2022 |
Thiruvenkatarajan V, Dharmalingam A, Arenas G, Wahba M, Liu W-M, Zaw Y, et al., 'Effect of high-flow vs. low-flow nasal plus mouthguard oxygen therapy on hypoxaemia during sedation: a multicentre randomised controlled trial.', Anaesthesia, 77 46-53 (2022) [C1]
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Nova |
2022 |
Panwar R, Van Haren F, Cazzola F, Nourse M, Brinkerhoff G, Quail A, 'Standard care versus individualized blood pressure targets among critically ill patients with shock: A multicenter feasibility and preliminary efficacy study', Journal of Critical Care, 70 (2022) [C1]
Purpose: Emerging evidence suggests that minimizing mean perfusion pressure (MPP) deficit during vasopressor therapy for shock can potentially reduce adverse kidney-related outcom... [more]
Purpose: Emerging evidence suggests that minimizing mean perfusion pressure (MPP) deficit during vasopressor therapy for shock can potentially reduce adverse kidney-related outcomes in ICU. We assessed feasibility and preliminary efficacy of individualizing MPP targets based on patients' own pre-illness basal-MPP among vasopressor-treated patients with shock. Material and methods: In this prospective before-and-after trial, 31 patients during the ¿before¿/observational phase and 31 patients during the ¿after¿/intervention phase were enrolled at two tertiary-level Australian ICUs. Feasibility endpoint was time-weighted average MPP-deficit during vasopressor therapy. Preliminary efficacy outcomes were new significant AKI, major adverse kidney events within 14 days (MAKE-14), and 90-day mortality. Results: Patients in the after group had lower MPP-deficit (median 18%, [interquartile range [IQR]: 11¿23] vs. 4%, [IQR: 2¿9], p < 0.001) and lower incidence of new significant AKI (8/31 [26%] vs. 1/31 [3%], p = 0.01) than the before group. The between-group differences in MAKE-14 (9/31 [29%] vs. 4/31 [13%], p = 0.12) and 90-day mortality (6/31 [19%] vs. 2/31 [6%], p = 0.13) were not statistically significant. Conclusions: An individualized blood pressure target strategy during vasopressor therapy in ICU was feasible and appeared to be efficacious in this preliminary study. Testing this strategy in a larger randomized controlled trial is warranted. Study registration: ACTRN12617001459314.
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Nova |
2020 |
Thiruvenkatarajan V, Dharmalingam A, Arenas G, Wahba M, Steiner R, Kadam VR, et al., 'High-flow nasal cannula versus standard oxygen therapy assisting sedation during endoscopic retrograde cholangiopancreatography in high risk cases (OTHER): study protocol of a randomised multicentric trial', TRIALS, 21 (2020)
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2018 |
Panwar R, Sullohern B, Shiel E, Alexis Brown C, Quail A, 'Validity of a protocol to estimate patients pre-morbid basal blood pressure
Purpose: The pre-illness basal mean arterial BP (MAP) is an important reference point to gauge the degree of relative hypotension among unwell patients. We aimed to assess mean bi... [more]
Purpose: The pre-illness basal mean arterial BP (MAP) is an important reference point to gauge the degree of relative hypotension among unwell patients. We aimed to assess mean bias, correlation, and agreement between basal MAP measured during nighttime ambulatory BP monitoring (ABPM) and basal MAP estimated using a standardized protocol. Materials and methods: For a cohort of 137 consecutive patients, aged =40 years, who recently underwent ABPM, a blinded investigator estimated basal MAP from up to five most recent clinic BP measurements. Both basal MAP values, measured and estimated, were compared pairwise for each participant. Results: We traced a median of 4 [interquartile range 3¿5] previous BP measurements per patient over a median period of 132 [interquartile range 55¿277] days up until the ABPM test. The estimated basal MAP (mean 88 ± 8 mmHg) was linearly related (Pearson¿s r = 0.41, p = 0.0001) to the measured basal MAP (mean 88 ± 12 mmHg). Bland-Altman plot revealed a mean bias of 0.3 mmHg with agreement limits of ±22 mmHg. Conclusions: The mean bias between estimated and measured values for basal MAP was insignificant and modest. When a recent nighttime ABPM is unavailable, a protocol based on recent clinic BP readings can be used to estimate patient¿s basal MAP. Study registration: Australian New Zealand Clinical Trials Registry ACTRN12613001382763.
