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Dr Damian McLeod

Postdoctoral Fellow

School of Biomedical Sciences and Pharmacy (Human Physiology)

Career Summary

Biography

Research Expertise
- Stroke / cerebral ischaemia - Imaging the ischaemic penumbra using perfusion computed tomography (CTP) - Improving outcome and safety for thrombolysis in stroke - Mechanisms of hypothermic neuroprotection following ischaemic stroke - Effects of therapeutic hypothermia on intracranial pressure following stroke - Proteomic changes following stroke and therapeutic hypothermia - Cardiovascular and respiratory physiology - Neural control of the bronchial circulation during exercise - Exercise-induced asthma

Qualifications

  • PhD (Human Physiology), University of Newcastle
  • Bachelor of Biomedical Sciences (Hons), University of Newcastle

Keywords

  • Clinical Science
  • Medical Physiology
  • Stroke

Fields of Research

Code Description Percentage
110399 Clinical Sciences not elsewhere classified 100

Professional Experience

UON Appointment

Title Organisation / Department
Postdoctoral Fellow University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia
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Publications

For publications that are currently unpublished or in-press, details are shown in italics.


Journal article (22 outputs)

Year Citation Altmetrics Link
2015 Murtha LA, McLeod DD, Pepperall D, McCann SK, Beard DJ, Tomkins AJ, et al., 'Intracranial pressure elevation after ischemic stroke in rats: Cerebral edema is not the only cause, and short-duration mild hypothermia is a highly effective preventive therapy', Journal of Cerebral Blood Flow and Metabolism, 35 592-600 (2015)

In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equa... [more]

In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equates to higher ICP. We recently demonstrated a dramatic ICP elevation 24 hours after small ischemic strokes in rats, with minimal edema. This ICP elevation was completely prevented by short-duration moderate hypothermia soon after stroke. Here, our aims were to determine the importance of edema in ICP elevation after stroke and whether mild hypothermia could prevent the ICP rise. Experimental stroke was performed in rats. ICP was monitored and short-duration mild (35 °C) or moderate (32.5 °C) hypothermia, or normothermia (37 °C) was induced after stroke onset. Edema was measured in three studies, using wet-dry weight calculations, T 2 -weighted magnetic resonance imaging, or histology. ICP increased 24 hours after stroke onset in all normothermic animals. Short-duration mild or moderate hypothermia prevented this rise. No correlation was seen between ¿ICP and edema or infarct volumes. Calculated rates of edema growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than cerebral edema are the primary cause of the ICP elevation 24 hours after stroke onset.

DOI 10.1038/jcbfm.2014.230
Co-authors Neil Spratt
2015 Schmidt B, Reinhard M, Lezaic V, McLeod DD, Weinhold M, Mattes H, Klingelhöfer J, 'Autoregulation monitoring and outcome prediction in neurocritical care patients: Does one index fit all?', Journal of Clinical Monitoring and Computing, (2015)

Indexes PRx and Mx have been formerly introduced to assess cerebral autoregulation and have been shown to be associated with 3-month clinical outcome. In a mixed cohort of neurocr... [more]

Indexes PRx and Mx have been formerly introduced to assess cerebral autoregulation and have been shown to be associated with 3-month clinical outcome. In a mixed cohort of neurocritical care patients, we retrospectively investigated the impact of selected clinical characteristics on this association. Forty-one patients (18¿77 years) with severe traumatic (TBI, N = 20) and non-traumatic (N = 21) brain injuries were studied. Cerebral blood flow velocity, arterial blood pressure and intracranial pressure were repeatedly recorded during 1-h periods. Calculated PRx and Mx were correlated with 3-month clinical outcome score of modified Rankin Scale (mRS) in different subgroups with specific clinical characteristics. Both PRx and Mx correlated significantly with outcome (PRx: r = 0.38, p < 0.05; AUC = 0.64, n.s./Mx: r = 0.48, p < 0.005; AUC = 0.80, p < 0.005) in the overall group, and in patients with hemicraniectomy (N = 17; PRx: r = 0.73, p < 0.001; AUC = 0.89, p < 0.01/Mx: r = 0.69, p < 0.005; AUC = 0.87, p < 0.05). Mx, not PRx, correlated significantly with mRS in patients with heart failure (N = 17; r = 0.69, p < 0.005; AUC = 0.92, p < 0.005), and in non-traumatic patients (r = 0.49, p < 0.05; AUC = 0.79, p < 0.05). PRx, not Mx, correlated significantly with mRS in TBI patients (r = 0.63, p < 0.01; AUC = 0.89, p < 0.01). Both indexes did not correlate with mRS in diabetes patients (N = 15), PRx failed in hypocapnic patients (N = 26). Both PRx and Mx were significantly associated with 3-month clinical outcome, even in patients with hemicraniectomy. PRx was more appropriate for TBI patients, while Mx was better suited for non-traumatic patients and patients with heart failure. Prognostic values of indexes were affected by diabetes (both Mx and PRx) and hypocapnia (PRx only).

