Stroke gives rise to an immediately infarcted area surrounded by an area of critically perfused neural tissue (‘area at risk’); the fate of this tissue being dependent on increased perfusion subacutely. Using experimental temporary occlusion of the middle cerebral artery (MCA) in the rat we studied the possible upregulation of the 5-HT(1) receptor in the MCA. Experimental stroke: The MCA of an anaesthetised rat was exposed and temporarily occluded with a hook for 120 mins. Afterwards the rat was revitalised. In vitro pharmacological examination: After two days the rat was killed and the MCA's were harvested and suspended on wires for measurement of contractile properties. Selective 5-HT(1) agonists and antagonists were used to study contractile responses. Contractile responses to 5-HT(1) stimulation were clearly enhanced after stroke (compared to the contralateral MCA). This receptor upregulation implies an increased sensitivity towards the endogenous agonist 5-hydroxytryptamine. It has earlier been shown that temporary occlusion leads to upregulation of a contractile ET(B) receptor. The combined upregulation of contractile receptors may further reduce the blood supply to the area at risk, thus, increasing the infarct size with subsequent increased neurological disability.