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Nova |
2018 |
Brady J, Hardy BM, Yoshino O, Buxton A, Quail A, Balogh ZJ, 'The effect of haemorrhagic shock and resuscitation on fracture healing in a rabbit model: An animal study', Bone and Joint Journal, 100B 1234-1240 (2018) [C1]
Aims: Little is known about the effect of haemorrhagic shock and resuscitation on fracture healing. This study used a rabbit model with a femoral osteotomy and fixation to examine... [more]
Aims: Little is known about the effect of haemorrhagic shock and resuscitation on fracture healing. This study used a rabbit model with a femoral osteotomy and fixation to examine this relationship. Materials and Methods: A total of 18 male New Zealand white rabbits underwent femoral osteotomy with intramedullary fixation with 'shock' (n = 9) and control (n = 9) groups. Shock was induced in the study group by removal of 35% of the total blood volume 45 minutes before resuscitation with blood and crystalloid. Fracture healing was monitored for eight weeks using serum markers of healing and radiographs. Results: Four animals were excluded due to postoperative complications. The serum concentration of osteocalcin was significantly elevated in the shock group postoperatively (p < 0.0001). There were otherwise no differences with regard to serum markers of bone healing. The callus index was consistently increased in the shock group on anteroposterior (p = 0.0069) and lateral (p = 0.0165) radiographs from three weeks postoperatively. The control group showed an earlier decrease of callus index. Radiographic scores were significantly greater in the control group (p = 0.0025). Conclusion: In a rabbit femoral osteotomy model with intramedullary fixation, haemorrhagic shock and resuscitation produced larger callus but with evidence of delayed remodelling.
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Nova |
2017 |
Laver DR, Attia J, Oldmeadow C, Quail AW, 'Cardiac Calcium Release Channel (Ryanodine Receptor 2) Regulation by Halogenated Anesthetics', Anesthesiology, 126 495-506 (2017) [C1]
Background: Halogenated anesthetics activate cardiac ryanodine receptor 2-mediated sarcoplasmic reticulum Ca 2+ release, leading to sarcoplasmic reticulum Ca 2+ depletion, reduced... [more]
Background: Halogenated anesthetics activate cardiac ryanodine receptor 2-mediated sarcoplasmic reticulum Ca 2+ release, leading to sarcoplasmic reticulum Ca 2+ depletion, reduced cardiac function, and providing cell protection against ischemia-reperfusion injury. Anesthetic activation of ryanodine receptor 2 is poorly defined, leaving aspects of the protective mechanism uncertain. Methods: Ryanodine receptor 2 from the sheep heart was incorporated into artificial lipid bilayers, and their gating properties were measured in response to five halogenated anesthetics. Results: Each anesthetic rapidly and reversibly activated ryanodine receptor 2, but only from the cytoplasmic side. Relative activation levels were as follows: halothane (approximately 4-fold; n = 8), desflurane and enflurane (approximately 3-fold,n = 9), and isoflurane and sevoflurane (approximately 1.5-fold, n = 7, 10). Half-activating concentrations (K a) were in the range 1.3 to 2.1 mM (1.4 to 2.6 minimum alveolar concentration [MAC]) with the exception of isoflurane (5.3 mM, 6.6 minimum alveolar concentration). Dantrolene (10 µM with 100 nM calmodulin) inhibited ryanodine receptor 2 by 40% but did not alter the K a for halothane activation. Halothane potentiated luminal and cytoplasmic Ca 2+ activation of ryanodine receptor 2 but had no effect on Mg 2+ inhibition. Halothane activated ryanodine receptor 2 in the absence and presence (2 mM) of adenosine triphosphate (ATP). Adenosine, a competitive antagonist to ATP activation of ryanodine receptor 2, did not antagonize halothane activation in the absence of ATP. Conclusions: At clinical concentrations (1 MAC), halothane desflurane and enflurane activated ryanodine receptor 2, whereas isoflurane and sevoflurane were ineffective. Dantrolene inhibition of ryanodine receptor 2 substantially negated the activating effects of anesthetics. Halothane acted independently of the adenine nucleotide-binding site on ryanodine receptor 2. The previously observed adenosine antagonism of halothane activation of sarcoplasmic reticulum Ca 2+ release was due to competition between adenosine and ATP, rather than between halothane and ATP.