DOI 10.1007/s10877-015-9726-3
2015 Beard DJ, McLeod DD, Logan CL, Murtha LA, Imtiaz MS, van Helden DF, Spratt NJ, 'Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke.', J Cereb Blood Flow Metab, 35 861-872 (2015)
DOI 10.1038/jcbfm.2015.2
Co-authors Neil Spratt, Dirk Vanhelden
2015 Beard DJ, Mcleod DD, Logan CL, Murtha LA, Imtiaz MS, Van Helden DF, Spratt NJ, 'Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke', Journal of Cerebral Blood Flow and Metabolism, 35 861-872 (2015)

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arter... [more]

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.

DOI 10.1038/jcbfm.2015.2
Co-authors Neil Spratt, Dirk Vanhelden
2015 Beard DJ, Mcleod DD, Logan CL, Murtha LA, Imtiaz MS, Van Helden DF, Spratt NJ, 'Intracranial pressure elevation reduces flow through collateral vessels and the penetrating arterioles they supply. A possible explanation for 'collateral failure' and infarct expansion after ischemic stroke', Journal of Cerebral Blood Flow and Metabolism, 35 861-872 (2015)

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arter... [more]

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels ('collateral failure') is associated with late infarct expansion despite stable arterial occlusion. The cause for 'collateral failure' is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by >450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for 'collateral failure' in stroke-in-progression.

DOI 10.1038/jcbfm.2015.2
Co-authors Dirk Vanhelden, Neil Spratt
2015 Mcleod DD, Parsons MW, Hood R, Hiles B, Allen J, Mccann SK, et al., 'Perfusion computed tomography thresholds defining ischemic penumbra and infarct core: Studies in a rat stroke model', International Journal of Stroke, 10 553-559 (2015)

Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stro... [more]

Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stroke and guide reperfusion therapies. Aims: The study aims to determine whether there are important changes in perfusion computed tomography thresholds defining ischemic penumbra and infarct core over time following stroke. Methods: Permanent middle cerebral artery occlusion was performed in adult outbred Wistar rats (n=6) and serial perfusion computed tomography scans were taken every 30 mins for 2h. To define infarction thresholds at 1h and 2h post-stroke, separate groups of rats underwent 1h (n=6) and 2h (n=6) of middle cerebral artery occlusion followed by reperfusion. Infarct volumes were defined by histology at 24h. Co-registration with perfusion computed tomography maps (cerebral blood flow, cerebral blood volume, and mean transit time) permitted pixel-based analysis of thresholds defining infarction, using receiver operating characteristic curves. Results: Relative cerebral blood flow was the perfusion computed tomography parameter that most accurately predicted penumbra (area under the curve=0·698) and also infarct core (area under the curve=0·750). A relative cerebral blood flow threshold of <75% of mean contralateral cerebral blood flow most accurately predicted penumbral tissue at 0·5h (area under the curve=0·660), 1h (area under the curve=0·659), 1·5h (area under the curve=0·636), and 2h (area under the curve=0·664) after stroke onset. A relative cerebral blood flow threshold of <55% of mean contralateral most accurately predicted infarct core at 1h (area under the curve=0·765) and at 2h (area under the curve=0·689) after middle cerebral artery occlusion. Conclusions: The data provide perfusion computed tomography defined relative cerebral blood flow thresholds for infarct core and ischemic penumbra within the first two hours after experimental stroke in rats. These thresholds were shown to be stable to define the volume of infarct core and penumbra within this time window.

DOI 10.1111/ijs.12147
Citations Scopus - 1
Co-authors Neil Spratt, Chris Levi
2014 Spratt NJ, Tomkins AJ, Pepperall D, McLeod DD, Calford MB, 'Allopregnanolone and its precursor progesterone do not reduce injury after experimental stroke in hypertensive rats - role of postoperative temperature regulation?', PLoS One, 9 e107752 (2014) [C1]
DOI 10.1371/journal.pone.0107752
Co-authors Neil Spratt
2014 Murtha LA, Mcleod DD, Mccann SK, Pepperall D, Chung S, Levi CR, et al., 'Short-duration hypothermia after ischemic stroke prevents delayed intracranial pressure rise', International Journal of Stroke, 9 553-559 (2014)
DOI 10.1111/ijs.12181
Citations Scopus - 1
Co-authors Chris Levi, Neil Spratt
2014 Murtha LA, Mcleod DD, Mccann SK, Pepperall D, Chung S, Levi CR, et al., 'Short-duration hypothermia after ischemic stroke prevents delayed intracranial pressure rise', International Journal of Stroke, 9 553-559 (2014) [C1]

Background: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Thera... [more]

