Wiles D, Yeginsu O, Ozden A, Covington S M, Rice J, Ertan A
Section of Gastroenterology, Tulane University Medical School, New Orleans, Louisiana 70112.
Dig Dis Sci. 1988 Jul;33(7):878-82. doi: 10.1007/BF01550979.
Because hypovolemic shock is known to cause gastric ulcers in animals and human beings, we investigated the tissue levels of somatostatin-like immunoreactivity (SLI) in the gastric corpus and antrum, duodenum, and pancreas during hypovolemic shock in rats. We studied male Wistar rats (N = 10 each) 15 min, 2 hr, and 12 hr after hypovolemic shock and compared results to a control group (N = 15). Two rats in both 2-hr and 12-hr groups showed gastric ulcers: three corporal and one antral. One animal developed multiple ulcers. In the gastric corpus and antrum and in the duodenum, tissue SLI showed significant decrease 15 min and 2 hr after shock. Gastric SLI remained low, whereas duodenal SLI recovered and rose above control level at 12 hr. Pancreatic SLI showed no significant changes during hypovolemic shock. Gastric tissue SLI levels that were significantly lower after shock than those of normal controls may have contributed to the peptic ulcer disease induced by hypovolemic shock in this experimental model.
由于已知低血容量性休克会在动物和人类中引发胃溃疡,我们研究了大鼠低血容量性休克期间胃体、胃窦、十二指肠和胰腺中生长抑素样免疫反应性(SLI)的组织水平。我们研究了雄性Wistar大鼠(每组N = 10只)在低血容量性休克后15分钟、2小时和12小时的情况,并将结果与对照组(N = 15只)进行比较。2小时和12小时组各有两只大鼠出现胃溃疡:3只在胃体,1只在胃窦。1只动物出现多处溃疡。在胃体、胃窦和十二指肠中,休克后15分钟和2小时组织SLI显著降低。胃SLI维持在低水平,而十二指肠SLI在12小时时恢复并升至对照组水平以上。低血容量性休克期间胰腺SLI无显著变化。休克后胃组织SLI水平显著低于正常对照组,这可能在该实验模型中导致了低血容量性休克诱发的消化性溃疡疾病。