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Titolo:
Kupffer cells end neutrophils as paracrine regulators of the heme oxygenase-1 gene in hepatocytes after hemorrhagic shock
Autore:
Paxian, M; Rensing, H; Rickauer, A; Schonhofen, S; Schmeck, J; Pannen, BHJ; Bauer, I; Bauer, M;
Indirizzi:
Univ Saarland, Dept Anesthesiol & Crit Care Med, D-66421 Homburg, Germany Univ Saarland Homburg Germany D-66421 Care Med, D-66421 Homburg, Germany Univ Heidelberg, Fac Clin Med Mannheim, Dept Anesthesiol & Intens Care Med, D-68135 Mannheim, Germany Univ Heidelberg Mannheim Germany D-68135 Med, D-68135 Mannheim, Germany Univ Freiburg, Dept Anesthesiol & Crit Care Med, D-79106 Freiburg, GermanyUniv Freiburg Freiburg Germany D-79106 re Med, D-79106 Freiburg, Germany
Titolo Testata:
SHOCK
fascicolo: 6, volume: 15, anno: 2001,
pagine: 438 - 445
SICI:
1073-2322(200106)15:6<438:KCENAP>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
CARBON-MONOXIDE; HEAT-SHOCK; RAT-LIVER; TRANSCRIPTIONAL ACTIVATION; HEPATOCELLULAR INJURY; EXPRESSION PATTERN; CIRCULATORY SHOCK; SUPEROXIDE ANION; HEPATIC ISCHEMIA; OXIDANT STRESS;
Keywords:
hemorrhage; stress response; oxygen free radicals; Kupffer cell blockade; neutrophil depletion; gadolinium chloride; vinblastine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Bauer, M Univ Saarland, Dept Anesthesiol & Crit Care Med, D-66421 Homburg,Germany Univ Saarland Homburg Germany D-66421 D-66421 Homburg, Germany
Citazione:
M. Paxian et al., "Kupffer cells end neutrophils as paracrine regulators of the heme oxygenase-1 gene in hepatocytes after hemorrhagic shock", SHOCK, 15(6), 2001, pp. 438-445

Abstract

Heme oxygenase (HO) plays a pivotal role for the maintenance of liver blood flow and hepatocellular integrity after hemorrhagic shock. We investigated the role of Kupffer cells and neutrophils as paracrine modulators of hepatocellular HO-1. gene expression in a rat model of hemorrhage and resuscitation. Male Sprague-Dawley rats (n = 6-10/group) were anesthetized (pentobarbital, 50 mg/kg intraperitonal) and subjected to hemorrhagic shock (mean arterial blood pressure: 35 mmHg for 60 min) or a sham protocol. Based on thetime course of HO-1 gene expression, the effect of various antioxidants, Kupffer cell blockade [gadolinium chloride (GdCl3); 10 mg/kg; 24 h prior to hemorrhage or dichloromethylene diphosphonate (Cl2MDP); 1 mg/kg; 2 days prior to hemorrhage], or neutrophil depletion (vinblastine, 0.5 mg/kg, 5 days prior to hemorrhage) on induction of the HO-1 gene was assessed at 5 h of resuscitation, i.e., the time point of maximal induction. Kupffer cell blockade and antioxidants abolished HO-1 mRNA and protein induction after hemorrhage, while neutrophil depletion failed to affect hepatocellular HO-1 gene expression. In addition, Kupffer cell blockade aggravated hepatocellular injury. N-formyl-methionine-leucyl-phenylalanin (fMLP) induced a substantial influx of neutrophils into the liver but failed to induce hepatocellular HO-1 mRNA expression. These data suggest that Kupffer cells but not neutrophils induce an adaptive hepatocellular stress response after hemorrhage and resuscitation. Oxygen-free radicals released by Kupffer cells may serve as paracrine regulators of a hepatocellular stress gene which is necessary to maintain liver blood flow and integrity under stress conditions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/05/20 alle ore 12:22:40