Tumor necrosis factor suppression and microcirculatory disturbance amelioration in ischemia/reperfusion injury of rat liver after ischemic preconditioning

Masahiro Shinoda, Motohide Shimazu, Go Wakabayashi, Minoru Tanabe, Ken Hoshino, Masaki Kitajima

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: Brief periods of hepatic ischemia produce immediate tolerance for subsequent prolonged ischemia. Although the beneficial effect of this ischemic preconditioning is recognized, the mechanism itself remains poorly understood. Methods: Male Wistar rats were divided into two groups: a control group that was subjected to 30 min of ischemia + following reperfusion, and an ischemic preconditioning group that was subjected to 5 min of ischemia + 5 min of reperfusion + 30 min of ischemia + following reperfusion. By using this model, hepatic damage, microcirculatory disturbances, and tumor necrosis factor-α protein production and mRNA expression were analyzed during the course of reperfusion in both groups. For the hepatic damage evaluations, hepatic enzyme levels, histology, apoptosis analysis, and intravital microfluorography for dead cells were examined. For the microcirculatory disturbance analysis, an adhesion molecule and intravital microfluorography for endothelial-adherent leukocytes were examined. Results: In the ischemic preconditioning group, ischemia/reperfusion injuries (shown by hepatic enzymes elevation, histological degeneration, and increases in the number of apoptotic cells and microfluorographic dead cells) were markedly reduced. Moreover, microcirculatory disturbances represented by intercellular adhesion molecule-1 expression and leukocyte adhesion on the endothelium were ameliorated. Tumor necrosis factor-α protein production and mRNA expression were also suppressed in the ischemic preconditioning group. Conclusion: The suppression of tumor necrosis factor-α and the subsequent amelioration of microcirculatory disturbances were observed, suggesting that the mechanism underlying the protective effect of ischemic preconditioning in hepatic ischemia/reperfusion injuries may involve tumor necrosis factor-α and microcirculatory regulation.

Original languageEnglish
Pages (from-to)1211-1219
Number of pages9
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume17
Issue number11
DOIs
Publication statusPublished - 2002

Fingerprint

Ischemic Preconditioning
Reperfusion Injury
Tumor Necrosis Factor-alpha
Ischemia
Reperfusion
Liver
Leukocytes
Messenger RNA
Intercellular Adhesion Molecule-1
Enzymes
Endothelium
Wistar Rats
Histology
Proteins
Cell Count
Apoptosis
Control Groups

Keywords

  • Ischemia reperfusion
  • Ischemic preconditioning
  • Liver
  • Microcirculation
  • Tumor necrosis factor

ASJC Scopus subject areas

  • Gastroenterology
  • Hepatology

Cite this

Tumor necrosis factor suppression and microcirculatory disturbance amelioration in ischemia/reperfusion injury of rat liver after ischemic preconditioning. / Shinoda, Masahiro; Shimazu, Motohide; Wakabayashi, Go; Tanabe, Minoru; Hoshino, Ken; Kitajima, Masaki.

In: Journal of Gastroenterology and Hepatology (Australia), Vol. 17, No. 11, 2002, p. 1211-1219.

Research output: Contribution to journalArticle

@article{9fa0687acc6046b383c617d83d34f2d4,
title = "Tumor necrosis factor suppression and microcirculatory disturbance amelioration in ischemia/reperfusion injury of rat liver after ischemic preconditioning",
abstract = "Background: Brief periods of hepatic ischemia produce immediate tolerance for subsequent prolonged ischemia. Although the beneficial effect of this ischemic preconditioning is recognized, the mechanism itself remains poorly understood. Methods: Male Wistar rats were divided into two groups: a control group that was subjected to 30 min of ischemia + following reperfusion, and an ischemic preconditioning group that was subjected to 5 min of ischemia + 5 min of reperfusion + 30 min of ischemia + following reperfusion. By using this model, hepatic damage, microcirculatory disturbances, and tumor necrosis factor-α protein production and mRNA expression were analyzed during the course of reperfusion in both groups. For the hepatic damage evaluations, hepatic enzyme levels, histology, apoptosis analysis, and intravital microfluorography for dead cells were examined. For the microcirculatory disturbance analysis, an adhesion molecule and intravital microfluorography for endothelial-adherent leukocytes were examined. Results: In the ischemic preconditioning group, ischemia/reperfusion injuries (shown by hepatic enzymes elevation, histological degeneration, and increases in the number of apoptotic cells and microfluorographic dead cells) were markedly reduced. Moreover, microcirculatory disturbances represented by intercellular adhesion molecule-1 expression and leukocyte adhesion on the endothelium were ameliorated. Tumor necrosis factor-α protein production and mRNA expression were also suppressed in the ischemic preconditioning group. Conclusion: The suppression of tumor necrosis factor-α and the subsequent amelioration of microcirculatory disturbances were observed, suggesting that the mechanism underlying the protective effect of ischemic preconditioning in hepatic ischemia/reperfusion injuries may involve tumor necrosis factor-α and microcirculatory regulation.",
keywords = "Ischemia reperfusion, Ischemic preconditioning, Liver, Microcirculation, Tumor necrosis factor",
author = "Masahiro Shinoda and Motohide Shimazu and Go Wakabayashi and Minoru Tanabe and Ken Hoshino and Masaki Kitajima",
year = "2002",
doi = "10.1046/j.1440-1746.2002.02864.x",
language = "English",
volume = "17",
pages = "1211--1219",
journal = "Journal of Gastroenterology and Hepatology (Australia)",
issn = "0815-9319",
publisher = "Wiley-Blackwell",
number = "11",

