Hass H J, Wilhelm W, Kemnitz P, Letko G
Division of Experimental Surgery of the Clinic of Surgery; Medical Academy of Magdeburg, Germany.
Int J Pancreatol. 1991 Sep;10(1):39-49. doi: 10.1007/BF02924252.
In the pathogenesis of acute pancreatitis, the events and mechanisms increasing the digestibility of the pancreatic acinar cells are widely unknown. Therefore, the possible contribution of a disturbed energy supply (provoked by anoxia or partial uncoupling) to the induction of autodigestion was studied in experiments on acinar cells isolated from the pancreas. During incubation viability, respiration under normal and maximally stimulated conditions, and trypsin-inhibiting capacity (TIC) of these cells were determined. With increasing duration of anoxia, the portion of surviving cells was strongly diminished, and the number of cells with blebs and vesicularly transformed endoplasmic reticulum was increased. Although the endogenous respiration was not influenced up to 1.5 h of anoxia, 30 min of anoxia substantially decreased the capacity of oxidative energy production. The survival curves were characterized by a self-accelerating course of cell destruction. The alteration of the cellular energy metabolism found its reflection in the decreased TIC of the cells.
在急性胰腺炎的发病机制中，增加胰腺腺泡细胞消化性的事件和机制尚不明确。因此，在从胰腺分离的腺泡细胞实验中，研究了能量供应紊乱（由缺氧或部分解偶联引起）对自消化诱导的可能作用。在孵育过程中，测定了这些细胞的活力、正常和最大刺激条件下的呼吸以及胰蛋白酶抑制能力（TIC）。随着缺氧时间的延长，存活细胞的比例显著降低，出现气泡和内质网囊泡样改变的细胞数量增加。尽管在缺氧1.5小时内，内源性呼吸未受影响，但缺氧30分钟显著降低了氧化能量产生的能力。存活曲线的特征是细胞破坏呈自我加速过程。细胞能量代谢的改变反映在细胞TIC的降低上。
