Effects of intestinal ischemia/reperfusion injury on gastric acid secretion.
Effects of intestinal ischemia/reperfusion injury on gastric acid secretion.
复制标题
肠道缺血/再灌注损伤对胃酸分泌的影响。
DOI:
10.1006/jsre.2000.5853
复制
发表时间:
2000
期刊:
影响因子:
--
通讯作者:
Mercer,DW
中科院分区:
文献类型:
--
作者:
Castañeda,A;Vilela,R;Chang,L;Mercer,DW
BackgroundThe mechanism responsible for gastric colonization in critically injured ICU patients remains to be fully elucidated. Moreover, the effects of gut ischemia/reperfusion (I/R) injury on gastric function are unclear. It was our hypothesis that gut I/R injury would cause gastric dysfunction.Materials and methodsRats were anesthetized and, via laparotomy, the superior mesenteric artery (SMA) was clamped at its aortic origin for 45 min followed by clamp removal. Rats were allowed to awaken and then killed after 6 h of reperfusion. Control rats underwent laparotomy with SMA isolation. Stomachs were removed, gastric fluid was aspirated, and the volume, pH, and protein, bicarbonate, and glucose contents were determined. Serum and antral mucosa were prepared for gastrin radioimmunoassay and the glandular mucosa was assessed for morphologic injury.ResultsSMA I/R injury caused significant accumulation of gastric luminal fluid that was alkaline and rich in protein, glucose, and bicarbonate content when compared with sham controls. SMA I/R injury also caused gastric surface epithelial cell injury and significantly increased serum and antral gastrin levels. In additional rats, gut I/R injury inhibited basal acid secretion and blunted the acid secretory response to pentagastrin.ConclusionsThis study demonstrated for the first time that small intestinal I/R injury causes significant gastric dysfunction. The findings suggest that this type of injury, a frequent occurrence in critically injured ICU patients, may predispose patients to gastric colonization due to stasis and loss of the natural bactericidal effects of gastric acid.