Factors affecting the cerebrovascular response to noradrenaline in the dog

Abstract

1 Noradrenaline infused into the internal carotid artery of the dog (0.01-1 mug kg(-1) min(-1)) constricts the blood vessels of the cortex. This constriction is mediated by the action of noradrenaline on alpha-adrenoceptors of the cerebral arteries.2 Intravenous (1 mug kg(-1) min(-1)) or intra common carotid arterial (0.01-1 mug kg(-1) min(-1)) infusions of noradrenaline cause an increase in cortical blood flow that can be dissociated from changes in blood pressure.3 The effect of intravenous noradrenaline on the cortical blood vessels and metabolism is blocked by high PaCO(2) levels, or by the prior administration of (+/-)-propranolol. (+)-Propranolol is without such effect.4 Following section of both vagi and both sinus nerves, intravenous noradrenaline fails to cause an increase in cortical blood flow.5 In another series of animals the area of the carotid bifurcation was vascularly isolated and perfused with blood from a second dog. Chemoreceptor and baroreceptor activity was shown to be intact.6 Administration of 5% CO(2) to the donor dog caused an increase in cerebral blood flow in the recipient dog.7 Administration of intravenous noradrenaline (1.0 mug kg(-1) min(-1)) to the donor animal caused an increase in cerebral blood flow, cerebral O(2) and glucose utilization of the recipient.8 Administration of 5% CO(2) and intravenous (-)-noradrenaline (1.0 mug kg(-1) min(-1)) caused a further increase in flow and metabolism.9 This evidence suggests that the cerebrovasodilatation observed following intravenous noradrenaline is reflex and is triggered by chemoreceptor activity.10 The evidence also suggests that the antagonism of the cortical dilatory effects of intravenous noradrenaline by raised PaCO(2) in the intact animal must be at a site different from the peripheral chemoreceptors.