Plusczyk T, Westermann S, Rathgeb D, Feifel G
Department of General Surgery, University of Saarland, Homburg/Saar, Germany.
Am J Physiol. 1997 Feb;272(2 Pt 1):G310-20. doi: 10.1152/ajpgi.1997.272.2.G310.
With use of in vivo microscopy, pancreatic duct permeability, red blood cell (RBC) velocities, functional capillary density (FCD), and overall changes in capillary blood flow (perfusion index) were estimated after intraductal infusion of sodium taurocholate (0.8 ml, 4%) alone or in combination with systemic administration of cholecystokinin (CCK, 0.3 microg/100 g body wt) or secretin (Sec, 10 microg/100 g body wt). Sodium taurocholate mediated a significant increase in pancreatic duct and capillary permeability within 105 +/- 26 s followed by a transient decrease in RBC velocities and a sustained decrease in FCD, which were paralleled by dramatic flow heterogeneity. Therefore, a significant reduction in overall capillary blood flow was calculated. CCK stimulation aggravated the microcirculatory failure due to a decrease in RBC velocities, which was accompanied by an increase in acinar cellular necrosis. Sec stimulation attenuated microcirculatory failure due to a more moderate reduction of FCD. The enhanced pancreatic duct and capillary permeability, which enables free diffusion of pancreatic digestive enzymes into the parenchyma, is the initiating event in acute biliary pancreatitis, causing microcirculatory failure and tissue damage. The microcirculatory changes are secondary and a propagating factor for the development of acini necrosis. Stimulation with CCK worsened the course of acute biliary pancreatitis.
通过体内显微镜检查，在单独经导管注入牛磺胆酸钠（0.8毫升，4%）或与胆囊收缩素（CCK，0.3微克/100克体重）或促胰液素（Sec，10微克/100克体重）全身给药联合使用后，评估胰腺导管通透性、红细胞（RBC）速度、功能性毛细血管密度（FCD）以及毛细血管血流的总体变化（灌注指数）。牛磺胆酸钠在105±26秒内使胰腺导管和毛细血管通透性显著增加，随后红细胞速度短暂下降，FCD持续下降，同时伴有明显的血流不均一性。因此，计算出毛细血管总体血流显著减少。CCK刺激因红细胞速度降低而加重微循环衰竭，同时伴有腺泡细胞坏死增加。Sec刺激因FCD降低程度较为适中而减轻微循环衰竭。胰腺导管和毛细血管通透性增强，使胰腺消化酶能够自由扩散到实质中，这是急性胆源性胰腺炎的起始事件，导致微循环衰竭和组织损伤。微循环变化是继发性的，是腺泡坏死发展的一个传播因素。CCK刺激会使急性胆源性胰腺炎的病程恶化。