}

TY - JOUR

T1 - Tumor necrosis factor suppression and microcirculatory disturbance amelioration in ischemia/reperfusion injury of rat liver after ischemic preconditioning

AU - Shinoda, Masahiro

AU - Shimazu, Motohide

AU - Wakabayashi, Go

AU - Tanabe, Minoru

AU - Hoshino, Ken

AU - Kitajima, Masaki

PY - 2002

Y1 - 2002

N2 - Background: Brief periods of hepatic ischemia produce immediate tolerance for subsequent prolonged ischemia. Although the beneficial effect of this ischemic preconditioning is recognized, the mechanism itself remains poorly understood. Methods: Male Wistar rats were divided into two groups: a control group that was subjected to 30 min of ischemia + following reperfusion, and an ischemic preconditioning group that was subjected to 5 min of ischemia + 5 min of reperfusion + 30 min of ischemia + following reperfusion. By using this model, hepatic damage, microcirculatory disturbances, and tumor necrosis factor-α protein production and mRNA expression were analyzed during the course of reperfusion in both groups. For the hepatic damage evaluations, hepatic enzyme levels, histology, apoptosis analysis, and intravital microfluorography for dead cells were examined. For the microcirculatory disturbance analysis, an adhesion molecule and intravital microfluorography for endothelial-adherent leukocytes were examined. Results: In the ischemic preconditioning group, ischemia/reperfusion injuries (shown by hepatic enzymes elevation, histological degeneration, and increases in the number of apoptotic cells and microfluorographic dead cells) were markedly reduced. Moreover, microcirculatory disturbances represented by intercellular adhesion molecule-1 expression and leukocyte adhesion on the endothelium were ameliorated. Tumor necrosis factor-α protein production and mRNA expression were also suppressed in the ischemic preconditioning group. Conclusion: The suppression of tumor necrosis factor-α and the subsequent amelioration of microcirculatory disturbances were observed, suggesting that the mechanism underlying the protective effect of ischemic preconditioning in hepatic ischemia/reperfusion injuries may involve tumor necrosis factor-α and microcirculatory regulation.

AB - Background: Brief periods of hepatic ischemia produce immediate tolerance for subsequent prolonged ischemia. Although the beneficial effect of this ischemic preconditioning is recognized, the mechanism itself remains poorly understood. Methods: Male Wistar rats were divided into two groups: a control group that was subjected to 30 min of ischemia + following reperfusion, and an ischemic preconditioning group that was subjected to 5 min of ischemia + 5 min of reperfusion + 30 min of ischemia + following reperfusion. By using this model, hepatic damage, microcirculatory disturbances, and tumor necrosis factor-α protein production and mRNA expression were analyzed during the course of reperfusion in both groups. For the hepatic damage evaluations, hepatic enzyme levels, histology, apoptosis analysis, and intravital microfluorography for dead cells were examined. For the microcirculatory disturbance analysis, an adhesion molecule and intravital microfluorography for endothelial-adherent leukocytes were examined. Results: In the ischemic preconditioning group, ischemia/reperfusion injuries (shown by hepatic enzymes elevation, histological degeneration, and increases in the number of apoptotic cells and microfluorographic dead cells) were markedly reduced. Moreover, microcirculatory disturbances represented by intercellular adhesion molecule-1 expression and leukocyte adhesion on the endothelium were ameliorated. Tumor necrosis factor-α protein production and mRNA expression were also suppressed in the ischemic preconditioning group. Conclusion: The suppression of tumor necrosis factor-α and the subsequent amelioration of microcirculatory disturbances were observed, suggesting that the mechanism underlying the protective effect of ischemic preconditioning in hepatic ischemia/reperfusion injuries may involve tumor necrosis factor-α and microcirculatory regulation.

KW - Ischemia reperfusion

KW - Ischemic preconditioning

KW - Liver

KW - Microcirculation

KW - Tumor necrosis factor

UR - http://www.scopus.com/inward/record.url?scp=0036917097&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036917097&partnerID=8YFLogxK

U2 - 10.1046/j.1440-1746.2002.02864.x

DO - 10.1046/j.1440-1746.2002.02864.x

M3 - Article

VL - 17

SP - 1211

EP - 1219

JO - Journal of Gastroenterology and Hepatology (Australia)

JF - Journal of Gastroenterology and Hepatology (Australia)

SN - 0815-9319

IS - 11

ER -