[Opioid system and cardiac resistance to ischemic and reperfusion injuries].

Abstract

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.

• Authors: Iu B Lishmanov, L N Maslov, S V Tam, S A Bogomaz
• Journal: Rossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova (Ross Fiziol Zh Im I M Sechenova) Vol. 86 Issue 2 Pg. 164-73 (Feb 2000) ISSN: 0869-8139 [Print] Russia (Federation)
• Vernacular Title: Opioidnaia sistema i ustoĭchvost' serdtsa k povrezhdeniiam pri ishemii-reperfuzii.
• PMID: 10808507 (Publication Type: English Abstract, Journal Article)

Chemical References

• Narcotic Antagonists
• Receptors, Opioid
• Enkephalin, Methionine
• Enkephalin, Leucine
• Creatine Kinase

Topics

• Animals
• Creatine Kinase (metabolism)
• Enkephalin, Leucine (metabolism)
• Enkephalin, Methionine (metabolism)
• In Vitro Techniques
• Myocardial Reperfusion Injury (metabolism)
• Myocardium (metabolism)
• Narcotic Antagonists (pharmacology)
• Rats
• Rats, Wistar
• Receptors, Opioid (agonists, metabolism)