Recovery of hepatocellular ATP and “pericentral apoptosis” after hemorrhage and resuscitation

ABSTRACT Progressive liver dysfunction contributes significantly to the development of multiple organ failure after trauma/hemorrhage. This study tested the relative impact of necrotic and apoptotic cell death in a graded model of hemorrhagic shock (mean arterial blood pressure=35±5 mmHg for 1, 2, o...

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Published in:The FASEB journal 2003-06, Vol.17 (9), p.993-1002
Main Authors: PAXIAN, MARKUS, BAUER, INGE, RENSING, HAUKE, JAESCHKE, HARTMUT, MAUTES, ANGELIKA E. M., KOLB, STEFAN A., WOLF, BEATE, STOCKHAUSEN, ANDRE, JEBLICK, SILKE, BAUER, MICHAEL
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Amino Acid Chloromethyl Ketones - pharmacology
Animals
Antioxidants - pharmacology
Apoptosis
ATP
Caspase Inhibitors
Cyclic N-Oxides - pharmacology
Cysteine Proteinase Inhibitors - pharmacology
Hepatocytes - pathology
Hypotension - physiopathology
Indocyanine Green - analysis
Ischemia - pathology
liver
Liver - blood supply
Liver - metabolism
Liver - pathology
Liver - physiopathology
Male
necrapoptosis
Necrosis
oxygen free radicals
Rats
Rats, Sprague-Dawley
Resuscitation
Shock, Hemorrhagic - metabolism
Shock, Hemorrhagic - pathology
Shock, Hemorrhagic - physiopathology
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Summary:ABSTRACT Progressive liver dysfunction contributes significantly to the development of multiple organ failure after trauma/hemorrhage. This study tested the relative impact of necrotic and apoptotic cell death in a graded model of hemorrhagic shock (mean arterial blood pressure=35±5 mmHg for 1, 2, or 3 h, followed by 2 h, 1 h, or no resuscitation, respectively) in rats. Prolonged periods of hemorrhagic hypotension (3 h) were paralleled by a profound decrease of hepatic ATP levels and occurrence of pericentral necrosis. Resuscitation after shorter periods of hemorrhagic hypotension resulted in restoration of tissue ATP whereas hepatocellular function as assessed by indocyanine green clearance remained depressed (49.9±1.6 mL/(min·kg) at baseline, 28.8± 1.2 mL/(min·kg) after 2 h of resuscitation; P
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.02-0624com