Document Detail

A protective role of nitric oxide in isolated ischaemic/reperfused rat heart.
MedLine Citation:
PMID:  8746217     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: The importance of NO-induced vasodilator tone in maintaining adequate coronary flow to sustain hemodynamic function in aerobically perfused heart and the role of NO in the injury development in ischaemic/reperfused heart was studied. METHODS: Effect of NO synthesis inhibitor (N omega-nitro-L-arginine, L-NOARG) on isolated working rat hearts subjected to either 90 min of aerobic perfusion or to a global ischaemia (27.5 to 42.5 min) followed by 40 min reperfusion was studied. To overcome coronary flow reducing effect of L-NOARG either perfusion pressure was raised from 75 to 120 cm H2O or adenosine (400 nM) was administered. RESULTS: In the hearts perfused at coronary pressure of 75 and 120 cm H2O, L-NOARG (10 microM) reduced coronary flow by 30% and 17%, respectively, while cardiac output was not affected. Only a transient increase in adenosine and lactate outflow occurred in L-NOARG-treated hearts. The post-ischaemic recovery of functions was impaired in L-NOARG-treated hearts, an effect not correlating with L-NOARG-induced reduction in coronary flow. Although the pre-ischaemic coronary flow was similar in the untreated hearts perfused at 75 cm H2O and in L-NOARG-treated hearts perfused at 120 cm H2O, the post-ischaemic recovery in the latter group was still impaired as compared to that in the untreated hearts. Likewise, coronary flow was similar in the untreated hearts and in those treated with L-NOARG plus adenosine, nevertheless, the post-ischaemic recovery in the latter group was impaired as compared to that in the untreated hearts. CONCLUSIONS: While the inhibition of NO synthesis resulted in coronary flow reduction it did not induce a state of permanent ischaemia in isolated rat heart. L-NOARG-induced augmentation of the ischaemia/reperfusion injury was related to the deficit of NO, itself, rather than to the reduction in myocardial perfusion.
A Beresewicz; E Karwatowska-Prokopczuk; B Lewartowski; K Cedro-Ceremuåzyńska
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  30     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  1995 Dec 
Date Detail:
Created Date:  1996-10-10     Completed Date:  1996-10-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  1001-8     Citation Subset:  IM    
Department of Clinical Physiology, Medical Centre of Postgraduate Education, Warsaw, Poland.
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MeSH Terms
Adenosine / metabolism,  pharmacology
Arginine / analogs & derivatives,  pharmacology
Coronary Circulation / drug effects
Heart / physiopathology
Lactates / metabolism
Lactic Acid
Myocardial Ischemia / metabolism*,  physiopathology
Myocardial Reperfusion Injury / metabolism*,  physiopathology
Nitric Oxide / metabolism,  physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Rats, Wistar
Reg. No./Substance:
0/Lactates; 10102-43-9/Nitric Oxide; 2149-70-4/Nitroarginine; 50-21-5/Lactic Acid; 58-61-7/Adenosine; 74-79-3/Arginine; EC Oxide Synthase

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

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