血小板活化因子（PAF）抑制剂（TCV-309）可减轻蛙皮素和PAF诱导的胰腺炎。大鼠的形态学和功能研究。

Platelet activating factor (PAF) inhibitor (TCV-309) reduces caerulein- and PAF-induced pancreatitis. A morphologic and functional study in the rat.

作者信息

Tomaszewska R, Dembiński A, Warzecha Z, Banaś M, Konturek S J, Stachura J

机构信息

Department of Clinical and Experimental Pathomorphology, University Medical School, Kraków, Poland.

出版信息

J Physiol Pharmacol. 1992 Dec;43(4):345-52.

PMID:1294265

Abstract

Caerulein-induced acute pancreatitis was studied in rats. Consistent with this type of acute pancreatitis morphological (edema, leukocytic infiltration and acinar cell vaculization) and biochemical (increase in pancreatic protein content. PAF release and serum amylase) changes developed 5 hours after caerulein administration. In addition increase in pancreatic weight and decrease in pancreatic blood flow were noticed. PAF administration caused pancreatic damage similar in some parameters to caerulein-induced pancreatitis, along with reduction of pancreatic blood flow, increase in pancreatic protein content, and serum amylase. TCV-309, a selective PAF antagonist, administered prior to caerulein and/or PAF, reduced caerulein-induced pancreatitis and prevented PAF-induced pancreatitis. Results of our present studies indicate the crucial role of PAF in pathogenesis of experimental acute pancreatitis.

摘要

在大鼠中研究了蛙皮素诱导的急性胰腺炎。与这种类型的急性胰腺炎一致，在给予蛙皮素5小时后出现了形态学（水肿、白细胞浸润和腺泡细胞空泡化）和生化（胰腺蛋白含量增加、血小板活化因子释放和血清淀粉酶升高）变化。此外，还观察到胰腺重量增加和胰腺血流减少。给予血小板活化因子导致胰腺损伤，在某些参数上与蛙皮素诱导的胰腺炎相似，同时伴有胰腺血流减少、胰腺蛋白含量增加和血清淀粉酶升高。在给予蛙皮素和/或血小板活化因子之前给予选择性血小板活化因子拮抗剂TCV-309，可减轻蛙皮素诱导的胰腺炎并预防血小板活化因子诱导的胰腺炎。我们目前的研究结果表明血小板活化因子在实验性急性胰腺炎发病机制中起关键作用。