INHIBITION OF NITRIC OXIDE SYNTHESIS AGGRAVATES REPERFUSION INJURY AFTER HEPATIC ISCHEMIA AND ENDOTOXEMIA
| Autor: | David M. Guido, Hartmut Jaeschke, Ying Wang, Anwar Farhood, W.R. Mathews |
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| Rok vydání: | 1995 |
| Předmět: |
Male
Neutrophils Salmonella enteritidis Toxemia Priming (immunology) Pharmacology Arginine Nitric Oxide Critical Care and Intensive Care Medicine Nitric oxide chemistry.chemical_compound Ischemia medicine Animals Enzyme Inhibitors Liver injury Nitric oxide synthesis business.industry Alanine Transaminase Free Radical Scavengers medicine.disease Glutathione Rats Inbred F344 Pathophysiology Rats Hepatic ischemia Endotoxins NG-Nitroarginine Methyl Ester Liver chemistry Vasoconstriction Reperfusion Injury Emergency Medicine Lipid Peroxidation Nitric Oxide Synthase business Reperfusion injury |
| Zdroj: | Shock. 4:282-288 |
| ISSN: | 1073-2322 |
| Popis: | The potential role of nitric oxide (NO) was investigated in the pathophysiology of liver injury after priming with 20 min hepatic ischemia-reperfusion and administration of .5 mg/kg Salmonella enteritidis endotoxin. Liver injury during the early reperfusion phase of 4 h was characterized by severe vascular oxidant stress, lipid peroxidation (LPO), neutrophil infiltration, and a 33% reduction of the microvascular blood flow in the liver. Inhibition of NO synthesis with N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME) aggravated liver injury by 90%, reduced LPO, and did not affect liver neutrophils but further impaired microvascular blood flow. Treatment with the NO-donor spermine-NONOate or L-arginine did not affect these parameters in postischemic animals, however, treatment did restore all values of L-NAME-treated animals back to disease control levels. These data suggest that endogenous NO formation is sufficient to limit ischemic liver injury during reperfusion but inhibition of NO synthesis will result in additional ischemic damage. NO may also be involved in scavenging of superoxide in the vasculature and in inducing LPO. |
| Databáze: | OpenAIRE |
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