Document Detail

Role of polymorphonuclear leukocytes in cardiovascular depression and cellular injury in hemorrhagic shock and reinfusion.
MedLine Citation:
PMID:  8891664     Owner:  NLM     Status:  MEDLINE    
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.
R Kapoor; K Prasad
Related Documents :
414554 - Intraaortic counterpulsation balloon: radiographic considerations.
12197604 - Oozing-type of left ventricular rupture treated under percutaneous cardiopulmonary supp...
9607464 - Current concepts of ventricular defibrillation.
15520304 - Extracorporeal cardiac shock wave therapy markedly ameliorates ischemia-induced myocard...
8774824 - Evaluation of asynchronous left ventricular relaxation by doppler echocardiography duri...
17462414 - Use of conventional dual chamber pacemakers with custom lead adapters to induce atrial ...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Free radical biology & medicine     Volume:  21     ISSN:  0891-5849     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  1996  
Date Detail:
Created Date:  1997-03-10     Completed Date:  1997-03-10     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  609-18     Citation Subset:  IM    
Department of Physiology, College of Medicine, University of Saskatchewan, Canada.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Antioxidants / metabolism
Cardiac Output, Low / etiology*,  pathology,  physiopathology
Catalase / metabolism
Creatine Kinase / blood
Free Radicals / metabolism
Glutathione Peroxidase / metabolism
Lipid Peroxidation
Myocardial Reperfusion Injury / etiology,  pathology,  physiopathology
Myocardium / metabolism
Neutrophils / physiology*
Oxidative Stress
Reactive Oxygen Species / metabolism
Shock, Hemorrhagic / complications*,  pathology,  physiopathology
Superoxide Dismutase / metabolism
Reg. No./Substance:
0/Antioxidants; 0/Free Radicals; 0/Reactive Oxygen Species; EC; EC Peroxidase; EC Dismutase; EC Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Inhibition of pleural mesothelial cell collagen synthesis by nitric oxide.
Next Document:  Fetal growth retardation in rats may result from apoptosis: role of peroxynitrite.