Jin Xue-Long, Zheng Yang, Shen Hai-Ming, Jing Wen-Li, Zhang Zhao-Qiang, Huang Jian-Zhong, Tan Qing-Lin
Department of Physiology, Tianjin Medical University, Tianjin 300070, China.
World J Gastroenterol. 2005 Mar 21;11(11):1610-5. doi: 10.3748/wjg.v11.i11.1610.
To explore the dynamic changes in the pressure of the lateral ventricle during acute brainstem hemorrhage and the changes of neural discharge of vagus nerve under the load of intracranial hypertension, so as to analyze their effects on the congestive degree of intestinal mucous membrane and the morphologic changes of intestinal mucous membrane.
An operation was made to open the skull to obtain an acute brainstem hemorrhage animal model. Microcirculatory microscope photography device and video recording system were used to determine the changes continuously in the caliber of jejunal mesenteric artery during brainstem hemorrhage and the changes with time in the congestion of jejunal mucosal villi. We used HE stain morphology to analyze the changes of duodenal mucosal villi. A recording electrode was used to calculate and measure the electric discharge activities of cervical vagus nerve.
(1) We observed that the pressure of lateral cerebral ventricle increased transiently during acute brainstem hemorrhage; (2) The caliber of the jejunal mesenteric artery increased during brainstem hemorrhage. Analysis of red color coordinate values indicated transient increase in the congestion of jejunal mucous membrane during acute brainstem hemorrhage; (3) Through the analysis of the pathologic slice, we found enlarged blood vessels, stagnant blood, and transudatory red blood cells in the duodenal submucous layer; (4) Electric discharge of vagus nerve increased and sporadic hemorrhage spots occurred in duodenal mucous and submucous layer, when the lateral ventricle was under pressure.
Brainstem hemorrhage could cause intracranial hypertension, which would increase the neural discharge of vagus nerve and cause the transient congestion of jejunal mucous membrane. It could cause hyperemia and diffused hemorrhage in the duodenal submucous layer 48 h after brainstem hemorrhage.
探讨急性脑干出血时侧脑室压力的动态变化及颅内高压负荷下迷走神经神经放电的变化,分析其对肠黏膜充血程度及肠黏膜形态学变化的影响。
通过开颅手术建立急性脑干出血动物模型。采用微循环显微镜摄像装置及视频记录系统,连续测定脑干出血时空肠肠系膜动脉管径的变化及空肠黏膜绒毛充血随时间的变化。采用苏木精-伊红染色形态学方法分析十二指肠黏膜绒毛的变化。用记录电极计算并测量颈迷走神经的放电活动。
(1)观察到急性脑干出血时侧脑室压力短暂升高;(2)脑干出血时空肠肠系膜动脉管径增宽。红色坐标值分析表明急性脑干出血时空肠黏膜充血短暂增加;(3)通过病理切片分析,发现十二指肠黏膜下层血管扩张、血流淤滞及红细胞渗出;(4)侧脑室受压时,迷走神经放电增加,十二指肠黏膜及黏膜下层出现散在出血点。
脑干出血可导致颅内高压,增加迷走神经神经放电,引起空肠黏膜短暂充血。脑干出血48小时后可导致十二指肠黏膜下层充血及弥漫性出血。