[A symptomatic ectopic pancreas in the stomach--a case report]. / Objawowa ektopowa tkanka trzustkowa w zolqdku--opis przypadku.

Ectopic pancreas (heterotopic pancreas) is a congenital anomaly and the most common type of ectopic tissue in the gastrointestinal tract. It is typically located in the stomach, duodenum and jejunum. Ectopic pancreas is usually an asymptomatic and benign lesion, in a majority of cases found incidentally during endoscopy or surgery. Generally appears as submucosal lesion with characteristic central umbilication. Complications of heterotopic pancreas are secondary to pathologic changes occurring in the normal pancreatic tissue or caused by ,,mass effect". Asymptomatic cases of ectopic pancreatic tissue are seldom recognized at a preoperative stage. In this paper we reported a case of symptomatic heterotopic pancreatic tissue in a young man, requiring surgical treatment.

Protease inhibitor leupeptin attenuates myocardial stunning in rat heart.

BACKGROUND: In order to test the hypothesis that cardiac protein degradation contributes to the pathogenesis of myocardial stunning, the effect of protease inhibitor leupeptin on the postischemic hemodynamics and metabolic functioning was measured in isolated rat hearts. MATERIAL/METHODS: Isolated rat hearts were perfused in Langendorff mode in the presence or absence of leupeptin (10 Kg/ml for 10 min.), and then subjected to 20 min. of normothermic ischemia and 30 min. of reperfusion. Aortic pressure, cardiac output, coronary flow (CF), global oxygen consumption (MVO2), carbon dioxide and [H+] release, and [Ca2+] uptake were investigated. RESULTS: Hearts pretreated with leupeptin exhibited better postischemic return of systolic, diastolic and developed aortic pressure and faster return of CF to preischemic values during reperfusion. MVO2 and CO2 release were lower in this group in the 10th and 15th min. of reperfusion and [Ca2+] uptake higher in the 5th and 15th min. of reperfusion CONCLUSIONS: Leupeptin protects the heart from myocardial stunning, which is consistent with the idea that proteases contribute to the pathogenesis of this phenomenon.

Ischemic preconditioning diminishes oxygen demand and increases coronary flow in the early phase of reperfusion in rat heart.

BACKGROUND: Ischemic preconditioning (IPC) can be defined as an adaptive mechanism induced by a brief period of reversible ischemia increasing the heart's resistance to a subsequent longer period of ischemia. The objective of our research was to describe the effects of IPC on the hemodynamic function and metabolism of the myocardium during postischemic reperfusion. MATERIAL/METHODS: 20 rat hearts were assigned to a preconditioning group (n=10) or to a control group (n=10). Preconditioning was achieved with 5 min. of global ischemia and 10 min. of reperfusion followed by 40 min. of ischemia. We investigated the postischemic recovery of aortic pressure, cardiac output, and coronary flow, as well as oxygen consumption, carbon dioxide release, and [H+] release. RESULTS: No significant intergroup differences in aortic pressure and cardiac output were observed during reperfusion. In both groups, increased coronary flow (greater in the IPC group: 11.4+/-0.6 ml/min. vs 9.1+/-0.5 ml/min. in control group) was observed in the early phase of reperfusion. This was accompanied by a rise in CO2 and [H+] release, which was also greater in the IPC group. Oxygen consumption was significantly lower in the IPC group in the later phase of reperfusion (9.39+/-0.53 vs 11.79+/-0.54 micromol/min/g dry weight), as were CO2 and [H+] release. CONCLUSIONS: IPC diminishes oxygen demand during reperfusion without changing the hemodynamic function considerably. IPC results in a transient increase of coronary flow accompanied by a rise in CO2 and [H+] release.