论文部分内容阅读
目的探讨致损害因素及其作用强度与门脉高压性胃病变粘膜出血（ＰＨＧＭＨ）的关系．方法用３０ｇ／Ｌ硫代乙酰胺腹部ｓｃ法诱导大鼠慢性肝损害肝硬变及门脉高压，继用饥饿诱导法使大鼠发生门脉高压性胃粘膜出血（ＰＨＧＭＨ，ｎ＝３４），分期观察（注药４５ｄ，ＰＨＴＭＨⅠ，ｎ＝１４；注药６５ｄ，ＰＨＴＭＨⅡ，ｎ＝２０）饥饿１２ｈ～３６ｈ后的胃粘膜出血率及严重性分级的变化．结果①ＰＨＧＭＨ鼠的出血率（９１２％）、严重性分级（ｇｒａｄｅ，２６３±０２０）均显著大于对照（４３８％，ｇｒａｄｅ０６３±０２０，Ｐ＜００１）．②分期观察ＰＨＧＭＨⅠ和ＰＨＧＭＨⅡ鼠的粘膜出血率（８５７％和９５０％）、严重性分级（ｇｒａｄｅ，１７９±０２０和２６０±０２５）均大于对照（４２９％及４４４％，Ｐ＜００５；ｇｒａｄｅ，０５７±０３０及０６７±０２９，Ｐ＜００１）．③随饥饿时间延长，出血率及严重性分级逐渐增加，尤其饥饿２４ｈ后与对照差异显著（Ｐ＜００５和Ｐ＜００１）．④饥饿持续时间与出血严重性分级间有显著正相关关系（ｒ＝０５０２，ｔｒ＝２４６０，Ｐ＜００５）．结论门脉高压性胃?
Objective To investigate the relationship between the damage factors and their effect intensity and mucosal hemorrhage (PHGMH) in portal hypertensive gastropathy. Methods Chronic hepatic cirrhosis and portal hypertension were induced by 30g / L thioacetamide in abdomen in rats, followed by starvation-induced portal hypertension gastric mucosal hemorrhage (PHG-MH, n = 34 ), Staged observation (injection 45d, PHT MH Ⅰ, n = 14; injection of 65d, PHT MH Ⅱ, n = 20) 12h ~ 36h after starvation of gastric mucosal hemorrhage and severity changes. Results ① The bleeding rate (912%) and severity grade (263 ± 020) in PHGMH mice were significantly higher than those in control (438%, grade063 ± 020, P <0 01). (2) The mucosal hemorrhage rates of PHGMHⅠ and PHGMHⅡ mice were observed by staging (857% and 950% respectively), and the grade of grade (grade Ⅰ 79 ± 020 and 2 60 ± 0 25) were higher than the control (429% and 444%, P <005; grade, 057 ± 030 and 067 ± 029, P <001). ③ With the prolongation of starvation, the hemorrhage rate and severity grading increased gradually, especially after 24h of starvation, the difference with the control was significant (P <005 and P <001). There was a significant positive correlation between the duration of starvation and the severity of bleeding (r = 0502, tr = 2460, P <005). Conclusion portal hypertension stomach?