title: A protective role of nitric oxide in isolated ischaemic/reperfused rat heart.
abstract: OBJECTIVE
  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.
authors: Department of Clinical Physiology, Medical Centre of Postgraduate Education, Warsaw, Poland.
authors: A
authors: A
authors: Beresewicz
authors: E
authors: E
authors: Karwatowska-Prokopczuk
authors: B
authors: B
authors: Lewartowski
authors: K
authors: K
authors: Cedro-Ceremuåzyńska
mesh_terms: D000241:Adenosine / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects; D006321:Heart / Q000503:physiopathology; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar
chemical_list: D007773:Lactates; D019335:Nitroarginine; D009569:Nitric Oxide; D019344:Lactic Acid; D001120:Arginine; D019001:Nitric Oxide Synthase; D000241:Adenosine