A Research for, cellular Dysfunction in Acta Stroke

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Nitroglycerin, as well as nitric oxied, causes hyperpolarization and cGMP elevation in vascular smooth muscle cells. It is unknown whether nitroglycerin ameliorates vasospasm by an increase in cGMP levels after sudarachnoid hemorrhage (SAH). The purpose of the first study was to measure the levels of cGMP and cAMP in the cerebral arteries and parietal cerebral cortices in a primate model and to determine the effect of nitroglycerin on vasospasm after SAH.Chronic vasospasm was induced by clot placement around the right middle cerebral artery (MCA). Seven days after the surgery, angiography was repeated and either nitroglycerin or saline was administered intrevenously. A significant vasospasm occurredin the cerebral arteries on both sides, more prominently on the right side. Concomittantly, rCBF on the right side was significantly decreased. In the right MCA,cGMP levels were significantly lower than in the normal MCA.After the administration of nitroglycerin for 3 hours, the cerebral vessels were significantly dilated on both sides, and rCBF was singnificantly increased on the right side but not on the left side. Although depressed cGMP levels in the right MCA were not recovered by nitroglycerin, a significant increase in cGMP levels was observed in the basilar artery. In both parietal cortices, cGMP levels were significantly decreased after SAH and unchanged after nitroglycerin treatment. There were no significant changer in cAMP levels in SAH and after nitroglycerin treatment. In conclusion, the vasodilator effect of nitroglycerin in spastic MCA may not be mediated by an increase in cGMP levels, suggesting an involvement of hyperpolarization of the smooth muscle cells.