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嘌呤核苷磷酸化酶:内皮细胞游离氧自由基损伤的新标志物。

Purine nucleoside phosphorylase: a new marker for free oxygen radical injury to the endothelial cell.

作者信息

Rao P N, Walsh T R, Makowka L, Rubin R S, Weber T, Snyder J T, Starzl T E

机构信息

Department of Surgery, University Health Center of Pittsburgh, University of Pittsburgh, Pennsylvania 15261.

出版信息

Hepatology. 1990 Feb;11(2):193-8. doi: 10.1002/hep.1840110206.

DOI:10.1002/hep.1840110206
PMID:2155167
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2972712/
Abstract

The effect of ischemia and reperfusion on purine nucleoside phosphorylase was studied in an isolated perfused rat liver model. This enzyme is localized primarily in the cytoplasm of the endothelial and Kupffer cells; some activity is associated with the parenchymal cells. Levels of this enzyme accurately predicted the extent of ischemia and reperfusion damage to the microvascular endothelial cell of the liver. Livers from Lewis rats were subjected to 30, 45 and 60 min of warm (37 degrees C) no flow ischemia that was followed by a standard reperfusion period lasting 45 min. Purine nucleoside phosphorylase was measured at the end of the no flow ischemia and reperfusion periods as was superoxide generation (O2-). Bile production was monitored throughout the no flow ischemia and reperfusion periods. Control perfusions were carried out for 120 min. A significant rise in purine nucleoside phosphorylase levels as compared with controls was observed at the end of ischemia in all the three groups. The highest level, 203.5 +/- 29.2 mU/ml, was observed after 60 min of ischemia. After the reperfusion period, levels of purine nucleoside phosphorylase decreased in the 30- and 45-min groups 58.17 +/- 9.66 mU/ml and 67.5 +/- 17.1 mU/ml, respectively. These levels were equal to control perfusions. In contrast, after 60 min of ischemia, levels of purine nucleoside phosphorylase decreased early in the reperfusion period and then rose to 127.8 +/- 14.8 mU/ml by the end of reperfusion (p less than 0.0001). Superoxide generation at the beginning of reperfusion was higher than in controls with similar values observed at the end of 30, 45 and 60 min of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在离体灌注大鼠肝脏模型中研究了缺血再灌注对嘌呤核苷磷酸化酶的影响。该酶主要定位于内皮细胞和库普弗细胞的细胞质中;一些活性与实质细胞相关。该酶的水平准确预测了肝脏微血管内皮细胞缺血再灌注损伤的程度。将Lewis大鼠的肝脏进行30、45和60分钟的温(37℃)无血流缺血,随后进行持续45分钟的标准再灌注期。在无血流缺血和再灌注期结束时测量嘌呤核苷磷酸化酶以及超氧化物生成(O2-)。在整个无血流缺血和再灌注期监测胆汁生成。进行120分钟的对照灌注。在所有三组缺血结束时,观察到嘌呤核苷磷酸化酶水平与对照相比显著升高。缺血60分钟后观察到最高水平,为203.5±29.2 mU/ml。再灌注期后,30分钟和45分钟组的嘌呤核苷磷酸化酶水平分别降至58.17±9.66 mU/ml和67.5±17.1 mU/ml。这些水平与对照灌注相等。相比之下,缺血60分钟后,嘌呤核苷磷酸化酶水平在再灌注期早期下降,然后在再灌注结束时升至127.8±14.8 mU/ml(p<0.0001)。再灌注开始时的超氧化物生成高于对照,在缺血30、45和60分钟结束时观察到相似的值。(摘要截断于250字)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/b08b7e5602d1/nihms244726f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/083a41fa38dc/nihms244726f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/8d1b15991e9a/nihms244726f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/da3bbcf187ec/nihms244726f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/16b28651f124/nihms244726f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/b08b7e5602d1/nihms244726f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/083a41fa38dc/nihms244726f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/8d1b15991e9a/nihms244726f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/da3bbcf187ec/nihms244726f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/16b28651f124/nihms244726f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6503/2972712/b08b7e5602d1/nihms244726f5.jpg

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