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取雄性家免20只,随机等分为休克组和对照组。全麻、剖腹,用自制“∠”形分离钟分离并夹闭肠系膜上动脉复制肠系膜上动脉闭塞性休克模型。对照组除不夹闭外,其余操作与休克组全同。分别观察两组眼球结膜微循环动态变化,并分别检测两组中的若干血液流变学指标及血压和腹腔温度之动态变化。实验结果提示:该种休克模型休克的发生机理可能因红细胞带电量减少和微小血池的形成共同促使红细胞聚集加强,后者又与红细胞压积增高一起导致血粘度增加,并进而使血流减慢。微血管舒缩的异常和血流减慢可能是使该种休克模型动脉组织微循环灌流减少的两个重要因素。微血管的舒缩障碍似与肠道细菌及内毒素关系不大,但可能与小肠缺血坏死的范围与程度有关联。
Twenty males were excluded and randomly divided into shock group and control group. With general anesthesia and laparotomy, the superior mesenteric artery occlusive shock model was isolated and the superior mesenteric artery was isolated with a self-made “∠” shaped separation bell. The control group was identical to the shock group except that it was not clamped. The dynamic changes of the microcirculation of the conjunctiva of the eyeballs of the two groups were observed, and some of the hemorheological parameters and the dynamic changes of blood pressure and abdominal temperature were detected. The experimental results suggest that the mechanism of shock in this type of shock model may be due to the reduction of the red blood cell charge and the formation of the tiny blood pool that together promote the increase of red blood cell aggregation. The latter together with the increase of the hematocrit leads to an increase in blood viscosity, which in turn reduces the blood flow. SLOW. Abnormal microvasomotor systole and slowed blood flow may be two important factors that reduce the microcirculation and perfusion of the arterial tissue in this type of shock model. Microvasucular dyskinesia seems to have little to do with gut bacteria and endotoxins, but it may be related to the extent and extent of intestinal necrosis.