Cerebrovascular response to intracarotid injection of serotonin before and after middle cerebral artery occlusion

Abstract

SUMMARYThe effect of intracarotid injection of serotonin (5-HT) on internal carotid artery flow and oxygen availability (02a) of the cerebral cortex was studied in 10 baboons. Vasoconstriction occurred in the vascular bed of the territory supplied by the injected artery. After one middle cerebral artery was occluded the vasoconstrictor effect of 5-HT was more pronounced, particularly in the non-ischaemic hemisphere. The capacity of the cerebral vessels to provide collateral blood flow was reduced in both ischaemic and non-ischaemic areas of brain. As a result of focal cerebral ischaemia, 5-HT may accumulate in the brain and contribute to the progression of infarction.

Brain Hypoxia: The Turning-Point in the Genesis of the Migraine Attack?

“…-In conformity with the fact that this substance does not cross the BBB, it has been found that intracarotid application of serotonin produces equivocal effects upon intracranial blood flow (32,33,34), although it constricts the scalp arteries (32) and reduces the calibre of the internal carotid artery (35,36); -As reviewed by Rosenblum (37), serotonin has, likewise, failed to consistently produce marked degrees of constriction when locally applied to the pial microcirculation;…”

Photochemically Induced Cortical Infarction in the Rat. 1. Time Course of Hemodynamic Consequences

“…Progres sive ischemia in the border zone of an infarct re sulting in the gradual increase in infarct size has previously been reported (Welch et al, 1973). Pos sible mechanisms to account for progression of stroke include edema formation (O'Brien et al, 1974), release of serotonin or thromboxane A2 from aggregating platelets (Welch et al, 1973;Hallen beck and Furlow, 1979), and increased extracellular potassium (Wade et al, 1975). Our laboratory has demonstrated blood -brain barrier alterations within the infarcting tissue as early as 30 min fol lowing irradiation .…”

Cathecholamine and 5-hydroxytryptamine levels in ischemic brain. Influence of p-chlorophenylalanine.

“…Unilateral common carotid ligation in this animal consistently induces cerebral hemispheric ischemia in 40 to 50% of animals, 4 the incidence of ischemia and eventual infarction apparently depending on vascular anatomical variation. 6 Since the incidence of eventual infarction in the gerbil seems so dependent on adequacy of collateral circulation, it seemed appropriate to use this model to test the hypothesis that neuronal release of 5-HT with subsequent vasoconstriction may limit collateral vasocapacitance in foci of cerebral ischemia, thereby contributing to the progression of ischemia. 6 Therefore, a separate animal group was pretreated with the tryptophan-hydroxylase inhibitor, pchlorophenylalanine (PCPA), in order to deplete cerebral tissue 5-HT content and determine if the stroke incidence rate was thus modified.…”