Differential, histochemical and immunohistochemical changes in rat hepatocytes after isoflurane or sevoflurane exposure

Differential, histochemical and immunohistochemical changes were observed in hepatocytes from immediately to 7 days after isoflurane or sevoflurane exposure (at H 0 to on Day 7) to study the process of development and recovery in anesthetic-induced hepatic injury. A total of 570 7-week-old male Spra...

Full description

Saved in:
Bibliographic Details
Published inActa medica Okayama Vol. 57; no. 1; p. 1
Main Authors Honda, Mayumi, Yamada, Teruo, Nomura, Takako, Miki, Yukari, Kanda, Shigeto, Seki, Akihiko, Sasaki, Junzou
Format Journal Article
LanguageEnglish
Published Japan 01.02.2003
Subjects
Anesthetics, Inhalation - adverse effects
Animals
Halothane - adverse effects
Hepatocytes - chemistry
Hepatocytes - drug effects
Immunohistochemistry
Inhalation Exposure - adverse effects
Isoflurane - adverse effects
Liver Glycogen - metabolism
Male
Methyl Ethers - adverse effects
Rats
Rats, Sprague-Dawley
RNA, Ribosomal - metabolism
Online AccessGet full text

Cover

More Information
Summary:Differential, histochemical and immunohistochemical changes were observed in hepatocytes from immediately to 7 days after isoflurane or sevoflurane exposure (at H 0 to on Day 7) to study the process of development and recovery in anesthetic-induced hepatic injury. A total of 570 7-week-old male Sprague-Dawley rats with or without phenobarbital treatment were exposed to isoflurane or sevoflurane in 100%, 21%, or 10% oxygen, or to 10% oxygen alone for 2h. In phenobarbital-treated rats, hepatocytes both with and without anesthetic exposure markedly changed in 10% oxygen at H 0. Glycogen and ribosomal ribonucleic acid (rRNA) disappeared at H 0 and at H 6, respectively, and at H 6, AST levels in the blood rose. From H 6 to Day 1, necrosis developed more markedly and widely in zone 3 hepatocytes exposed to anesthetics in 10% oxygen than in those exposed to oxygen alone. All degenerated tissues had returned to normal levels by day 7. Recovery of the hepatolobular structure may be attributed to rearrangement of remaining hepatocytes in the portal vein area. Both the disappearance of glycogen and rRNA and the increase in blood AST levels after exposure to isoflurane or sevoflurane are considered to be factors contributing to the induction of necrosis around the central vein. The grade of isoflurane-induced hepatic injury was found to be significantly higher than that of sevoflurane.
ISSN:0386-300X