Background: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Therapeutic hypothermia improves outcome after cardiac arrest, is strongly neuroprotective in experimental stroke, and is under clinical trial in stroke. Hypothermia lowers elevated intracranial pressure; however, rebound intracranial pressure elevation and neurological deterioration may occur during rewarming. Hypotheses: (1) Intracranial pressure increases 24h after moderate and small strokes. (2) Short-duration hypothermia-rewarming, instituted before intracranial pressure elevation, prevents this 24h intracranial pressure elevation. Methods: Long-Evans rats with two hour middle cerebral artery occlusion or outbred Wistar rats with three hour middle cerebral artery occlusion had intracranial pressure measured at baseline and 24h. Wistars were randomized to 2·5h hypothermia (32·5°C) or normothermia, commencing 1h after stroke. Results: In Long-Evans rats (n=5), intracranial pressure increased from 10·9±4·6mmHg at baseline to 32·4±11·4mmHg at 24h, infarct volume was 84·3±15·9mm3. In normothermic Wistars (n=10), intracranial pressure increased from 6·7±2·3mmHg to 31·6±9·3mmHg, infarct volume was 31·3±18·4mm3. In hypothermia-treated Wistars (n=10), 24h intracranial pressure did not increase (7·0±2·8mmHg, P<0·001 vs. normothermia), and infarct volume was smaller (15·4±11·8mm3, P<0·05). Conclusions: We saw major intracranial pressure elevation 24h after stroke in two rat strains, even after small strokes. Short-duration hypothermia prevented the intracranial pressure rise, an effect sustained for at least 18h after rewarming. The findings have potentially important implications for design of future clinical trials. © 2013 The Authors. International Journal of Stroke © 2013 World Stroke Organization.

DOI 10.1111/ijs.12181
Citations Scopus - 6Web of Science - 5
Co-authors Neil Spratt, Chris Levi
2014 Murtha LA, McLeod DD, Pepperall D, McCann SK, Beard DJ, Tomkins AJ, et al., 'Intracranial pressure elevation after ischemic stroke in rats: cerebral edema is not the only cause, and short-duration mild hypothermia is a highly effective preventive therapy', Journal of Cerebral Blood Flow and Metabolism, (2014)

In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equa... [more]

In both the human and animal literature, it has largely been assumed that edema is the primary cause of intracranial pressure (ICP) elevation after stroke and that more edema equates to higher ICP. We recently demonstrated a dramatic ICP elevation 24 hours after small ischemic strokes in rats, with minimal edema. This ICP elevation was completely prevented by short-duration moderate hypothermia soon after stroke. Here, our aims were to determine the importance of edema in ICP elevation after stroke and whether mild hypothermia could prevent the ICP rise. Experimental stroke was performed in rats. ICP was monitored and short-duration mild (35¿°C) or moderate (32.5¿°C) hypothermia, or normothermia (37¿°C) was induced after stroke onset. Edema was measured in three studies, using wet¿dry weight calculations, T2-weighted magnetic resonance imaging, or histology. ICP increased 24 hours after stroke onset in all normothermic animals. Short-duration mild or moderate hypothermia prevented this rise. No correlation was seen between ¿ICP and edema or infarct volumes. Calculated rates of edema growth were orders of magnitude less than normal cerebrospinal fluid production rates. These data challenge current concepts and suggest that factors other than cerebral edema are the primary cause of the ICP elevation 24 hours after stroke onset.Journal of Cerebral Blood Flow & Metabolism advance online publication, 17 December 2014; doi:10.1038/jcbfm.2014.230.

DOI 10.1038/jcbfm.2014.230
Co-authors Neil Spratt
2014 Murtha LA, Yang Q, Parsons MW, Levi CR, Beard DJ, Spratt NJ, McLeod DD, 'Cerebrospinal fluid is drained primarily via the spinal canal and olfactory route in young and aged spontaneously hypertensive rats', Fluids and Barriers of the CNS, 11 (2014) [C1]

Background: Many aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the... [more]

Background: Many aspects of CSF dynamics are poorly understood due to the difficulties involved in quantification and visualization. In particular, there is debate surrounding the route of CSF drainage. Our aim was to quantify CSF flow, volume, and drainage route dynamics in vivo in young and aged spontaneously hypertensive rats (SHR) using a novel contrast-enhanced computed tomography (CT) method.Methods: ICP was recorded in young (2-5 months) and aged (16 months) SHR. Contrast was administered into the lateral ventricles bilaterally and sequential CT imaging was used to visualize the entire intracranial CSF system and CSF drainage routes. A customized contrast decay software module was used to quantify CSF flow at multiple locations.Results: ICP was significantly higher in aged rats than in young rats (11.52 ± 2.36 mmHg, versus 7.04 ± 2.89 mmHg, p = 0.03). Contrast was observed throughout the entire intracranial CSF system and was seen to enter the spinal canal and cross the cribriform plate into the olfactory mucosa within 9.1 ± 6.1 and 22.2 ± 7.1 minutes, respectively. No contrast was observed adjacent to the sagittal sinus. There were no significant differences between young and aged rats in either contrast distribution times or CSF flow rates. Mean flow rates (combined young and aged) were 3.0 ± 1.5 µL/min at the cerebral aqueduct; 3.5 ± 1.4 µL/min at the 3rd ventric= and 2.8 ± 0.9 µL/min at the 4th ventricle. Intracranial CSF volumes (and as percentage total brain volume) were 204 ± 97 µL (8.8 ± 4.3%) in the young and 275 ± 35 µL (10.8 ± 1.9%) in the aged animals (NS).Conclusions: We have demonstrated a contrast-enhanced CT technique for measuring and visualising CSF dynamics in vivo. These results indicate substantial drainage of CSF via spinal and olfactory routes, but there was little evidence of drainage via sagittal sinus arachnoid granulations in either young or aged animals. The data suggests that spinal and olfactory routes are the primary routes of CSF drainage and that sagittal sinus arachnoid granulations play a minor role, even in aged rats with higher ICP. © 2014 Murtha et al.; licensee BioMed Central Ltd.

