Exogenous bradykinin enhances ischemia/reperfusion injury of pancreas in rats.

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.