Tsuji T, Cook D A
Department of Neurosurgery, Shinshu University School of Medicine, Matsumoto, Japan.
Eur J Pharmacol. 1994 Oct 13;264(1):77-80. doi: 10.1016/0014-2999(94)90638-6.
Bradykinin, substance P and vasopressin induced a vasodilatation followed by a vasoconstriction in control perfused canine basilar arteries with endothelium. The dilatation was significantly reduced and the constriction was significantly enhanced by endothelial removal with saponin. The potentiated constriction was significantly blocked by sodium ozagrel, a thromboxane synthetase inhibitor. These results suggest that the dilatation due to these neuropeptides may depend on endothelium-derived relaxing factor, and that the augmented constriction after endothelial removal may be related to the thromboxane A2 production in cerebral arterial smooth muscles. This mechanism following the damage of endothelium might be implicated in cerebral vasospasm after subarachnoid haemorrhage.
在对照灌注的有内皮犬基底动脉中,缓激肽、P物质和血管加压素引起血管舒张,随后是血管收缩。用皂角苷去除内皮后,舒张作用显著减弱,收缩作用显著增强。血栓素合成酶抑制剂奥扎格雷钠可显著阻断增强的收缩作用。这些结果表明,这些神经肽引起的舒张可能依赖于内皮源性舒张因子,而内皮去除后增强的收缩可能与脑动脉平滑肌中血栓素A2的产生有关。蛛网膜下腔出血后脑血管痉挛可能与内皮损伤后的这一机制有关。