Role of polymorphonuclear leukocytes in cardiovascular depression and cellular injury in hemorrhagic shock and reinfusion.
We investigated the role of polymorphonuclear leukocytes (PMNLs) in cardiac depression and cytotoxicity during hemorrhagic shock and reinfusion. The dogs were assigned to four groups: I (sham), 4 h duration; II, 2 h of shock followed by reinfusion for 2 h; III, shock and reinfusion in neutrophils depleted with immune serum; IV, same as III but pretreated with nonimmune serum. Cardiac function and contractility were depressed during shock while plasma creatine kinase (CK), and CK-MB increased. Reinfusion tended to return hemodynamic parameters towards control values while oxygen free radical producing activity of PMNLs, plasma CK, and CK-MB increased further. Cardiac malondialdehyde (lipid peroxidation product) and superoxide dismutase activity were higher while left ventricular chemiluminescence was lower in group II as compared to group I. Despite the increase in the antioxidant reserve and antioxidant enzymes, there was oxidative damage. PMNL depletion attenuated the deleterious effects of shock and reinfusion on the hemodynamic and biochemical parameters. The changes in group IV were similar to those in group II. These results suggest that PMNLs may partly be involved in the deterioration of cardiac function, and contractility and cellular injury during hemorrhagic shock and reinfusion.
Department of Physiology, College of Medicine, University of Saskatchewan, Canada.
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Kapoor
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Prasad
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002303:Cardiac Output, Low / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D002374:Catalase / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D005260:Female; D005609:Free Radicals / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006439:Hemodynamics; D015227:Lipid Peroxidation; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D009504:Neutrophils / Q000502:physiology*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012771:Shock, Hemorrhagic / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D005609:Free Radicals; D017382:Reactive Oxygen Species; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003402:Creatine Kinase