Turkish Neurosurgery 1992 , Vol 2 , Num 3
Erol TADEMROLU1, Robert MACFARLANE1, Michael A. MOSKOWITZ1, Enoch P. WEI2, Hermes A. KANTOS2
1Neurology & Neurosurgery Services , Massachusetts General Hospital, The effects of 10 global cerebral ischaemia on cortical arteriolar responses to Acetylcholine (ACh) application was examined in anaesthetized cats by closed cranial window technique. The physiological response of the pial arterioles to topical ACh (10-7 M) was endothelium- dependent vasodilation. Following 10 min global ischaemia pial vessel diameters were measured during minutes 30, 45, 60, 75, 90, and 120 of the reperfusion period before and after Ach application. During the reperfusion period the pial arteriolar response to Ach was reversed and sustained up to 75 minutes of reperfusion and then vasodilatory response to Ach recovered. However, vasodilatory responses to ACh at 120 min of reperfusion were stil less than the baseline values.

We concluded that; 1) Endothelium-dependent vasodilation with ACh is present in pial arterioles. 2) 10 min global cerebral ischaemia temporarily reverses the endothelium- dependent pial arteriolar responses to ACh. 3) Since the production of free oxygen radicals following 10 min global ischaemia has been demonstrated, inhibition of endothelium- dependent vasodilation of the pial arterioles during the reperfusion period, depends on inactivation of the endothelium-dependent relaxing factors) (EDRFs) by free oxygen radicals. 4) Since the vasodilatory responses of the pial arterioles recovered in the late reperfusion period we concluded that EDRF(s) were still produced and the endothelial cells were intact or minimally damaged. These findings suggest that elimination of endothelium-dependent vasodilation is the result of relatively minor injury rather than complete destruction of the pial arteriolar endothelial cells. 5) Vasoconstriction of the cerebral arterioles after ACh application during the early reperfusion period was the unmasked vasoconstrictory effect of ACh on the vascular smooth muscle, because of EDRF inactivation by free oxygen radicals. Keywords : Cerebral ischaemia. endothelium-dependent relaxing factors (EDRFs), acetylcholine, vasodilation, free oxygen radicals

Corresponding author : Erol Tademirolu