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对接受化合物48/80诱导的过敏性休克的大鼠肝细胞进行形态计量分析。

Morphometric analysis of hepatocytes from rats subjected to compound 48/80-induced anaphylactic shock.

作者信息

Dimlich R V, Cardell R R

出版信息

Tissue Cell. 1985;17(3):293-308. doi: 10.1016/0040-8166(85)90049-7.

DOI:10.1016/0040-8166(85)90049-7
PMID:4012763
Abstract

Morphometric and biochemical techniques were used to analyze hepatic glycogen, endoplasmic reticulum, and mitochondrial matrix granules in rats treated with compound 48/80 to induce an anaphylactic-like state of shock. Thirty minutes after insult there was a significant decrease in glycogen and mitochondrial matrix granules, an increase in rough endoplasmic reticulum (RER), and no change in smooth endoplasmic reticulum (SER). Less glycogen in experimental rats substantiated a previously described glycogenolytic response to compound 48/80. The decrease in matrix granules implies a loss and/or shift in intramitochondrial calcium as occurs in epinephrine-induced glycogenolysis in the rat. Since other glycogenolytic agents, e.g. glucagon, and starvation stimulate an increase in SER presumably from RER, the present morphological data suggest the increase in RER may precede proliferation of SER from RER.

摘要

采用形态测量和生化技术分析用化合物48/80处理以诱导类过敏休克状态的大鼠的肝糖原、内质网和线粒体基质颗粒。损伤30分钟后,糖原和线粒体基质颗粒显著减少,粗面内质网(RER)增加,滑面内质网(SER)无变化。实验大鼠体内糖原减少证实了先前描述的对化合物48/80的糖原分解反应。基质颗粒的减少意味着线粒体内钙的丢失和/或转移,这与肾上腺素诱导的大鼠糖原分解中发生的情况相同。由于其他糖原分解剂,如胰高血糖素和饥饿,可能会刺激SER从RER增加,目前的形态学数据表明RER的增加可能先于SER从RER的增殖。

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Morphometric analysis of hepatocytes from rats subjected to compound 48/80-induced anaphylactic shock.对接受化合物48/80诱导的过敏性休克的大鼠肝细胞进行形态计量分析。
Tissue Cell. 1985;17(3):293-308. doi: 10.1016/0040-8166(85)90049-7.
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