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Nova |
2017 |
Yoshino O, Brady J, Young K, Hardy B, Matthys R, Buxton T, et al., 'Reamed locked intramedullary nailing for studying femur fracture and its complications', European Cells and Materials, 34 99-107 (2017) [C1]
Morbidity associated with femur fractures in polytrauma patients is known to be high. The many unsolved clinical questions include the immunological effect of the fracture and its... [more]
Morbidity associated with femur fractures in polytrauma patients is known to be high. The many unsolved clinical questions include the immunological effect of the fracture and its fixation, timing of fracture fixation, management of fracture non-union, effect of infection and critical size of bone defects. The aim of this study was to establish a clinically-relevant and reproducible animal model with regards to histological, biomechanical and radiological changes during bone healing. A custom-designed intramedullary nail with interlocking system (RabbitNail, RISystem AG, Davos Platz, Switzerland) was used for fixation, following femur fracture. New Zealand White rabbits were assigned to two groups: 1. closed fracture model (CF; non-survival model: n = 6, survival model: n = 3) with unilateral mid-shaft femur fracture created by blunt force; 2. osteotomy model (OT; survival model: n = 14) with unilateral transverse osteotomy creating femur fracture. There were no intraoperative complications and full-weight bearing was achieved in all survival rabbits. Significant periosteal reaction and callus formation were confirmed from 2 weeks postoperatively, with a significant volume formation (739.59 ± 62.14 mm3) at 8 weeks confirmed by micro-computed tomography (µ-CT). 2 months after fixation, there was no difference between the osteotomised and contralateral control femora in respect to the maximum torque (3.47 ± 0.35 N m vs. 3.26 ± 0.37 N m) and total energy (21.11 ± 3.09 N m × degree vs. 20.89 ± 2.63 N m × degree) required to break the femur. The data confirmed that a standardised internal fixation technique with an intramedullary nail for closed fracture or osteotomy produced satisfactory bone healing. It was concluded that important clinically-relevant studies can be conducted using this rabbit model.
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Nova |
2014 |
Walweel K, Li J, Molenaar P, Imtiaz MS, Quail A, dos Remedios CG, et al., 'Differences in the regulation of RyR2 from human, sheep, and rat by Ca² and Mg² in the cytoplasm and in the lumen of the sarcoplasmic reticulum.', J Gen Physiol, 144 263-271 (2014) [C1]
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Nova |
2012 |
Yoshino O, Quail AW, Oldmeadow CJ, Balogh ZJ, 'The interpretation of intra-abdominal pressures from animal models: The rabbit to human example', Injury: International Journal of the Care of the Injured, 43 169-173 (2012) [C1]
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Nova |
2012 |
Hardy BM, Yoshino O, Quail AW, Balogh ZJ, 'Influence of the timing of internal fixation of femur fractures during shock resuscitation on remote organ damage', ANZ Journal of Surgery, 82(S1) 177 (2012) [E3]
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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]
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Nova |
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]
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Nova |
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]
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Nova |
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]
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Nova |
2003 |
Quail A, Cottee D, McLeod D, Blake R, Bishop R, McIlveen S, White S, 'Analysis of bronchovascular downstream blood pressure changes in exercising sheep.', Arch Physiol Biochem, 111 309-313 (2003)
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2003 |
Bishop R, McLeod D, McIlveen S, Blake R, Gunther R, Davis J, et al., 'Long-term measurement of bronchial vascular resistance in awake sheep and dogs.', Arch Physiol Biochem, 111 315-316 (2003)
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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]
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Nova |
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]
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Nova |
2003 |
White S, McIlveen S, Parsons G, Quail A, Cottee D, Gunther R, et al., 'Neural control of the bronchial circulation.', Archives of physiology and biochemistry, 111 305-308 (2003)
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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]