DOI 10.1186/2045-8118-11-12
Citations Scopus - 5
Co-authors Mark Parsons, Chris Levi, Neil Spratt
2013 Mcleod DD, Parsons MW, Hood R, Hiles B, Allen J, Mccann SK, et al., 'Perfusion computed tomography thresholds defining ischemic penumbra and infarct core: Studies in a rat stroke model', International Journal of Stroke, (2013)

Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stro... [more]

Background: Perfusion computed tomography is becoming more widely used as a clinical imaging tool to predict potentially salvageable tissue (ischemic penumbra) after ischemic stroke and guide reperfusion therapies. Aims: The study aims to determine whether there are important changes in perfusion computed tomography thresholds defining ischemic penumbra and infarct core over time following stroke. Methods: Permanent middle cerebral artery occlusion was performed in adult outbred Wistar rats (n=6) and serial perfusion computed tomography scans were taken every 30 mins for 2h. To define infarction thresholds at 1h and 2h post-stroke, separate groups of rats underwent 1h (n=6) and 2h (n=6) of middle cerebral artery occlusion followed by reperfusion. Infarct volumes were defined by histology at 24h. Co-registration with perfusion computed tomography maps (cerebral blood flow, cerebral blood volume, and mean transit time) permitted pixel-based analysis of thresholds defining infarction, using receiver operating characteristic curves. Results: Relative cerebral blood flow was the perfusion computed tomography parameter that most accurately predicted penumbra (area under the curve=0·698) and also infarct core (area under the curve=0·750). A relative cerebral blood flow threshold of <75% of mean contralateral cerebral blood flow most accurately predicted penumbral tissue at 0·5h (area under the curve=0·660), 1h (area under the curve=0·659), 1·5h (area under the curve=0·636), and 2h (area under the curve=0·664) after stroke onset. A relative cerebral blood flow threshold of <55% of mean contralateral most accurately predicted infarct core at 1h (area under the curve=0·765) and at 2h (area under the curve=0·689) after middle cerebral artery occlusion. Conclusions: The data provide perfusion computed tomography defined relative cerebral blood flow thresholds for infarct core and ischemic penumbra within the first two hours after experimental stroke in rats. These thresholds were shown to be stable to define the volume of infarct core and penumbra within this time window. © 2013 World Stroke Organization.

