Ohkuma H, Ogane K, Fujita S, Manabe H, Suzuki S
Department of Neurosurgery, Hirosaki University School of Medicine, Japan.
Stroke. 1993 Oct;24(10):1541-5; discussion 1545-6. doi: 10.1161/01.str.24.10.1541.
Serial changes of anti-platelet-aggregating activity in the endothelial cells after experimental subarachnoid hemorrhage were studied in 30 feline two-hemorrhage models.
One hour or 2, 4, 7, or 14 days after mimic subarachnoid hemorrhage, ADP (40 mg/kg) was infused into the basilar artery via the right vertebral artery to activate circulating platelets. Immediately after ADP infusion, the basilar artery was fixed by intra-arterial perfusion with 1.5% glutaraldehyde in 0.1 mol/L phosphate buffer and was removed. The luminal surface was examined under a scanning electron microscope.
One hour after subarachnoid hemorrhage, no platelets adhered or aggregated on the luminal surface. However, 4 to 7 days after subarachnoid hemorrhage, many platelets were observed adhering or aggregating on the luminal surface.
These findings suggest the impairment of anti-platelet-aggregating activity of endothelial cells after subarachnoid hemorrhage. This impairment may be involved in inducing cerebral ischemia during cerebral vasospasm by causing platelet adhesion and aggregation.
在30只猫的双次出血模型中研究实验性蛛网膜下腔出血后内皮细胞抗血小板聚集活性的系列变化。
在模拟蛛网膜下腔出血后1小时或2、4、7或14天，通过右椎动脉将ADP（40mg/kg）注入基底动脉以激活循环中的血小板。在注入ADP后立即通过在0.1mol/L磷酸盐缓冲液中用1.5%戊二醛进行动脉内灌注固定基底动脉并将其取出。在扫描电子显微镜下检查管腔表面。
蛛网膜下腔出血后1小时，管腔表面未见血小板黏附或聚集。然而，蛛网膜下腔出血后4至7天，观察到许多血小板黏附或聚集在管腔表面。
这些发现提示蛛网膜下腔出血后内皮细胞抗血小板聚集活性受损。这种损伤可能通过引起血小板黏附和聚集而参与脑血管痉挛期间诱导脑缺血。