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Nova |
2002 |
Chen C-Y, Munch P, Quail AW, Bonham A, 'Postexercise hypotension in conscious SHR is attenuated by blockade of substance P receptors in NTS', American Journal of Physiology-Heart and Circulatory Physiology, 283 H1856-H1862 (2002) [C1]
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Nova |
2002 |
Quail AW, White S, 'Differential Response of Canine Left Coronary Beds to Calcitonin Gene-Related Peptide and Adenosine', Journal of the American College of Cardiology, 39, No 9 Sup B 451B (2002) [C3] |
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2002 |
Chen CY, Munch PA, Quail AW, Bonham AC, 'Post-exercise hypotension in conscious SHR is attenuated by blockade of substance P receptors in nucleus tractus solitarius', FASEB JOURNAL, 16 A115-A115 (2002) |
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2002 |
White S, McIlveen S, Bishop R, Quail AW, Cottee D, Parsons G, et al., 'Mechanisms of Bronchial Blood Flow Response During and After Exercise in Sheep', Proceedings of the Australian Health and Medical Research Congress 2002, n/a #2427 (2002) [C3] |
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2000 |
Quail AW, 'Proceedings of the Australian Physiological and Pharmacological Society Symposium: Integrative cardiovascular function', CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 27 1013-1013 (2000)
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2000 |
Porges W, Hennessy E, Quail AW, Cottee D, Moore P, McIlveen SA, et al., 'Heart-Lung Interactions: The sigh and autonomic control in the bronchial and coronary circulations', Clinical and Experimental Pharmacology and Physiology, 27 1022-1027 (2000) [C1]
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Nova |
2000 |
Quail AW, Cottee D, Porges W, White SW, 'Recent views on integrated coronary control: significance of non-uniform regional control of coronary flow conductance', Clinical and Experimental Pharmacology and Physiology, 27 1039-1044 (2000) [C1]
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Nova |
2000 |
Cottee D, Quail AW, Porges W, Moore P, White SW, 'Effects of anaesthesia on regional coronary control mechanisms', Clinical and Experimental Pharmacology and Physiology, 27 1034-1038 (2000) [C1]
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Nova |
2000 |
Moore P, Quail AW, Cottee D, McIlveen SA, White SW, 'Effect of fentanyl on baroreflex control of circumflex coronary conductance', Clinical and Experimental Pharmacology and Physiology, 27 1028-1033 (2000) [C1]
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Nova |
1999 |
MacPherson R, Quail AW, 'Halothane Attentuates Myogenicity in the Rabbit Ear Artery', Anesthesia & Analgesia, 89(6) 1400-1405 (1999) [C1]
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1999 |
Buckner PS, Quail AW, Cottee DB, White SW, 'Venous hydrostatic indifference point as a marker of postnatal adaptation to orthostasis in swine', Journal of Applied Physiology, 87 882-888 (1999) [C1]
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1997 |
Sestan JR, Quail A, Leitch J, 'A dynamic graphical arrhythmia trainer', JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 29 12512-12512 (1997) |
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1996 |
Quail AW, Cottee DB, White SW, Porges WL, Hennessy EJ, 'Baroreflex Control of Coronary Blood Flow Varies Regionally in Awake Dogs', Clinical and Experimental Pharmacology and Physiology, 23 866-873 (1996) [C1]
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Nova |
1996 |
Harrigan PWJ, Browne SM, Quail AW, 'Multiple seizures following re-exposure to propofol', ANAESTHESIA AND INTENSIVE CARE, 24 261-264 (1996)
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1993 |
Hennessy E, White S, Van Der Touw T, Quail AW, Porges WL, Glenfield P, 'Control of Resting Bronchial Hemodynamics in the Awake Dog', American Journal of Physiology 265: (Heart Circ Physiol. 34), 265 649-660 (1993) [C1]
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Nova |
1993 |
Quail AW, Cottee DB, White SW, 'Limitation of a pulsed Doppler velocimeter for blood flow measurement in small vessels', Journal Applied Physiology, 75 2745-2754 (1993) [C1]
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Nova |
1991 |
Buchanan A, White SW, Walters WA, Redman S, Quail AW, Cottee DBF, Hennessy EJ, 'Teenage ballet dancers as a model of the female athlete: sensitivity of endocrine control in the menstrual cycle to exercise', Australian Journal of Science and Medicine in Sport, 24 63-67 (1991)
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1990 |
