[Opioid system and cardiac resistance to ischemic and reperfusion injuries].
In vivo pre-treatment with the opioid receptor antagonist D,L-naloxone completely eliminated the reperfusion-induced creatine kinase (CK) leakage from the rat isolated perfused haert. The inactive isomer L-naloxone decreased the CK release by half. The (-antagonist ICI 174,864 and k-antagonist nor-binanltorphimine exerted a weaker protective effect. The (-antagonist DAMGO, the (2-agonist DSLET, the k1-agonist spiradolin, or the sigma-agonist (+)-SKF 10047, improved myocardial cell viability after ischemia/reperfusion.
Lishmanov
Iu B
IuB
Research Institute of Cardiology, Siberian Branch of the Russian Acad. Med. Sci., Tomsk.
Maslov
L N
LN
Tam
S V
SV
Bogomaz
S A
SA
D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D004743:Enkephalin, Leucine / Q000378:metabolism; D004744:Enkephalin, Methionine / Q000378:metabolism; D066298:In Vitro Techniques; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D009292:Narcotic Antagonists / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011957:Receptors, Opioid / Q000819:agonists / Q000378:metabolism*
D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D004744:Enkephalin, Methionine; D004743:Enkephalin, Leucine; D003402:Creatine Kinase