DOI 10.1111/ijs.12147
Citations Scopus - 3
Co-authors Mark Parsons, Chris Levi, Neil Spratt
2013 McLeod DD, Beard DJ, Parsons MW, Levi CR, Calford MB, Spratt NJ, 'Inadvertent Occlusion of the Anterior Choroidal Artery Explains Infarct Variability in the Middle Cerebral Artery Thread Occlusion Stroke Model', PLOS ONE, 8 (2013) [C1]
DOI 10.1371/journal.pone.0075779
Citations Scopus - 3Web of Science - 2
Co-authors Neil Spratt, Chris Levi, Mark Parsons
2012 McLeod DD, Parsons G, Gunther R, Quail AW, Cottee DB, White SW, 'Differential effects of inhaled methacholine on circumferential wall and vascular smooth muscle of third-generation airways in awake sheep', Journal of Applied Physiology, 113 1233-1242 (2012) [C1]
Citations Scopus - 2Web of Science - 1
Co-authors Tony Quail, Saxon White
2011 McLeod DD, Parsons MW, Levi CR, Beautement S, Buxton D, Roworth B, Spratt NJ, 'Establishing a rodent stroke perfusion computed tomography model', International Journal of Stroke, 6 284-289 (2011) [C1]
DOI 10.1111/j.1747-4949.2010.00564.x
Citations Scopus - 10Web of Science - 9
Co-authors Mark Parsons, Neil Spratt, Chris Levi
2011 McIlveen SA, White SW, Quail AW, McLeod DD, Parsons G, 'Integration of baroreflex and autoregulation control of bronchial blood flow in awake dogs', Acta Physiologica, 203 299-310 (2011) [C1]
Citations Scopus - 2Web of Science - 2
Co-authors Tony Quail, Saxon White
2011 Spratt NJ, Donnan GA, McLeod DD, Howells DW, ''Salvaged' stroke ischaemic penumbra shows significant injury: Studies with the hypoxia tracer FMISO', Journal of Cerebral Blood Flow and Metabolism, 31 934-943 (2011) [C1]
DOI 10.1038/jcbfm.2010.174
Citations Scopus - 6Web of Science - 5
Co-authors Neil Spratt
2007 Parsons G, White SW, Quail AW, McIlveen SA, Bishop R, McLeod DD, et al., 'Autonomic control of bronchial blood flow and airway dimensions during strenuous exercise in sheep', Pulmonary Pharmacology & Therapeutics, 20 190-199 (2007) [C1]
DOI 10.1016/j.pupt.2006.03.010
Citations Scopus - 6Web of Science - 6
Co-authors Saxon White, Tony Quail
2007 Bishop R, McLeod DD, McIlveen SA, Blake RJ, Gunther R, Davis J, et al., 'Effects of graded exercise on bronchial blood flow and airway dimensions in sheep', Pulmonary Pharmacology & Therapeutics, 20 178-189 (2007) [C1]
DOI 10.1016/j.pupt.2006.03.003
Citations Scopus - 6Web of Science - 6
Co-authors Saxon White, Tony Quail
2003 Quail AW, Cottee DB, McLeod DD, Blake RJ, Bishop R, McIlveen SA, White SW, 'Analysis of Bronchovascular Downstream Blood Pressure Changes in Exercising Sheep', Archives of Physiology and Biochemistry, 111 309-313 (2003) [C1]
DOI 10.1080/13813450312331337469
Citations Scopus - 3
Co-authors Tony Quail, Saxon White
2003 Bishop R, McLeod DD, McIlveen SA, Blake RJ, Gunther R, Davis J, et al., 'Long-Term Measurement of Bronchial Vascular Resistance in Awake Sheep and Dogs', Archives of Physiology and Biochemistry, 111 315-315 (2003) [C1]
DOI 10.1080/13813450312331337478
Citations Scopus - 2
Co-authors Saxon White, Tony Quail
2003 White SW, McIlveen SA, Parsons G, Quail AW, Cottee DB, Gunther R, et al., 'Neural Control of the Bronchial Circulation', Archives of the Physiology and Biochemistry, 111 305-308 (2003) [C1]
DOI 10.1080/13813450312331337450
Citations Scopus - 6
Co-authors Tony Quail, Saxon White
Show 19 more journal articles

Conference (31 outputs)

