Document Detail


Intracoronary nitric oxide improves postischemic coronary blood flow and myocardial contractile function.
MedLine Citation:
PMID:  7573509     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the present study a novel nitric oxide (NO) donor, CAS-1609, was utilized as a means of coronary NO replenishment in a canine model of myocardial ischemia-reperfusion. Administration of CAS-1609 (1.25 mg iv) 10 min before reperfusion, followed by a 1 mg/h intracoronary infusion throughout the 4.5-h reperfusion period, resulted in significant improvement in postischemic transmural myocardial blood flow (0.66 +/- 0.09 vs. 0.37 +/- 0.08 ml.min-1.g-1 for saline vehicle, P < 0.05). Dogs receiving NO supplementation also exhibited a significant recovery of myocardial contractility after 4.5 h of reperfusion (30 +/- 2% area ejection fraction vs. 22 +/- 2% for saline vehicle, P < 0.05). Moreover, myocardial necrosis as a percentage of the area at risk was reduced from 28.9 +/- 4.3% in the saline group to 8.5 +/- 2.6% in the CAS-1609 group (P < 0.01), while ischemic zone myeloperoxidase activity, indicative of neutrophil infiltration, was also attenuated by 70% with NO therapy. Injection of acetylcholine and nitroglycerin into the left circumflex coronary artery revealed a significant impairment of vasodilator responses in the saline vehicle dogs at 2 h of reperfusion. However, dogs treated with the NO donor demonstrated postischemic vasodilator responses which were similar to baseline (P = not significant vs. baseline). These studies demonstrate that intracoronary administration of NO significantly augments postischemic coronary blood flow and contractile function following ischemia and reperfusion. In addition, NO therapy reduces coronary vascular injury, attenuates myocardial necrosis, and reduces neutrophil infiltration. The cardioprotective actions of intracoronary NO administration may be related to the potent antineutrophil actions of NO.
Authors:
R Pabla; A J Buda; D M Flynn; D B Salzberg; D J Lefer
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  269     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1995 Sep 
Date Detail:
Created Date:  1995-11-02     Completed Date:  1995-11-02     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1113-21     Citation Subset:  IM    
Affiliation:
Department of Medicine, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Movement
Coronary Circulation*
Coronary Vessels / physiopathology
Dogs
Female
Hemodynamics
Male
Myocardial Contraction / drug effects*
Myocardial Reperfusion Injury / physiopathology*
Myocardium / enzymology,  pathology
Necrosis
Neutrophils / physiology
Nitric Oxide / pharmacology*
Oxadiazoles / pharmacology*
Peroxidase / metabolism
Vasodilator Agents / pharmacology*
Vasomotor System / physiopathology
Grant Support
ID/Acronym/Agency:
R01 HL-34691/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/4-hydroxynethyl-furoxan-3-carboxamide; 0/Oxadiazoles; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; EC 1.11.1.7/Peroxidase

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


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