Document Detail

Changes in P-selectin expression on cardiac microvessels in blood-perfused rat hearts subjected to ischemia-reperfusion.
MedLine Citation:
PMID:  15620944     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: During cardiac surgery involving cardiopulmonary bypass, activation of polymorphonuclear cells is believed to contribute to ischemia-reperfusion injury and subsequent myocardial impairment of function. The early tethering of polymorphonuclear cells to blood vessel walls depends upon recognition of the adhesion molecule P-selectin on endothelium. The purpose of this study was to define the kinetic changes in expression of P-selectin on myocardial vessels in a model of global ischemia-reperfusion injury. METHODS: In a novel recirculating blood-based perfusion system, rat hearts were subjected to 30 minutes of aerobic perfusion, 60 minutes of global ischemia, and 60 minutes of reperfusion, or to 120 minutes of continuous aerobic blood perfusion (with or without leukocyte/platelet depletion). Heart function (left ventricular developed pressure), heart rate, and perfusion pressure were monitored throughout. Hearts were sampled at defined periods for microvascular expression of P-selectin, identified by immunohistochemistry. RESULTS: In control (nonperfused) hearts and in hearts subjected to perfusion and ischemia, few cardiac vessels (8% to 16%) expressed P-selectin. After 15 minutes of reperfusion, P-selectin was present on the majority of vessels (77%; p < 0.05) but expression decreased subsequently throughout the remaining duration of reperfusion. Interestingly, upregulation of P-selectin also occurred when hearts were subjected to continuous perfusion alone (no ischemia), but this upregulation was less rapid. Depletion of leukocytes/platelets from the blood perfusate did not modify P-selectin expression. CONCLUSIONS: The augmented expression of P-selectin on myocardial vessels during reperfusion of ischemic hearts probably reflects changes induced during global ischemia and by the duration of perfusion through the nonbiological tubing of the circuit. That is likely to mimic the effects initiated during cardiopulmonary bypass.
Andrew O Chukwuemeka; K Alun Brown; Graham E Venn; David J Chambers
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Annals of thoracic surgery     Volume:  79     ISSN:  1552-6259     ISO Abbreviation:  Ann. Thorac. Surg.     Publication Date:  2005 Jan 
Date Detail:
Created Date:  2004-12-28     Completed Date:  2005-08-12     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  15030100R     Medline TA:  Ann Thorac Surg     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  204-11     Citation Subset:  AIM; IM    
Cardiac Surgical Research/Cardiothoracic Surgery, Rayne Institute, Guy's and St. Thomas' NHS Trust, St. Thomas' Campus, London, United Kingdom.
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MeSH Terms
Capillaries / metabolism
Cardiopulmonary Bypass
Cell Adhesion
Coronary Vessels / metabolism*
Equipment Design
Leukocyte Reduction Procedures
Myocardial Ischemia / genetics,  metabolism*
Myocardial Reperfusion / instrumentation,  methods
Myocardial Reperfusion Injury / genetics,  metabolism*
Neutrophils / physiology
P-Selectin / biosynthesis*,  genetics
Rats, Wistar
Reg. No./Substance:

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