MECHANISM WHEREBY HALOTHANE REVERSES THE PRESSOR RESPONSES TO ACETYLCHOLINE

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Abstract
The initial and secondary components of the biphasic pressor response to acetylcholine in the atropinized dog were analysed separately. Deep halothane anaesthesia reversed the initial pressor response to acetylcholine owing to a decrease in total peripheral vascular resistance in the absence of an increase in cardiac output. The secondary pressor response was not reversed but was suppressed owing to a marked reduction of the increase in cardiac output responsible for this pressor response; total peripheral resistance increased. Conversely, halothane anaesthesia did not block the increase in blood glucose concentration resulting from the injection of acetylcholine. Thus, the change induced by halothane in the secondary pressor phase was apparently a consequence of cardiac depression rather than of adrenal medullary blockade. Compound P‐286 (N‐diethylaminoethyl‐N‐isopentyl‐N‐di‐isopropylurea), which produces a change in the pressor response to acetylcholine similar to that induced by halothane, prevents the hyperglycaemia due to acetylcholine. In some experiments, deep halothane anaesthesia depressed the cardiac inotropic but not the chronotropic response to acetylcholine. Such selective blocking action is believed to have a bearing on production of arrhythmias.

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