Abstract
1 Noradrenaline infused into the internal carotid artery of the dog (0.01-1 μg kg-1 min-1) constricts the blood vessels of the cortex. This constriction is mediated by the action of noradrenaline on α-adrenoceptors of the cerebral arteries.
2 Intravenous (1 μg kg-1 min-1) or intra common carotid arterial (0.01-1 μg 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 PaCO2 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% CO2 to the donor dog caused an increase in cerebral blood flow in the recipient dog.
7 Administration of intravenous noradrenaline (1.0 μg kg-1 min-1) to the donor animal caused an increase in cerebral blood flow, cerebral O2 and glucose utilization of the recipient.
8 Administration of 5% CO2 and intravenous (-)-noradrenaline (1.0 μg 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 PaCO2 in the intact animal must be at a site different from the peripheral chemoreceptors.
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