Onoue H, Kaito N, Akiyama M, Tomii M, Tokudome S, Abe T
Department of Neurosurgery, Jikei University School of Medicine, Tokyo, Japan.
J Neurosurg. 1995 Sep;83(3):510-5. doi: 10.3171/jns.1995.83.3.0510.
To investigate the effects of subarachnoid hemorrhage (SAH) on the responsiveness of human cerebral arteries to vasoactive substances, the authors measured the isometric tension generated in helical strips of basilar and middle cerebral arteries isolated from human cadavers. Contractions caused by KCl, prostaglandin F2 alpha, noradrenaline, and serotonin were reduced in arteries obtained from cadavers with aneurysmal SAH damage and compared to those obtained from cadavers with no indication of intracranial diseases. Endothelium-dependent relaxation elicited by substance P and bradykinin, and endothelium-independent relaxation induced by prostaglandin I2 and nitroglycerin were also markedly decreased in arteries affected by SAH. However, the reduction in relaxation response to prostaglandin I2 was significantly less than that to the other vasodilator agents. These results indicate that human cerebral artery functions are severely impaired after SAH and that poor responses to vasoactive agents may result primarily from dysfunction of smooth-muscle cells.
为研究蛛网膜下腔出血（SAH）对人脑动脉对血管活性物质反应性的影响，作者测量了从人类尸体分离的基底动脉和大脑中动脉螺旋条带产生的等长张力。与无颅内疾病迹象的尸体所获取的动脉相比，患有动脉瘤性SAH损伤的尸体所获取的动脉中，由氯化钾、前列腺素F2α、去甲肾上腺素和5-羟色胺引起的收缩减弱。在受SAH影响的动脉中，由P物质和缓激肽引起的内皮依赖性舒张以及由前列腺素I2和硝酸甘油引起的非内皮依赖性舒张也明显降低。然而，对前列腺素I2的舒张反应降低明显小于对其他血管舒张剂的降低。这些结果表明，SAH后人脑动脉功能严重受损，对血管活性物质的反应不佳可能主要源于平滑肌细胞功能障碍。
