Document Detail

Supplement of nitric oxide attenuates neutrophil-mediated reperfusion injury.
MedLine Citation:
PMID:  7586447     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Nitric oxide (NO) derived from the endothelial cell has been identified as a constitutive chemical mediator that regulates the function of the endothelial cell in association with neutrophil (PMN) adhesion and activation. However, its role in the pathogenesis of myocardial reperfusion injury is not clear. METHODS AND RESULTS: Fifteen isolated rat hearts were perfused with modified Krebs-Henseleit solution and subjected to 20 minutes of global and normothermic ischemia. Then the hearts were reperfused for 45 minutes with different protocols: the control (C) group was reperfused without PMNs, the P group was reperfused with PMNs, and the N group was reperfused with PMNs and nitroprusside (10(-5) mol/L). The ozone chemiluminescence method was used for direct measurement of NO in the coronary effluent during reperfusion. NO in the coronary effluent in the C group decreased at reperfusion after normoxic perfusion, and this decrease in NO continued for the first 15 minutes of reperfusion. Percentage recovery of left ventricular developed pressure and coronary flow was significantly lower in the P group than that in the N group. Also, the N group had a significantly lesser Luminol-elicited chemiluminescence of the coronary effluent and ratio of PMN adherence to myocardial vasculature compared with the P group. CONCLUSIONS: This study demonstrated directly the decrease in NO production during reperfusion and showed that supplement of NO with NO donor attenuated the injury in which PMNs were involved. The results suggest that NO plays a significant role in reperfusion injury and that supplement of NO during reperfusion appears to be useful to attenuate this injury.
H Fukuda; Y Sawa; K Kadoba; K Taniguchi; Y Shimazaki; H Matsuda
Related Documents :
8891867 - Left ventricular dysfunction due to the new ischemic outcomes: stunning and hibernation.
14519437 - Overexpression of calpastatin by gene transfer prevents troponin i degradation and amel...
16309567 - The role of exogenous carbon monoxide in the recovery of post-ischemic cardiac function...
7484207 - Mr imaging of contrast-enhanced porcine myocardial infarction. assessment of reperfusio...
18422517 - Vascular endothelial growth factor-165 gene therapy promotes cardiomyogenesis in reperf...
20228327 - Ct of left ventricular assist devices.
Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article    
Journal Detail:
Title:  Circulation     Volume:  92     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1995 Nov 
Date Detail:
Created Date:  1995-12-28     Completed Date:  1995-12-28     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  II413-6     Citation Subset:  AIM; IM    
First Department of Surgery, Osaka University School of Medicine, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Chemiluminescent Measurements
Myocardial Ischemia / physiopathology*
Myocardial Reperfusion Injury / prevention & control*
Myocardium / metabolism
Neutrophils / physiology*
Nitric Oxide / physiology*
Nitroprusside / administration & dosage
Rats, Sprague-Dawley
Reg. No./Substance:
10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside

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

Previous Document:  Magnesium cardioplegia enhances mRNA levels and the maximal velocity of cytochrome oxidase I in the ...
Next Document:  Improved 4- and 6-hour myocardial preservation by hypoxic preconditioning.