Conjoint Professor Tony Quail

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.

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.

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.

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.

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.

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.