摘要
夹闭成年大耳白兔肠系膜上动脉60min后松夹,以复制肠系膜上动脉闭塞性休克(SMAO休克,以血压下降50％以上视为休克)。休克组120min后,颈动脉血压由夹闭前11.88±0.77kPa下降至5.01±0.45kPa(P<0.01);全血比粘度由5.60±0.41上升到6.82±0.86(P<0.01);血细胞压积由41.10±0.97％上升到47.60±1049％(P<0.05);血小板聚集率由0.810±0.022下降到0.607±0.038(P<0.01)。对照组连续观察120min后,上述指标的数值前后相差不显著。实验结果表明;血液浓缩,全血粘度增加,血小板粘滞性增高,在SMAO休克发病机制中起着重要作用。
The superior mesenterie artery occlusion shock model was induced by Clamping the superior mesenterie artery (SMA) for 60 minuts and the releasing the artery clamp. Shock was considered if the blood plessure at 120 minutes after releasing the artery clamp reduced to 50％ of that before clamping SMA. In the shock group, at 120 minuts after releasing the artery clamp, the blood pressure of the cervical artery decreased from 11.88±0.77 kPa before clamping SMA to 5.01±0.45kPa; blood vicosiy inerased from 5.60±0.41 to 6.82±0.86, while the hemotocrit increased from 41.1±1.0％ to 47.6±1.5％ and the platelet aggregate counting rate reduced from 0.810±0.022 to 0.607±0.0a8, the difffences were all sigaificent (P<0.01).
@ The control group had on significant changes in the above itms.
@ This result suggests that the blood concentration, the increase of the blood viscoity and platelet play an inportant pair in inducing SMA occlusion shock.
出处
《锦州医学院学报》
1993年第1期12-13,共2页
Journal of Jinzhou Medical College
关键词
肠系膜上动脉
血凝粘度
SMAO
休克
superior mesenteric artery
blood viscosity
hemotocrit
platelet aggregate counting ratio