WHITE SW, QUAIL AW, DELEEUW PW, TRAUGOTT FM, BROWN WJ, PORGES WL, COTTEE DB, 'IMPEDANCE CARDIOGRAPHY FOR CARDIAC-OUTPUT MEASUREMENT - AN EVALUATION OF ACCURACY AND LIMITATIONS', EUROPEAN HEART JOURNAL, 11 79-92 (1990)
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1989 |
QUAIL AW, 'MODERN INHALATIONAL ANESTHETIC AGENTS - A REVIEW OF HALOTHANE, ISOFLURANE AND ENFLURANE', MEDICAL JOURNAL OF AUSTRALIA, 150 95-102 (1989)
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1989 |
QUAIL AW, 'THE SURGEON AS A PATIENT - COMMENT', MEDICAL JOURNAL OF AUSTRALIA, 150 223-223 (1989) |
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1988 |
MOORE PG, WHITE SW, PORGES WL, GAZIBARICH GJ, QUAIL AW, 'ROLE OF ARGININE VASOPRESSIN IN OPIOID MEDIATED CORONARY VASOCONSTRICTION', AUSTRALIAN AND NEW ZEALAND JOURNAL OF MEDICINE, 18 367-367 (1988)
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1988 |
WHITE S, QUAIL A, 'NASOPHARYNGEAL REFLEXES - ROLE OF BRAIN MONOAMINES IN CENTRAL INTEGRATION - A REVIEW', CANADIAN JOURNAL OF ZOOLOGY-REVUE CANADIENNE DE ZOOLOGIE, 66 173-181 (1988)
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1987 |
Head GA, Quail AW, Woods RL, 'Lesions of A1 noradrenergic cells affect AVP release and heart rate during hemorrhage', American Journal of Physiology - Heart and Circulatory Physiology, 253 (1987)
The role of A1 noradrenergic cells of the ventrolateral medulla in the changes in mean arterial pressure (MAP), heart rate (HR), and plasma arginine vasopressin (AVP) after slow c... [more]
The role of A1 noradrenergic cells of the ventrolateral medulla in the changes in mean arterial pressure (MAP), heart rate (HR), and plasma arginine vasopressin (AVP) after slow continuous hemorrhage (2% blood vol/min up to 35%) was examined by comparing responses in conscious rabbits before and 3 wk after a sham operation or A1 lesions. In the control experiments, MAP fell minimally up to the withdrawal of 20% of blood volume after which it fell abruptly to 20-30 mm Hg below control by the 35% level. Plasma AVP increased nonlinearly during progressive hemorrhage with significant increases occurring only after 25% of blood volume was removed. In contrast, HR increased linearly after the onset of bleeding. After A1 lesions, which destroyed 84% (range 80-94%) of the noradrenergic cells, the amount of AVP released and the tachycardia during hemorrhage were reduced by 83 and 61%, respectively (P < 0.005), but the fall in MAP was minimally affected. Basal values of MAP, HR, or plasma AVP were not affected by the lesions. These results suggest that during hemorrhage in conscious rabbits A1 nonadrenergic neurons are important for the secretion of AVP and the reflex tachycardia but play little role in the maintenance of blood pressure.
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1987 |
Lew MJ, Ludbrook J, Pavia JM, Quail AW, Rutter PC, 'Selective manipulation of neurohumoral control of the cardiac pacemaker by drugs given intrapericardially', Journal of Pharmacological Methods, 17 137-148 (1987)
A technique of intrapericardial administration of ß-adrenoceptor and muscarinic cholinergic receptor antagonist drugs has been tested in conscious rabbits. Intrapericardial propra... [more]
A technique of intrapericardial administration of ß-adrenoceptor and muscarinic cholinergic receptor antagonist drugs has been tested in conscious rabbits. Intrapericardial propranolol or atenolol (50 µg/kg) had the same effect on isoprenaline heart rate dose-response curves and on the sympathetic component of the arterial baroreceptor-heart rate reflex as did conventional, 5-fold greater, intravenous doses of the drugs. The action of intrapericardial propranolol was attributable to its (-)isomer. Intrapericardial propranolol (50 µg/kg) had little effect on ventricular contractility. Plasma levels of propranolol and atenolol after intrapericardial administration were, respectively, 7- and 40-fold less than after the usual intravenous doses. Intrapericardial hyoscine methyl bromide (10 µg/kg) abolished baroreflex vagal effects on heart rate as effectively as did the conventional, 5-fold greater, intravenous dose. The duration of receptor blockade by both classes of drugs when given intrapericardially was at least 2 hr. We conclude that the rapid diffusion of ß-adrenoceptor and muscarinic cholinergic receptor blocking drugs from the pericardial sac to receptors on the sinoatrial cardiac pacemaker, and their prolonged actions, provides a useful technique for preventing the actions of the sympathetic and vagus nerves, and of circulating catecholamines, on the chronotropic functions of the heart. © 1987.
