Saito A, Handa J, Toda N
Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
Surg Neurol. 1991 Jun;35(6):461-7. doi: 10.1016/0090-3019(91)90180-h.
Autologous blood was injected into the cisterna magna of mongrel dogs twice with an interval of 48 hours. They were killed 3 days, 1 week, or 4 weeks after the first injection of blood, and helical strips of the basilar artery were prepared. Contractions induced by 5-hydroxytryptamine, noradrenaline, prostaglandin F2 alpha, and oxyhemoglobin were significantly potentiated. Relaxations caused by nicotine, K+, arachidonic acid, and prostaglandin I2 were suppressed, but the relaxant response to calcium ionophore A23187 and substance P did not change significantly. These results suggest that contractions mediated via activation of alpha, 5-hydroxytryptamine, and prostaglandin F2 alpha receptors are potentiated, and relaxations caused by stimulation of vasodilator nerves and by endogenous and exogenous prostaglandin I2 are attenuated in dog basilar arteries exposed to subarachnoid clot. On the other hand, certain relaxations possibly mediated by endothelium-derived relaxing factor do not appear to be significantly influenced.
将自体血注入杂种狗的枕大池，间隔48小时注射两次。在首次注射血液后3天、1周或4周将狗处死，制备基底动脉的螺旋条。5-羟色胺、去甲肾上腺素、前列腺素F2α和氧合血红蛋白诱导的收缩明显增强。尼古丁、钾离子、花生四烯酸和前列腺素I2引起的舒张受到抑制，但对钙离子载体A23187和P物质的舒张反应没有明显变化。这些结果表明，在暴露于蛛网膜下腔血凝块的狗基底动脉中，通过激活α、5-羟色胺和前列腺素F2α受体介导的收缩增强，由血管舒张神经刺激以及内源性和外源性前列腺素I2引起的舒张减弱。另一方面，某些可能由内皮源性舒张因子介导的舒张似乎没有受到明显影响。
