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一种诱导大鼠肝实质缺血性坏死的模型及其定量分析。

A model for provoking ischemic necrosis in rat liver parenchyma and its quantitative analysis.

作者信息

Frederiks W M, James J, Bosch K S, Schröder M J, Schuyt H C

出版信息

Exp Pathol. 1982;22(4):245-52. doi: 10.1016/s0232-1513(82)80015-7.

Abstract

Ischemia in the left lateral and median lobe of the rat liver was provoked by means of a small clip, as applied in human microvascular surgery. After various periods of ischemia (30, 40, 50, 60 and 90 min) the blood flow to these lobes was restored. Twenty-four hours after restoration, the extent of necrosis was estimated quantitatively via morphometric measurements of the relative surfaces of necrotic tissue in photomicrographs of gallocyanin-stained serial sections. After periods of ischemia longer than 40 min, the percentage of necrotic tissue increased linearly with the period of clamping. After 40 min of total ischemia the changes in hepatocytes are for the greater part reversible, whereas after 90 min the majority of the cells have passed the "point of no return" and will no more be able to maintain their integrity.

摘要

按照人体微血管手术的操作方式,用一个小夹子造成大鼠肝脏左外侧叶和中叶的缺血。在经历不同时长的缺血(30、40、50、60和90分钟)后,恢复这些叶的血流。血流恢复24小时后,通过对用胆青素染色的连续切片显微照片中坏死组织相对面积进行形态测量,定量评估坏死程度。缺血时长超过40分钟后,坏死组织的百分比随夹闭时长呈线性增加。全缺血40分钟后,肝细胞的变化大部分是可逆的,而缺血90分钟后,大多数细胞已越过“不可逆点”,将无法再维持其完整性。

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