Year Citation Altmetrics Link
2013 Beard D, McLeod D, Spratt N, 'The collateral circulation: key to outcome in mice and men', INTERNATIONAL JOURNAL OF STROKE (2013) [E3]
Co-authors Neil Spratt
2012 Murtha LA, McLeod DD, Spratt NJ, 'The effects of therapeutic hypothermia on intracranial pressure after experimental ischemic stroke', Abstracts. Australian Neuroscience Society 32nd Annual Meeting, Gold Coast, Queensland (2012) [E3]
Co-authors Neil Spratt
2012 Arulampalam A, McLeod DD, Spratt NJ, 'Fluid shifts in the rat brain after ischaemic stroke', Abstracts. Australian Neuroscience Society 32nd Annual Meeting, Gold Coast, Queensland (2012) [E3]
Co-authors Neil Spratt
2012 White SW, McLeod DD, Parsons G, Gunther R, Cottee DB, Quail AW, 'Selective effects of inhaled methacholine on 3rd generation bronchial blood flow and airway dimensions in awake sheep', FASEB Journal, San Diego, CA (2012) [E3]
Co-authors Tony Quail, Saxon White
2012 McLeod DD, Murtha LA, Pitsillides K, 'A new method of attaching a solid-state pressure sensor for measurement of chronic intracranial pressure in freely moving rats using biotelemetry', FASEB Journal, San Diego, CA (2012) [E3]
2012 Beard DJ, McLeod DD, Imtiaz MS, Spratt NJ, 'Quantitative assessment of leptomeningeal collateral flow in experimental stroke', The Stroke Interventionalist, Los Angeles, CA (2012) [E3]
Co-authors Neil Spratt
2012 McLeod DD, Beard DJ, Imtiaz MS, Spratt NJ, 'Validating a novel method for measuring leptomeningeal collateral flow in experimental stroke', The Stroke Interventionalist, Los Angeles, CA (2012) [E3]
Co-authors Neil Spratt
2012 Quail AW, Cottee DB, McLeod DD, Hamut M, White SW, 'Comparative effects of isoflurane, sevoflurane and desflurane on resting airway dimensions in the sheep', ANZCA ASM 2012. Evolution: Grow Develop Thrive: ePoster Sessions 2012, Perth, WA (2012) [E3]
Co-authors Saxon White, Tony Quail
2011 Murtha LA, McLeod DD, McCann S, Pepperall D-G, Spratt NJ, 'Short duration hypothermia results in sustained prevention of intracranial pressure elevation following experimental stroke', International Journal of Stroke, Adelaide, SA (2011) [E3]
Co-authors Neil Spratt
2011 White SW, McLeod DD, Parsons GH, Gunther RA, Cottee DB, Quail AW, 'Inhaled and intravenous methacholine evoke differential effects on bronchial blood flow and 3rd generation airway dimensions in awake sheep', Proceedings of the Australian Physiological Society 2011, Perth (2011) [E3]
Co-authors Saxon White, Tony Quail
2011 Hamut M, Quail AW, Seah PW, McLeod DD, Cottee DB, White SW, 'Mammalian differences in vagal-cholinoceptor control of coronary conductance', The FASEB journal, Washington, DC (2011) [E3]
Co-authors Tony Quail, Saxon White
2009 McLeod DD, Spratt NJ, Levi CR, Beautement S, Roworth B, Buxton D, et al., 'Experimental validation of perfusion computed tomography in acute middle cerebral artery occlusion', ACBRC 2009 Abstracts, Tianjin, China (2009) [E3]
Co-authors Neil Spratt, Chris Levi, Mark Parsons
2009 McLeod DD, Parsons MW, Levi CR, Beautement S, Roworth B, Buxton D, et al., 'An experimental model to investigate CT brain perfusion after stroke', ANS 2009 Abstracts: Posters, Canberra, ACT (2009) [E3]
Co-authors Mark Parsons, Neil Spratt, Chris Levi
2009 McLeod DD, 'Evaluation of a modified airways internal diameter assessment: Sonomicrometer for analysis of third generation airway reflexes in anesthetized and awake sheep', ISAN Satellite Meeting. Autonomic Adjustments to Environmental Challenges. Final Program, Newcastle, NSW (2009) [E3]
2009 McLeod DD, Spratt NJ, Levi CR, Beautement S, Roworth B, Buxton D, et al., 'Perfusion computed tomography for acute stroke: A model for experimental validation', Cerebrovascular Diseases, Stockholm, Sweden (2009) [E3]
DOI 10.1159/000221776
Co-authors Chris Levi, Mark Parsons, Neil Spratt
2008 McLeod DD, Gunther R, Seah PW, Quail AW, Cottee DB, Parsons G, White SW, 'Integrated autonomic control of the bronchial circulation and 3rd generation bronchus in the exercising sheep', American Journal of Respiratory and Critical Care Medicine, Toronto, ONT (2008) [E3]
Co-authors Tony Quail, Saxon White
2008 Hamut M, Quail AW, Cottee DB, Seah PW, McLeod DD, Blake RJ, White SW, 'Effects of evoked acute and steady-state high blood pressure on control of right and left coronary blood flow and conductance in awake sheep', Journal of Hypertension, Berlin, Germany (2008) [E3]
Co-authors Tony Quail, Saxon White
2007 Robinson S, McLeod DD, Gunther R, Quail AW, White SW, Parsons G, 'High frequency oscillatory ventilation (HFOV) effects on airway blood flow and airway caliber in sheep', American Journal of Respiratory and Critical Care Medicine, San Francisco, Calif. (2007) [E3]
Co-authors Saxon White, Tony Quail
2007 McLeod DD, Robinson S, Gunther R, Quail AW, Cottee DB, Seah P, et al., 'Effects of graded PEEP on bronchial blood flow and dimensions', American Journal of Respiratory and Critical Care Medicine, San Francisco, Calif. (2007) [E3]
Co-authors Saxon White, Tony Quail
2007 Hamut M, Quail AW, Cottee DB, Seah PW, McLeod DD, Blake RJ, White SW, 'Baroreflex-autonomic control of regional coronary blood flow conductance in awake sheep', Proceedings of the Australian Physiological Society, Newcastle, N.S.W. (2007) [E3]
Co-authors Tony Quail, Saxon White
2007 White SW, Parsons G, MacTaggart G, McLeod DD, Hamut M, Cottee DB, Quail AW, 'Controversy: Exercise-induced pulmonary haemorrhage in the horse', Proceedings of the Australian Physiological Society, Newcastle, N.S.W. (2007) [E3]
Co-authors Saxon White, Tony Quail
2007 McLeod DD, Gunther R, Seah PW, Quail AW, Cottee DB, Parsons G, White SW, 'Integrated autonomic control of the bronchial circulation and 3rd generation airway dimensions during exercise in awake sheep', Proceedings of the Australian Physiological Society, Newcastle, N.S.W. (2007) [E3]
Co-authors Tony Quail, Saxon White
2007 Quail AW, Cottee DB, Seah PW, McLeod DD, Blake RJ, White SW, 'Evolutionary aspects of neural control of coronary blood flow', Proceedings of the Australian Physiological Society, Newcastle, N.S.W. (2007) [E3]
Co-authors Saxon White, Tony Quail
2006 McLeod DD, Bastian F, Parsons G, Gunther R, Quail AW, Cottee DB, White SW, 'Graded exercise evokes bronchovascular and lower airway smooth muscle constriction', Abstracts from AuPS/Combio Brisbane 2006 (Proceedings of the Australian Physiological Society Vol 37), Brisbane (2006) [E3]
Co-authors Tony Quail, Saxon White
2006 White SW, McLeod DD, McIlveen SA, Bishop R, Gunther R, Cottee DB, Parsons G, 'Autonomic control of bronchial blood flow, airway circumference and airway wall thickness during strenuous exercise in sheep (Poster presentation)', Abstracts of the Experimental Biology 2006 Meeting (FASEB Journal vol 20, no 5), San Francisco, CA (2006) [E3]
Co-authors Saxon White
2006 McLeod DD, Parsons G, Bishop R, McIlveen SA, Gunther R, Cottee DB, et al., 'Effects of graded exercise on bronchial blood flow and airway dimensions in sheep', Experimental Biology 2006: Meeting Abstracts, San Francisco (2006) [E3]
Co-authors Saxon White, Tony Quail
2006 Hamut M, Quail AW, Cottee DB, Seah PW, Blake RJ, White SW, et al., 'Development of a chronic sheepp model for the study of regional coronary control mechanisms', Experimental Biology 2006: Meeting Abstracts, San Francisco (2006) [E3]
Co-authors Saxon White, Tony Quail
2006 White SW, McLeod DD, Parsons G, Gunther R, McIlveen SA, Bishop R, et al., 'Autonomic control of airways vascular and wall smooth muscle during exercise', Proceedings of the Australian Physiological Society, Brisbane (2006) [E3]
Co-authors Saxon White, Tony Quail
2005 McLeod DD, Parsons G, Gunther R, McIlveen SA, Bishop R, White SW, et al., 'Neural factors controlling bronchial blood flow during exercise', The FASEB Journal, San Diego, USA (2005) [E3]
Citations Web of Science - 2
Co-authors Saxon White, Tony Quail
2004 White SW, McIlveen SA, Bishop R, McLeod DD, Blake RJ, Gunther R, et al., 'Mechanisms controlling airways circulation during exercise', Proccedings of the Australian Health and Medical Research Congress 2004, Sydney (2004) [E3]
Co-authors Tony Quail, Saxon White
2004 Quail AW, Cottee DB, McLeod DD, Blake RJ, Bishop R, McIlveen SA, et al., 'Neural and pressure gradient factors controlling bronchial blood flow in exercising sheep', -, Royal North Shore Hospital, Sydney (2004) [E1]
Co-authors Tony Quail, Saxon White
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Grants and Funding