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1987 |
Quail AW, Woods RL, Korner PI, 'Cardiac and arterial baroreceptor influences in release of vasopressin and renin during hemorrhage', American Journal of Physiology - Heart and Circulatory Physiology, 252 (1987)
We studied the role of arterial and cardiac baroreceptors on mean arterial pressure (MAP) and release of arginine vasopressin (AVP) and plasma renin activity (PRA) during hemorrha... [more]
We studied the role of arterial and cardiac baroreceptors on mean arterial pressure (MAP) and release of arginine vasopressin (AVP) and plasma renin activity (PRA) during hemorrhage in conscious rabbits. Each rabbit was bled at 2% of its blood volume (BV) per minute until 35% had been removed, after which the blood was reinfused. Each rabbit was studied on three occasions, 7 days apart, and in each experiment, BV-MAP and BV-hormone response curves were constructed. The response to hemorrhage was examined when the input from 1) arterial and cardiac baroreceptors were both intact; 2) arterial baroreceptors only were intact (cardiac receptors were blocked with intrapericardial procaine); 3) cardiac receptors only were intact (after sinoaortic denervation); 4) neither receptor was intact. Resting AVP and PRA levels were unaffected by the various deafferentation procedures. AVP steeply increased only after more than 25% BV had been removed; this response was entirely mediated by cardiac baroreceptors. Increases in PRA occurred at BV loss >15% and were largely independent of baroreceptor input. Maintenance of MAP during hemorrhage was mostly due to drive from the arterial baroreceptors. Thus AVP secretion during hemorrhage contributes little to the maintenance of MAP, and the hypovolemic stimulus to AVP release comes entirely from the cardiac baroreceptors.
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1985 |
WHITE SW, TRAUGOTT FM, QUAIL AW, 'CENTRAL NERVOUS-SYSTEM 5-HYDROXYTRYPTAMINE AND NORADRENALINE SPECIFICITY OF EAR VASCULAR AND VENTILATION REFLEXES IN THERMOREGULATING RABBITS', JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM, 12 131-144 (1985)
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1985 |
QUAIL AW, WHITE SW, TRAUGOTT FM, MOORE PG, 'ROLE OF CENTRAL NERVOUS-SYSTEM MONOAMINES IN CARDIOPULMONARY EFFECTS OF ALTHESIN IN RABBIT AND MAN', JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM, 12 159-174 (1985)
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1985 |
TRAUGOTT FM, WHITE SW, QUAIL AW, 'SUPRABULBAR AND BULBAR INTEGRATION OF VENTILATION AND EAR VASCULAR CONTROL DURING THERMOREGULATION IN THE RABBIT', JOURNAL OF THE AUTONOMIC NERVOUS SYSTEM, 12 227-238 (1985)
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1982 |
Traugott FM, Quail AW, White SW, 'Cardiopulmonary reflexes during thermoregulation in the conscious rabbit: Dependence on central nervous 5-hydroxytryptamine', Neuroscience Letters, 27 (1982)
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1981 |
TRAUGOTT FM, QUAIL AW, WHITE SW, 'EVALUATION OF BLOOD RESISTIVITY INVIVO FOR IMPEDANCE CARDIOGRAPHY IN MAN, DOG AND RABBIT', MEDICAL & BIOLOGICAL ENGINEERING & COMPUTING, 19 547-552 (1981)
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1981 |
QUAIL AW, TRAUGOTT FM, 'EFFECTS OF CHANGING HEMATOCRIT, VENTRICULAR RATE AND MYOCARDIAL INOTROPY ON THE ACCURACY OF IMPEDANCE CARDIOGRAPHY', CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, 8 335-343 (1981)
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1981 |
QUAIL AW, TRAUGOTT FM, PORGES WL, WHITE SW, 'THORACIC RESISTIVITY FOR STROKE VOLUME CALCULATION IN IMPEDANCE CARDIOGRAPHY', JOURNAL OF APPLIED PHYSIOLOGY, 50 191-195 (1981)
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1981 |
Traugott FM, Quail AW, White SW, Letchford PJ, Moore PG, 'IMPEDANCE CARDIOGRAPHY: CLINICAL LIMITATIONS AND ACCURACY. 21-24 (1981)
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Nova |
1979 |
QUAIL AW, TRAUGOTT FM, WHITE SW, 'MODIFICATION OF CARDIORESPIRATORY REGULATION IN ARTERIAL HYPOXIA BY INDUCTION-AGENTS OF DIFFERENT MOLECULAR-CONFIGURATION - BARBITURATES (SODIUM PENTOBARBITAL AND THIOPENTONE), STEROIDS (ALFATHESIN) AND OPIATES (FENTANYL)', ANAESTHESIA AND INTENSIVE CARE, 7 82-82 (1979)
