Document Detail


Vascular endothelial growth factor attenuates myocardial ischemia-reperfusion injury.
MedLine Citation:
PMID:  9354516     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Hypoxic endothelial cell activation plays a key role in the myocardial dysfunction resulting from ischemia-reperfusion injury. Recent evidence suggests that vascular endothelial growth factor (VEGF) may, in addition to promoting angiogenesis, modulate various aspects of endothelial function and repair. We examined whether administration of VEGF in the cardioplegic solution might have a beneficial effect on myocardial ischemia-reperfusion injury in an isolated rat heart model. METHODS: Hearts from Sprague-Dawley rats were perfused with Krebs-Henseleit solution in a modified Langendorff apparatus. Percent recovery of cardiac output, coronary flow, stroke work, and percent increase in coronary vascular resistance were measured after 2 hours of global ischemia and 40 minutes of reperfusion. Coronary effluent was collected after ischemia and reperfusion for measurement of creatine kinase. RESULTS: Hearts receiving cardioplegia solution containing 125 microg VEGF showed significantly improved recovery of cardiac output, coronary flow, and stroke work, and significantly reduced coronary vascular resistance compared with hearts receiving hyperkalemic cardioplegia only (p < 0.05). Coadministration of a nitric oxide synthase inhibitor attenuated the VEGF-induced cardiprotective effects. Hearts treated with VEGF released significantly less creatine kinase compared with control hearts. CONCLUSIONS: Addition of VEGF to hyperkalemic cardioplegia protects against myocardial ischemia-reperfusion injury in the isolated rat heart.
Authors:
Z Luo; M Diaco; T Murohara; N Ferrara; J M Isner; J F Symes
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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:  64     ISSN:  0003-4975     ISO Abbreviation:  Ann. Thorac. Surg.     Publication Date:  1997 Oct 
Date Detail:
Created Date:  1997-11-13     Completed Date:  1997-11-13     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  15030100R     Medline TA:  Ann Thorac Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  993-8     Citation Subset:  AIM; IM    
Affiliation:
Department of Surgery, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135-2997, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiac Output / drug effects
Cardioplegic Solutions
Creatine Kinase / metabolism
Endothelial Growth Factors / pharmacology,  therapeutic use*
Glucose
Heart / drug effects,  physiology
Lymphokines / pharmacology,  therapeutic use*
Male
Myocardial Reperfusion Injury / prevention & control*
Myocardium / enzymology
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors
Organ Culture Techniques
Rats
Rats, Sprague-Dawley
Tromethamine
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Vascular Resistance / drug effects
Chemical
Reg. No./Substance:
0/Cardioplegic Solutions; 0/Endothelial Growth Factors; 0/Krebs-Henseleit solution; 0/Lymphokines; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors; 50-99-7/Glucose; 50903-99-6/NG-Nitroarginine Methyl Ester; 77-86-1/Tromethamine; EC 1.14.13.39/Nitric Oxide Synthase; EC 2.7.3.2/Creatine Kinase

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


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