The effect of a lipid hydroperoxide of arachidonic acid on the canine basilar artery. An experimental study on cerebral vasospasm.
The effect of a lipid hydroperoxide of arachidonic acid on the canine basilar artery. An experimental study on cerebral vasospasm.
复制标题
花生四烯酸脂质过氧化氢对犬基底动脉的影响。
作者：
T. Sasaki;S. Wakai;T. Asano;T. Watanabe;T. Kirino;K. Sano
脂质氢过氧化物（15-氢过氧花生四烯酸：15-HPAA）在犬体内的诱发痉挛能力进行了慢性实验研究。将15-HPAA （0.2 mg或2 mg）在牛血清白蛋白溶液中乳化后注射到大池中。血管造影观察基底动脉直径变化，电镜观察基底动脉形态变化。池内注射0.2 mg 15-HPAA可引起基底动脉轻度收缩，持续约7小时。池内注射2 mg 15-HPAA可引起双期收缩，初始期为中度收缩，持续约10小时。第二阶段开始于注射后第2天或第3天。动脉狭窄的强度在第二阶段比第一阶段更明显。基底动脉继发性延长收缩持续至注射后第7天牺牲。电镜观察显示内皮细胞明显退行性改变，中膜肌坏死。第二阶段延长的动脉收缩总是与内皮细胞的显著变性有关。另一方面，肌坏死改变仅限于少数平滑肌细胞。本研究的结果与假设一致，即与蛛网膜下腔血块溶解相关的脂质过氧化参与了蛛网膜下腔出血慢性血管痉挛的发生。
The in vivo spasmogenic capacity of a lipid hydroperoxide (15-hydroperoxy arachidonic acid: 15-HPAA) was studied in a chronic experiment using the dog. The 15-HPAA was injected into the cisterna magna (0.2 or 2 mg emulsified in bovine serum albumin solution). The changes in diameter of the basilar artery were followed by angiography, and the morphological changes were studied by electron microscopy. The cisternal injection of 0.2 mg of 15-HPAA caused a mild constriction of the basilar artery which lasted about 7 hours. The cisternal injection of 2 mg of 15-HPAA caused a biphasic constriction, the initial phase of which was a moderate narrowing lasting about 10 hours. The second phase started on the 2nd or the 3rd day after injection. The intensity of the arterial narrowing was more pronounced in the second phase than in the first. The prolonged secondary constriction of the basilar artery continued until sacrifice on the 7th day after injection. Electron microscopic study revealed a marked degenerative change in the endothelium and myonecrotic changes in the tunica media. The prolonged arterial constriction in the second phase was invariably associated with remarkable degeneration of the endothelium. On the other hand, myonecrotic changes were limited to a small number of smooth-muscle cells. The results of the present study are consonant with the hypothesis that lipid peroxidation associated with lysis of the subarachnoid clot is involved in the genesis of chronic vasospasm in subarachnoid hemorrhage.