Summary

Number of grants 15
Total funding $194,984

Click on a grant title below to expand the full details for that specific grant.


20153 grants / $41,845

Stroke In Progression: a new understanding of pathophysiology opening the door to effective therapy$25,222

Funding body: John Hunter Hospital Charitable Trust Fund

Funding body John Hunter Hospital Charitable Trust Fund
Project Team Doctor Ferdinand Miteff, Doctor Damian McLeod, Mr Daniel Beard, Doctor Lucy Murtha, Doctor Neil Spratt
Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500830
Type Of Funding Other Public Sector - State
Category 2OPS
UON Y

A better understanding of intracranial pressure changes after brain injury$15,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Neil Spratt, Doctor Damian McLeod, Miss Lucy Murtha, Mr Daniel Beard
Scheme Research Grant
Role Investigator
Funding Start 2015
Funding Finish 2015
GNo G1500709
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

The XXVIIth International SYmposium on Cerebral Blood Flow, Metabolism and Function & XIIthe International Conference on Quantification of Brain Function with PET, Canada 26-30 June$1,623

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Damian McLeod
Scheme Travel Grant
Role Lead
Funding Start 2015
Funding Finish 2015
GNo G1500883
Type Of Funding Internal
Category INTE
UON Y

20141 grants / $19,275

Cooling the brain via the skin to prevent intracranial pressure elevation after stroke$19,275

Funding body: National Stroke Foundation

Funding body National Stroke Foundation
Project Team Doctor Damian McLeod, Doctor Neil Spratt
Scheme Research Grant
Role Lead
Funding Start 2014
Funding Finish 2014
GNo G1301145
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20132 grants / $21,500

Novel mechanisms of ‘Stroke-in-Progression’: Intracranial pressure elevation and collateral blood vessel failure after minor stroke$20,000

Funding body: National Stroke Foundation

Funding body National Stroke Foundation
Project Team Doctor Damian McLeod, Doctor Neil Spratt
Scheme Research Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1201084
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

The XXVth International Symposium on Cerebral Blood flow, Metabolism and function & XIth International Conference on Quantification of Brain Function with PET, Shanghai, China, 20 - 23 May 2013$1,500

