Hoffmann T F, Steinbauer M, Waldner H, Messmer K
Institute for Surgical Research, Klinikum Innenstadt, Ludwig-Maximilians-University, Munich, Germany.
J Surg Res. 1996 Apr;62(1):144-51. doi: 10.1006/jsre.1996.0187.
We have investigated the effect of bradykinin on microvascular perfusion failure and enzyme release after ischemia/reperfusion of the pancreas in rats. Using intravital fluorescence microscopy in 21 anesthetized Sprague-Dawley rats, quantitative analysis of the microcirculation, including functional capillary density (FCD) and leukocyte-endothelium interaction, was performed in an ischemia/reperfusion model of the pancreas. Bradykinin was dissolved in phosphate buffer and given as a bolus injection (injection group, 10 microgram/kg body wt i.a.; n = 7) or continuously infused (infusion group, 125 microgram/kg body wt/hr i.a.; n = 7) 15 min before the end of 2 hr of ischemia. Two further groups underwent sham operation (control group, n = 7) or an ischemia of 2 hr (ischemia group, n = 7) without bradykinin administration. Continuous infusion of bradykinin resulted in a significant enhancement of capillary perfusion failure after ischemia during reperfusion. In the bradykinin infusion group less than 25% of the capillaries were perfused (FCD 98 +/- 9 cm -1) after 2 hr of reperfusion, whereas in the ischemia group without bradykinin, 50% of capillaries were perfused (FCD 192 +/- 11 cm -1). Both of these values are significantly different from the baseline value of the control group (408 +/- 9 cm -1). The rise in pancreas amylase concentration was significantly more pronounced in the infusion group (basal: 1812 +/- 114 U/1; 2 hr of reperfusion 3375 +/- 268 U/1) when compared to the ischemia group (basal: 2386 +/- 283 U/1; 2 hr of reperfusion 3486 +/- 268 U/1). These findings suggest that bradykinin has an additive role in aggravation of pancreatic microcirculatory failure after ischemia/reperfusion of the pancreas.
我们研究了缓激肽对大鼠胰腺缺血/再灌注后微血管灌注衰竭和酶释放的影响。在21只麻醉的Sprague-Dawley大鼠中使用活体荧光显微镜，在胰腺缺血/再灌注模型中对微循环进行定量分析，包括功能性毛细血管密度（FCD）和白细胞-内皮细胞相互作用。缓激肽溶解于磷酸盐缓冲液中，在2小时缺血结束前15分钟进行单次注射（注射组，腹腔注射10微克/千克体重；n = 7）或持续输注（输注组，腹腔注射125微克/千克体重/小时；n = 7）。另外两组分别接受假手术（对照组，n = 7）或2小时缺血（缺血组，n = 7）且不给予缓激肽。持续输注缓激肽导致再灌注期间缺血后毛细血管灌注衰竭显著加重。在缓激肽输注组，再灌注2小时后不到25%的毛细血管被灌注（FCD 98±9 cm-1），而在未给予缓激肽的缺血组，50%的毛细血管被灌注（FCD 192±11 cm-1）。这两个值均与对照组的基线值（408±9 cm-1）有显著差异。与缺血组（基础值：2386±283 U/1；再灌注2小时 3486±268 U/1）相比，输注组胰腺淀粉酶浓度升高明显更显著（基础值：1812±114 U/1；再灌注2小时 3375±268 U/1）。这些发现表明，缓激肽在胰腺缺血/再灌注后加重胰腺微循环衰竭方面具有叠加作用。
