In experimental small bowel obstruction an increased proportion of smooth endoplasmic reticulum and an increased number of lysosomes were seen in many liver cells. The occurrence of cytoplasmic vacuoles as well as the glycogen depletion were not pathognomonic and in the toxic pathogenesis the ultrastructural damage in the liver was only of a low degree and can be explained as a reactive (e.g. detoxication) phenomenon. The increase of plasma corticosterone content (stress reaction) differed only slightly from that of the controls, but a severe disturbance of fluid balance (increase of hematocrit and decrease of serum Na+ and C1-) and circulation failure were the more conspicuous findings, compared to toxic liver cell disturbance in the pathogenesis of small bowel obstruction.

译文

在实验性小肠梗阻中,在许多肝细胞中观察到光滑内质网的比例增加和溶酶体数量增加。细胞质空泡的发生以及糖原的耗竭不是病理性的,在毒性发病机理中,肝脏的超微结构损伤程度较低,可以解释为反应性 (例如解毒) 现象。血浆皮质酮含量 (应激反应) 的增加与对照组仅略有不同,但更明显的是体液平衡严重紊乱 (血细胞比容增加,血清Na和C1-降低) 和循环衰竭。在小肠梗阻的发病机理中与毒性肝细胞紊乱相比。

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