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大鼠肝脏质膜在短暂缺血后的生化及超微结构变化

Biochemical and ultrastructural changes in rat liver plasma membranes after temporary ischemia.

作者信息

Frederiks W M, Myagkaya G L, van Veen H A, Vogels I M

出版信息

Virchows Arch B Cell Pathol Incl Mol Pathol. 1984;46(4):269-82. doi: 10.1007/BF02890316.

DOI:10.1007/BF02890316
PMID:6150574
Abstract

In this study we have attempted to correlate reversible and irreversible cell damage induced by in vivo or in vitro ischemia with characteristics of the plasma membranes of liver parenchymal cells, as detected biochemically and ultrastructurally. The effects of in vivo or in vitro ischemia appeared to be similar. It was virtually impossible to isolate a substantial membrane fraction from ischemic livers, probably because of changes in the physical properties of the membranes by ischemia. The isolated membranes of ischemic liver cells show ultrastructural changes including the occurrence of many vesicular profiles and alterations in junctional complexes expressed by extended and smudged electron densities along the lateral surfaces. The microvilli of the bile canaliculi disappeared after only 15 min ischemia and cytoplasmic densities associated with junctional complexes also appeared extended and smudged. These changes correspond with the alterations observed in ischemic isolated membranes. After 30 min in vivo ischemia the activity of 5'-mononucleotidase used as a marker enzyme for plasma membranes, decreased by 75%, whereas the activity of thymidine 5'-phosphodiesterase was reduced only slightly. The changes in these enzyme activities were more prominent after in vitro ischemia than after in vivo. The morphological and biochemical changes observed in rat hepatocyte plasma membrane during the early stage of injury have no value in predicting the occurrence of necrosis in a later phase of the process since profound changes occur in plasma membrane properties after even short periods of ischemia (i.e. during the reversible stage).

摘要

在本研究中,我们试图将体内或体外缺血诱导的可逆性和不可逆性细胞损伤与肝实质细胞质膜的特性相关联,这些特性通过生物化学和超微结构检测。体内或体外缺血的影响似乎相似。从缺血肝脏中分离出大量膜组分几乎是不可能的,这可能是由于缺血导致膜的物理性质发生了变化。缺血肝细胞分离出的膜显示出超微结构变化,包括出现许多囊泡样结构以及连接复合体的改变,表现为沿着侧面的电子密度延长和模糊。仅缺血15分钟后,胆小管的微绒毛就消失了,与连接复合体相关的细胞质密度也出现延长和模糊。这些变化与在缺血分离膜中观察到的改变相对应。体内缺血30分钟后,用作质膜标记酶的5'-核苷酸酶活性降低了75%,而胸苷5'-磷酸二酯酶的活性仅略有降低。体外缺血后这些酶活性的变化比体内缺血后更明显。在大鼠肝细胞质膜损伤早期观察到的形态和生化变化对于预测该过程后期坏死的发生没有价值,因为即使在短时间缺血(即可逆阶段)后质膜性质也会发生深刻变化。

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Biochemical and ultrastructural changes in rat liver plasma membranes after temporary ischemia.大鼠肝脏质膜在短暂缺血后的生化及超微结构变化
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J Bioenerg Biomembr. 2012 Oct;44(5):571-7. doi: 10.1007/s10863-012-9459-7. Epub 2012 Jul 25.
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Microvascular changes in liver after ischemia-reperfusion injury. Protection with misoprostol.肝脏缺血再灌注损伤后的微血管变化。米索前列醇的保护作用。
Dig Dis Sci. 1994 Aug;39(8):1683-90. doi: 10.1007/BF02087776.
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Ischemia induces surface membrane dysfunction. Mechanism of altered Na+-dependent glucose transport.
缺血会导致表面膜功能障碍。钠依赖性葡萄糖转运改变的机制。
J Clin Invest. 1987 Sep;80(3):647-54. doi: 10.1172/JCI113117.
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Changes in acid phosphatase activity in rat liver after ischemia.缺血后大鼠肝脏酸性磷酸酶活性的变化。
Histochemistry. 1989;93(2):161-6. doi: 10.1007/BF00315970.