Hoffmann T F, Kübler J, Messmer K
Institut für Chirurgische Forschung, Klinikum Grosshadern, Ludwig-Maximilians-Universität München.
Langenbecks Arch Chir Suppl Kongressbd. 1998;115(Suppl I):443-6.
The selective bradykinin B1-receptor-antagonist CP-0298 reduces ischemia/reperfusion induced enhanced leukocyte adherence in postcapillary venules of the pancreas, but has no influence on the microvascular perfusion failure. The postischemic enzyme release will effectively attenuated by the antagonist. Wether the activation of the B1-receptor under pathophysiological conditions exerts protective effects to maintain the integrity of the pancreas, has to be evaluated in further experiments.
选择性缓激肽B1受体拮抗剂CP-0298可减少缺血/再灌注诱导的胰腺毛细血管后微静脉中白细胞黏附增强,但对微血管灌注衰竭无影响。该拮抗剂可有效减轻缺血后酶的释放。病理生理条件下B1受体的激活是否发挥保护作用以维持胰腺的完整性,有待进一步实验评估。