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Protective effect of liver ischemic preconditioning on liver and lung injury induced by hepatic ischemia-reperfusion in the rat.
Hepatology. 1999 Dec; 30(6):1481-9.Hep

Abstract

This study evaluates whether preconditioning could modulate the injurious effects of tumor necrosis factor (TNF) on liver and lung following hepatic ischemia-reperfusion (I/R) by inhibiting hepatic postischemic TNF release. The inhibition of hepatic TNF release from Kupffer cells with gadolinium chloride (GdCl(3)) previous to ischemia maintained TNF at control levels, attenuating the increases in transaminases, vascular permeability, and edema associated with hepatic I/R injury. TNF addition reverted this beneficial effect, indicating the implication of the TNF released mainly from Kupffer cells in hepatic I/R injury. Preconditioning prevented hepatic TNF increases, thus attenuating the liver injury, while TNF addition abolished the benefits of preconditioning. Inhibition of nitric oxide (NO) synthesis abolished the effect of preconditioning, whereas GdCl(3) addition avoided the injurious effect of NO inhibition. In addition, NO administration before I/R offered similar results to those found in preconditioning, while TNF addition abolished the benefits of NO. Thus, the effect of preconditioning on TNF release after hepatic I/R is mediated by NO. Inhibition of hepatic TNF release from Kupffer cells with GdCl(3) prevented both the increase in plasma TNF and the injurious effect in lung seen after hepatic I/R, and these effects were reverted with TNF addition. Preconditioning resulting in reduced hepatic TNF levels prevented the systemic TNF release, thus reducing the lung damage following hepatic I/R. However, TNF addition abolished the protective effect of preconditioning on lung injury. These findings indicate that preconditioning attenuates hepatic postischemic TNF release from Kupffer cells, thus probably reducing the liver and lung injury following hepatic I/R, and that this effect of preconditioning is mediated by NO.

Authors+Show Affiliations

Department of Medical Bioanalysis, Instituto de Investigaciones Biomédicas de Barcelona, Consejo Superior de Investigaciones Científicas, Barcelona, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10573528

Citation

Peralta, C, et al. "Protective Effect of Liver Ischemic Preconditioning On Liver and Lung Injury Induced By Hepatic Ischemia-reperfusion in the Rat." Hepatology (Baltimore, Md.), vol. 30, no. 6, 1999, pp. 1481-9.
Peralta C, Prats N, Xaus C, et al. Protective effect of liver ischemic preconditioning on liver and lung injury induced by hepatic ischemia-reperfusion in the rat. Hepatology. 1999;30(6):1481-9.
Peralta, C., Prats, N., Xaus, C., Gelpí, E., & Roselló-Catafau, J. (1999). Protective effect of liver ischemic preconditioning on liver and lung injury induced by hepatic ischemia-reperfusion in the rat. Hepatology (Baltimore, Md.), 30(6), 1481-9.
Peralta C, et al. Protective Effect of Liver Ischemic Preconditioning On Liver and Lung Injury Induced By Hepatic Ischemia-reperfusion in the Rat. Hepatology. 1999;30(6):1481-9. PubMed PMID: 10573528.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective effect of liver ischemic preconditioning on liver and lung injury induced by hepatic ischemia-reperfusion in the rat. AU - Peralta,C, AU - Prats,N, AU - Xaus,C, AU - Gelpí,E, AU - Roselló-Catafau,J, PY - 1999/11/26/pubmed PY - 1999/11/26/medline PY - 1999/11/26/entrez SP - 1481 EP - 9 JF - Hepatology (Baltimore, Md.) JO - Hepatology VL - 30 IS - 6 N2 - This study evaluates whether preconditioning could modulate the injurious effects of tumor necrosis factor (TNF) on liver and lung following hepatic ischemia-reperfusion (I/R) by inhibiting hepatic postischemic TNF release. The inhibition of hepatic TNF release from Kupffer cells with gadolinium chloride (GdCl(3)) previous to ischemia maintained TNF at control levels, attenuating the increases in transaminases, vascular permeability, and edema associated with hepatic I/R injury. TNF addition reverted this beneficial effect, indicating the implication of the TNF released mainly from Kupffer cells in hepatic I/R injury. Preconditioning prevented hepatic TNF increases, thus attenuating the liver injury, while TNF addition abolished the benefits of preconditioning. Inhibition of nitric oxide (NO) synthesis abolished the effect of preconditioning, whereas GdCl(3) addition avoided the injurious effect of NO inhibition. In addition, NO administration before I/R offered similar results to those found in preconditioning, while TNF addition abolished the benefits of NO. Thus, the effect of preconditioning on TNF release after hepatic I/R is mediated by NO. Inhibition of hepatic TNF release from Kupffer cells with GdCl(3) prevented both the increase in plasma TNF and the injurious effect in lung seen after hepatic I/R, and these effects were reverted with TNF addition. Preconditioning resulting in reduced hepatic TNF levels prevented the systemic TNF release, thus reducing the lung damage following hepatic I/R. However, TNF addition abolished the protective effect of preconditioning on lung injury. These findings indicate that preconditioning attenuates hepatic postischemic TNF release from Kupffer cells, thus probably reducing the liver and lung injury following hepatic I/R, and that this effect of preconditioning is mediated by NO. SN - 0270-9139 UR - https://www.unboundmedicine.com/medline/citation/10573528/Protective_effect_of_liver_ischemic_preconditioning_on_liver_and_lung_injury_induced_by_hepatic_ischemia_reperfusion_in_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0270913999005182 DB - PRIME DP - Unbound Medicine ER -