Okamoto S, Handa H, Toda N
Stroke. 1984 Jan-Feb;15(1):60-4. doi: 10.1161/01.str.15.1.60.
In helically-cut strips of dog basilar and mesenteric arteries, the isometric tension developed by application of ghost-free hemolysate from dog erythrocytes was recorded. The hemolysate contracted basilar arteries in a concentration-dependent fashion, the response being attenuated by treatment with either aspirin or polyphloretin phosphate, a prostaglandin antagonist. Mesenteric arteries were contracted only slightly by high concentrations of hemolysate. When the mesenteric arteries had partially been contracted with prostaglandin F2 alpha or norepinephrine, the hemolysate induced relaxations, which were abolished by aspirin in approximately half the preparations used. Studies on rat stomach strips exposed to superfusate of dog cerebral arteries showed a release of prostaglandin-like substance by the hemolysate application. It may be concluded that the hemolysate contracts basilar arteries and relaxes mesenteric arteries, mainly through prostaglandins synthesized in and released from the vascular wall. Such a mechanism may be involved in the pathogenesis of cerebral vasospasm following a subarachnoid hemorrhage.
在犬基底动脉和肠系膜动脉的螺旋状切片中，记录了应用犬红细胞无细胞溶血产物所产生的等长张力。溶血产物以浓度依赖的方式使基底动脉收缩，用阿司匹林或前列腺素拮抗剂聚磷酸根皮苷处理后，反应减弱。高浓度的溶血产物仅使肠系膜动脉轻微收缩。当肠系膜动脉用前列腺素F2α或去甲肾上腺素部分收缩后，溶血产物可诱导舒张，在所使用的约一半制剂中，这种舒张被阿司匹林消除。对暴露于犬脑动脉灌流液的大鼠胃切片的研究表明，应用溶血产物可释放前列腺素样物质。可以得出结论，溶血产物主要通过血管壁合成并释放的前列腺素使基底动脉收缩，使肠系膜动脉舒张。这种机制可能参与蛛网膜下腔出血后脑血管痉挛的发病过程。
