[Participation of K(ATP)-channels in cardioprotective effect of mu-opioid receptor agonists in acute ischemia and reperfusion of the isolated heart]. Eksp Klin Farmakol 2001;64(5):23-7
Date
01/05/2002Pubmed ID
11764493Scopus ID
2-s2.0-17144438355 (requires institutional sign-in at Scopus site) 5 CitationsAbstract
Preliminary administration of the mu-opioid receptor (mu-OR) agonist DAMGO (0.1 mg/kg) 15 min before heart isolation led to attenuation of the postischemic systolic and diastolic contractility dysfunction in isolated perfused rat heart. In addition, the mu-OR decreased creatine kinase (CK) release from the heart during the postischemic period, which was indicative of an increase in the sarcolemma tolerance to reperfusion injury. This protective effects are mediated by KATP channel activation. These data show that the mu-OR stimulation in vivo increases, by means of the KATP channel activation, the cardiac tolerance to the ischemia and reperfusion injury in vitro. Pretreatment with mu-OR agonists DAMGO or DALDA in vitro (0.5 mg/liter, 15 min prior to ischemia) exacerbated the postischemic contractility dysfunction of myocardium and did not affect the CK release. It is concluded that the protective effect of mu-OR simulation in vivo is mediated by the activation of these receptors localized outside the heart, probably with an unknown circulating humoral factor.
Author List
Maslov LN, Lasukova TV, Solenkova NV, Lishmanov AIu, Bogomaz SA, Tam SV, Gross GJMESH terms used to index this publication - Major topics in bold
Adenosine TriphosphateAnimals
Blood Pressure
Cardiotonic Agents
Creatine Kinase
Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
Glyburide
In Vitro Techniques
Myocardial Contraction
Myocardial Ischemia
Myocardial Reperfusion Injury
Oligopeptides
Potassium Channel Blockers
Potassium Channels
Rats
Rats, Wistar
Receptors, Opioid, mu