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Damian McLeod
Scheme Travel Grant
Role Lead
Funding Start 2013
Funding Finish 2013
GNo G1300541
Type Of Funding Internal
Category INTE
UON Y

20122 grants / $21,500

Experimental brain imaging to investigate novel protective mechanisms of short duration body cooling after stroke$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Damian McLeod, Doctor Neil Spratt, Professor Mark Parsons, Conjoint Professor Chris Levi
Scheme Project Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1101116
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

International Symposium of Collaterals to the Brain, Los Angeles, California, USA, 6 - 8 November 2012$1,500

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Damian McLeod
Scheme Travel Grant
Role Lead
Funding Start 2012
Funding Finish 2012
GNo G1200951
Type Of Funding Internal
Category INTE
UON Y

20112 grants / $4,100

The effect of stroke on cranial compartment volumes and intracranial pressure$2,600

Funding body: National Stroke Foundation

Funding body National Stroke Foundation
Project Team Doctor Damian McLeod, Doctor Neil Spratt
Scheme Research Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1100727
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

XXVth International Symposium on Cerebral Blood Flow, Metabolism and Function and the Xth International Conference on Quantification of Brain Function with PET$1,500

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Damian McLeod
Scheme Travel Grant
Role Lead
Funding Start 2011
Funding Finish 2011
GNo G1100304
Type Of Funding Internal
Category INTE
UON Y

20102 grants / $52,064

Improving patient selection for acute stroke therapies - an experimental model of CT brain perfusion after stroke$50,000

Funding body: BellBerry Limited

Funding body BellBerry Limited
Project Team Professor Mark Parsons, Doctor Neil Spratt, Conjoint Professor Chris Levi, Doctor Damian McLeod, Dr Peter Stanwell
Scheme Near Miss
Role Investigator
Funding Start 2010
Funding Finish 2010
GNo G0900222
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

Effects of therapeutic hypothermia and rewarming on intracranial pressure in experimental stroke$2,064

Funding body: National Stroke Foundation

Funding body National Stroke Foundation
Project Team Doctor Damian McLeod, Doctor Neil Spratt, Professor Mike Calford
Scheme Honours Grant
Role Lead
Funding Start 2010
Funding Finish 2010
GNo G1000608
Type Of Funding Grant - Aust Non Government
Category 3AFG
UON Y

20093 grants / $34,700

Establishing Computed Tomography Perfusion (CTP) imaging in an animal stroke model$20,000

Funding body: National Stroke Foundation

Funding body National Stroke Foundation
Project Team Doctor Damian McLeod, Doctor Neil Spratt, Professor Mike Calford, Conjoint Professor Chris Levi, Professor Mark Parsons
Scheme Research Grant
Role Lead
Funding Start 2009
Funding Finish 2009
GNo G0189942
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

Towards better early imaging in stroke: Use of an experimental model to investigate CT brain perfusion$13,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Doctor Neil Spratt, Professor Mark Parsons, Doctor Damian McLeod, Conjoint Professor Chris Levi
Scheme Stroke Research Project Grant
Role Investigator
Funding Start 2009
Funding Finish 2009
GNo G0189810
Type Of Funding Contract - Aust Non Government
Category 3AFC
UON Y

XVII European Stroke Conference, Stockholm Sweden, 26-29 May 2009$1,700

Funding body: University of Newcastle - Faculty of Health and Medicine

Funding body University of Newcastle - Faculty of Health and Medicine
Project Team Doctor Damian McLeod
Scheme Travel Grant
Role Lead
Funding Start 2009
Funding Finish 2009
GNo G0190140
Type Of Funding Internal
Category INTE
UON Y
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Research Supervision

Current Supervision

Commenced Research Title / Program / Supervisor Type
2015 Cooling the Skin while Maintaining Normal Core Temperature to Prevent Intracranial Pressure Elevation and Improve Outcome after Stroke
Human Biology, Faculty of Health and Medicine
Co-Supervisor
2011 A New Understanding of Factors Regulating Collateral Blood Flow during Ischaemic Stroke: Elevated Intracranial Pressure is a Potential Cause of Collateral Failure in Patients with Stroke-in-Progression
Human Biology, Faculty of Health and Medicine
Co-Supervisor

Past Supervision

Year Research Title / Program / Supervisor Type
2015 The Effects and Mechanisms of Therapeutic Hypothermia on Intracranial Pressure Regulation Following Ischaemic Stroke in Rats
Human Biology, Faculty of Health and Medicine
Co-Supervisor
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Dr Damian McLeod

Position

Postdoctoral Fellow
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine

Focus area

Human Physiology

Contact Details

Email damian.mcleod@newcastle.edu.au
Phone (02) 4921 7856
Fax (02) 4921 7903

Office

Room MS503
Building Medical Sciences
Location Callaghan
University Drive
Callaghan, NSW 2308
Australia
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