论文部分内容阅读
肠粘膜屏障功能减弱可导致肠道内内毒素的转运。本研究应用１２５Ｉ－ＬＰＳ作为示踪剂，通过对家兔离体和在体肠袢进行肠腔内施压，动态观察肠腔内毒素向肠外转运的模型，分析和探讨肠腔内压力、施压时间、肠屏障功能与肠内毒素转运的关系。实验结果表明：肠内压的升高可损害肠粘膜屏障，促进肠内毒素向体内的转运。高压力组的１２５Ｉ－ＬＰＳ入血总量明显高于低压力组（Ｐ＜０．０１）；离体肠管１２５Ｉ－ＬＰＳ入血量峰值出现在０．５小时，当肠腔内压大于２０ｃｍＨ２Ｏ时，在体肠管内１２５Ｉ－ＬＰＳ入血峰值向后延迟；肠内压力的升高有助于肠组织吸收１２５Ｉ－ＬＰＳ及肠内１２５Ｉ－ＬＰＳ的肠外渗漏。说明在肠道内内毒素转运过程中，肠内压升高及施压时间与内毒素入血呈正相关，并加重肠屏障的损伤。
Intestinal mucosal barrier function can lead to intestinal endotoxin transport. In this study, 125I-LPS was used as a tracer. The intestine was transplanted into the intestine to observe the intestinal cavity pressure, Pressure time, intestinal barrier function and intestinal endotoxin transport relationship. The experimental results show that the increase of intestinal pressure can damage the intestinal mucosal barrier and promote the transport of intestinal endotoxin to the body. The total amount of 125I-LPS in high-pressure group was significantly higher than that in low-pressure group (P <0.01). The peak value of 125I-LPS in isolated intestine was 0.5 hour. When the intestinal pressure was more than 20cmH2O , 125I-LPS in the body intestine into the peak postprandial peak delay; increased intestinal pressure to help intestinal absorption of 125I-LPS and enteral 125I-LPS extraintestinal leakage. This shows that in the process of intestinal endotoxin transport, increased intestinal pressure and pressure time and endotoxin into the blood was positively correlated, and increased intestinal barrier injury.