Hepatic phosphatidylcholine hydroperoxide content in noncirrhotic, cirrhotic, and antioxidant-treated rats with endotoxemia

Mohammad Masihur Rahman, Masanori Suzuki, Michiaki Unno, Kojin Endo, Heigo Takeuchi, Tetsuya Kakita, Seiki Matsuno

研究成果: Article査読

5 被引用数 (Scopus)

抄録

Hepatic phosphatidylcholine hydroperoxide (PCOOH) was studied intensively to delineate its role in the altered pathophysiology of liver failure associated with endotoxemic shock. Endotoxemia was induced by cecal ligation and puncture (CLP) in three models using rats. Model 1 consisted of normal healthy rats; model 2, cirrhotic rats; and model 3, rats treated with catalase and superoxide dismutase (SOD). Samples were taken before CLP, then 12h and 24h following CLP. A progressive and significant increase in serum endotoxin was seen in all models; however, a significantly low energy charge (EC) and high PCOOH were seen in models 1 and 2, whereas no change was observed in model 3. The regional blood flow remained unchanged throughout the experiment in models I and 3, but not in model 2. An initial increase in α-tocopherol was seen in model 1. The survival rate was markedly better in model 3 than in models 1 or 2. The fall in EC corresponded to the increase in serum endotoxin as well as to the increase in tissue PCOOH in models 1 and 2. It was more likely that the elevated lipid peroxidation in model 1 resulted from endotoxemia rather than from tissue hypoperfusion. The early increase in α-tocopherol that occurred in models 1 and 2, but not in model 3, indicated the antiradical defense response to oxidative injury. Thus, antioxidant therapy significantly improved the survival rate and tissue adenine nucleotide level in spite of the increased serum endotoxin level.

本文言語English
ページ(範囲)1047-1052
ページ数6
ジャーナルSurgery today
29
10
DOI
出版ステータスPublished - 1999 11 12

ASJC Scopus subject areas

  • 外科

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