Kusterer K, Enghofer M, Poschmann T, Usadel K H
Dept. of Endocrinology, Johann Wolfgang Goethe-University, Frankfurt, FRG.
Acta Physiol Hung. 1992;80(1-4):407-15.
In vivo microscopy was performed to assess the effect of dextran 40, gabexate mesilate and somatostatin on the microcirculation in sodium taurocholate-induced pancreatitis in rats. Intraductal infusion of 0.4 ml of a 4% solution of sodium taurocholate decreased capillary blood flow, induced capillary stasis and increased vascular permeability in the head of the pancreas. Dextran 40, gabexate mesilate and somatostatin improved capillary blood flow in the initial phase of acute pancreatitis significantly and prevented stasis in 5 of 9, 3 of 8 and 7 of 10 (p < 0.05) cases. Only dextran 40 reduced the increase of vascular permeability. Decrease of capillary blood flow, capillary stasis and vascular permeability changes are important factors contributing to the pathogenesis of sodium taurocholate-induced pancreatitis. Dextran 40, gabexate mesilate and somatostatin exert a beneficial effect on the microcirculatory changes in this model of acute pancreatitis.
采用体内显微镜技术评估右旋糖酐40、甲磺酸加贝酯和生长抑素对牛磺胆酸钠诱导的大鼠胰腺炎微循环的影响。向大鼠胰管内注入0.4 ml 4%的牛磺胆酸钠溶液可使胰腺头部的毛细血管血流减少，导致毛细血管淤滞，并增加血管通透性。右旋糖酐40、甲磺酸加贝酯和生长抑素在急性胰腺炎的初始阶段可显著改善毛细血管血流，并分别在9只中的5只、8只中的3只和10只中的7只（p<0.05）中预防了淤滞。只有右旋糖酐40降低了血管通透性的增加。毛细血管血流减少、毛细血管淤滞和血管通透性变化是牛磺胆酸钠诱导的胰腺炎发病机制的重要因素。右旋糖酐40、甲磺酸加贝酯和生长抑素对该急性胰腺炎模型的微循环变化具有有益作用。