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1979 |
TRAUGOTT FM, QUAIL AW, LETCHFORD P, WHITE SW, 'NON-INVASIVE MONITORING OF HUMAN CARDIAC-OUTPUT USING TRANS-THORACIC ELECTRICAL-IMPEDANCE', ANAESTHESIA AND INTENSIVE CARE, 7 83-84 (1979)
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1974 |
James O, Quail A, Gibbons J, 'Chest injury: the indications for artificial ventilation', Anaesthesia and Intensive Care, 2 27-32 (1974)
During the period April, 1968, to April, 1973, all patients admitted with respiratory failure following chest injury, were managed in the Acute Respiratory Unit. The great majorit... [more]
During the period April, 1968, to April, 1973, all patients admitted with respiratory failure following chest injury, were managed in the Acute Respiratory Unit. The great majority resulted from motor vehicle accidents. 130 patients suffered respiratory failure following chest injury, and were all seen by at least one of the authors. Only 21 patients had isolated chest injury, 109 having multiple injuries. Twenty four patients died, 9 from associated cerebral contusion. The place of artificial ventilation in the proper management of chest injuries is discussed and particular stress is laid on those patients with conditions or injuries likely to lead to respiratory failure. In this category are those patients with significant flail segment, associated head or abdominal injury, the obese, and those with pre existing chest disease.
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1973 |
Gibbons J, James O, Quail A, 'Relief of pain in chest injury', British Journal of Anaesthesia, 45 1136-1138 (1973)
Conservative measures were tried in 57 patients with respiratory failure following chest injury initially who were thought not to require artificial ventilation. In 30 of these th... [more]
Conservative measures were tried in 57 patients with respiratory failure following chest injury initially who were thought not to require artificial ventilation. In 30 of these thoracic epidural analgesia was considered unsuitable and in these patients pain was managed with either intercestal nerve block or parenteral narcotics. Thirteen of these eventually needed artificial ventilation. Of 27 patients in whom epidural analgesia was considered to be suitable, difficulty in obtaining adequate analgesia was initially encountered in 6 but adequate block was ultimately achieved. In 6 patients artificial ventilation was later needed. Conservative measures were successful in 38 of 57 patients. © 1973 Oxford University Press.
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1973 |
Gibbons J, James O, Quail A, 'Management of 130 cases of chest injury with respiratory failure', British Journal of Anaesthesia, 45 1130-1135 (1973)
The management of 130 consecutive patients who suffered respiratory failure following chest injuries is described. Ninety-two patients required artificial ventilation. Associated ... [more]
The management of 130 consecutive patients who suffered respiratory failure following chest injuries is described. Ninety-two patients required artificial ventilation. Associated injuries to the abdomen, the head, or the skeletal system were common and one-third suffered from pre-existing disease of the chest or other systems. In patients with respiratory failure but not requiring artificial ventilation, analgesia was provided by means of epidural injection of local anaesthetic, intercostal blocks or injection of morphine. In the artificially ventilated group continuous intravenous infusion of an analgesic, usually phenoperidine, was given. Laparotomy was performed in 38 patients of the series. Twenty-two of the ventilated patients died, 9 from cerebral injury and 5 from respiratory causes. Two of the non-ventilated group died. No long-term complications of tracheostomy were encountered in the 96 patients so managed in this series. © 1973 Oxford University Press.
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