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    A comparative study of adrenal medullary and cardiovascular responses to haemorrhage

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    From the foregoing results one can conclude that the superfused rat stomach fundic strip provides a sensitive method for continuously recording the release of cate¬ cholamines into the circulation. Injection of the animal with oestrogen subcutaneously 18 hours before the experi¬ ment gave a reliable and sensitive preparation for the assay of catecholamines released from the adrenal medulla during haemorrhage. Rat ascending colon soaked in a propranolol, (1G~^i) for half an hour before use provided a sensitive assay preparation for angiotensin generated during haemorrhage.The rabbit catecholamine released from the adrenal medulla increased at the end of the period of haetaorrhage which took 5 minutes to complete, at which time the blood pressure was lowered to about 50 - 60 cuaHg. The release of catecholamine is not continuous and decreased after the haemorrhage stopped. In some experiments catecholamine level had returned to control levels before the retransfusion of the shed blood commenced, although some intrinsic compensation and rise of arterial blood pressure had occurred. The blood pressure recovered slightly during the 30 minutes resting after the bleed, partly due to sympathetic influence, but also due to the rapid entrance of tissue fluid into the circulation as shown by decrease in both packed cell volume and haemoglobin con¬ centration. Heart rate did not increase significantly in this species during haemorrhage and fell below control levels 30 minutes after haemorrhage. This might be related to the increase of plasma volume due to entry of extra-cell liar fluid. This small rise in heart rate at the beginning of haemorrhage is probably related to the high resting heart rates in these anaesthetized animals.The release of catecholamine during haemorrhage in the rabbit was not reduced by muscarinic blockade but was abolished by nicotinic blockade which Indicates most of the receptor population are nicotinic, a finding supported by the experiments with carbachol.No evidence of increase in angiotensin generation luring or after haemorrhage suggests that no significant of the rabbit release of renin from the kidney occurs during or 30 minutes after the haemorrhage procedures, during which arterial blood pressure was reduced to 50 - 80 amHg. Angiotensin infusions into the aorta in 200, 400 and even 800 ng/kg/min did not give any evidence of releasing catecholamines from the adrenal medulla nor did discrete injections of angiotensin. This was taken as evidence that in the rabbit angiotensin does not act as a catecholamine releaser from the adrenal medulla.The above findings suggest that angiotensin neither releases catecholamine in significant amounts during haemorrhage, nor does it play any part in catecholamine release during haemorrhage in the rabbit .In dogs, catecholamine rele s« from the adrenal medulla commences as blood pressure falls and before the end of haemorrhage In most experiments when blood pressure was 50 - 80 mralig. Low levels of blood pressure did not have to be sustained for the increase in catecholamines to occur. Release was continuous over the whole period (30 minutes) after the bleed, in spite of the compensatory increase in arterial blood pressure. It returned to normal level when retransfusion of the shed blood began.The heart rate of the dog increased during haemorrhage especially towards the end and returned to control level within 30 minutes after haemorrhage. The increase in catecholamines released daring haemorrhage was not affected by muscarinic blockade. In animals treated with hexamethonium however, catecholamine release Increased during haemorrhage but not to the same level as during a bleed prior to blockade. Moreover, the output of catecholamine was a transient one persisting for only a few minutes in most of the animals studied and returning back to control levels before retransfusion started. Ligation of the renal veins together with prior administration of hexamethonlum totally abolished the release of catecholamine after haemorrhage.Angiotensin blood level in the dog increased markedly after haemorrhage and only returned to control levels after retransfusion of the shed blood. Infusion of angiotensin in 200 ng/kg/min significantly increased the release of catecholamine from the adrenal medulla In a transient burst which persisted for only 2-3 minutes and not for the whole period of the infusion. It resembled the responses noted during haemorrhage after ganglionic blockade with hexamethonluw.The above results suggest that the adrenal medulla of the dog Is very sensitive to angiotensin and that angiotension liberation during haemorrhage precedes the release of catecholamine in the dog and could play an important role in the initial release of catecholamine into the circulation during haemorrhage in this animal.The species differences noted are discussed in the context of the cardio vascular control in hypotensive states