Closa D, Hotter G, Bulbena O, Gelpi E, Rosello-Catafau J
Department of Medical Bioanalysis, Centro de Investigacion y Desarrollo, CSIC, Barcelona, Spain.
Pancreas. 1996 Mar;12(2):178-82. doi: 10.1097/00006676-199603000-00012.
The effect of verapamil administration on the changes of prostanoid synthesis, and on free radical production associated with acute pancreatitis, has been evaluated. A necrohemorrhagic model of pancreatitis was induced in Wistar rats by intraductal administration of sodium taurocholate (3.5%). This model is associated with initial increases in prostanoid synthesis and peroxidative damage. Verapamil, administered before pancreatitis induction, prevented initial increases in 6-keto prostaglandin F1alpha (PGF1alpha) and thromboxane B2 (TXB2) but had no effect on PGF2alpha or PGE2 or on lipoperoxidative damage. These results indicate that verapamil administration prevents the increases in pancreatic vasoactive prostanoids (TXB2 and 6-keto PGF1alpha) without affecting the increased levels of PGE2 and PGF2alpha and has no effect on oxygen free radical production in the initial stages of experimental acute pancreatitis.
已评估了维拉帕米给药对前列腺素合成变化以及与急性胰腺炎相关的自由基产生的影响。通过向Wistar大鼠胰管内注射牛磺胆酸钠(3.5%)诱导出坏死性出血性胰腺炎模型。该模型与前列腺素合成和过氧化损伤的初始增加有关。在诱导胰腺炎之前给予维拉帕米,可预防6-酮前列腺素F1α(PGF1α)和血栓素B2(TXB2)的初始增加,但对PGF2α或PGE2或脂质过氧化损伤没有影响。这些结果表明,给予维拉帕米可预防胰腺血管活性前列腺素(TXB2和6-酮PGF1α)的增加,而不影响PGE2和PGF2α的升高水平,并且对实验性急性胰腺炎初始阶段的氧自由基产生没有影响。