Letko G, Falkenberg B
Division of Experimental Surgery, Medical Academy of Magdeburg, Germany.
Gastroenterol J. 1991;51(3-4):159-63.
Aprotinin, a protease inhibitor, and promazine, an inhibitor of phospholipase A2, were tested for possible inhibition of pancreatic acinar cell (PAC) decline induced by uncoupling of oxidative phosphorylation with 2,4-dinitrophenol (DNP) or by temporary anoxia/reoxygenation. In incubates of acinar cells isolated from rat pancreas the presence of aprotinin did not influence the survival of cells treated with these noxae. This finding excludes that extracellulary acting trypsin, possibly released from damaged cells, contributes to further cell death. While promazine at concentrations of 15 to 20 nmol.(10(6) cells)-1 was well tolerated by untreated PAC, higher concentrations caused a clear reduction of cell viability. At optimum concentration promazine was without influence on DNP-treated cells, but it had a beneficial effect on survival and morphology of anoxia-treated PAC (p less than or equal to 0.05). Therefore, it can be assumed that after anoxia/reoxygenation the membrane phospholipase A2 becomes stimulated and causes phospholipid depletion with final death of the cells. It is suggested that such a mechanism may contribute to the initial cell damage in the pathogenesis of acute pancreatitis, too.
对蛋白酶抑制剂抑肽酶和磷脂酶A2抑制剂异丙嗪进行了测试，以考察它们对因2,4 -二硝基苯酚（DNP）使氧化磷酸化解偶联或因短暂缺氧/复氧所诱导的胰腺腺泡细胞（PAC）衰退是否有抑制作用。在从大鼠胰腺分离的腺泡细胞培养物中，抑肽酶的存在并不影响经这些损伤因素处理的细胞的存活。这一发现排除了可能从受损细胞释放的细胞外作用的胰蛋白酶导致进一步细胞死亡的可能性。虽然浓度为15至20 nmol·(10⁶细胞)⁻¹的异丙嗪对未处理的PAC耐受性良好，但更高浓度会导致细胞活力明显降低。在最佳浓度下，异丙嗪对DNP处理的细胞没有影响，但对缺氧处理的PAC的存活和形态有有益作用（p≤0.05）。因此，可以假定在缺氧/复氧后，膜磷脂酶A2被激活，导致磷脂耗竭，最终细胞死亡。有人提出，这样一种机制可能也在急性胰腺炎发病过程中的初始细胞损伤中起作用。
