Objective To investigate the possible roles of endothelin?1 (ET?1)and nitric oxide (NO) in the development of cerebral vasospasm(CVS) and related brain ischemic damage following subarachnoid hemorrhage (SAH).Methods 90 Wistar rats were divided into SAH group and sham operated group. Regional cerebral blood flow (rCBF),NO and ET?1 in both blood and brain tissue within 24?h after operation were detected.Diameter of basilar artery(BA) was measured.Results rCBF decreased rapidly and persistently within 24?h after induction of SAH. Spasm of BA occurred 30?min after SAH.NO in blood was decreased while that in brain tissue increased. Both blood and brain tissue ET?1 levels were increased.Conclusion Decrease of NO and increase of ET?1 in blood are involved in the development of CVS following SAH while increase of NO and ET?1 in brain tissue contributes to brain damage due to ischemia.
参考文献:
[1] Bederson J B, GERMANO M, GUARINO L. Cortical blood flow an d cerebral perfusi on pressure in a new noncraniotomy model of subarachnoid hemorrhage in rats, 1995 [2] 王成彬, 沈文梅, 田亚平. 铜离子活化镉还原法测定血清中硝酸盐浓度, 1996 [3] 高树生, 徐有奇. 正常妊娠中内皮素的测定, 1993 [4] ZELLERS T M, MCCOMICK J, WU Y Q. Interaction among ET 1 endothelium derive d nitric oxide and prostacyclin in pulmonary arteries and veins, 1994 [5] HARBERCHT B G, STADLER J, DEMETRICS A J. Nitric oxide and prost aglandi ns interact to prevent hepatic damage during murine endotoxemia, 1994 [6] Nishikawa T. Effect of nitric oxide synthase inhibition on cerebral blood flow and injury volume during focal ischemia in cats, 1993 [7] Ziv I, FLEMINGER G, DYALDETTI R. Increased plasma endothelin 1 in acute ischemic stroke, 1992