Opioid receptors have been found in peripheral vascular organs such as the heart. Opioid peptides contribute to myocardial function as their myocardial level alter during different physiological situation of the cardi~ ovascular system. However the role of opioid receptor in myocardial in~ farction is not fully clear. Also, ATP- sensitive potassium channels have been found in the heart and they markedly affect the myocardial function. However there is controversy about the role of these k+ channels in myo- cardial infarction and its relation to opioid receptors. The aim of the present work was to investigate the role of opioid receptors and ATP sensitive potassium channels in pathogenesis of myocardial infarction and the relation between them. The results of this work showed that morphine injection reduced the myocardial infarction induced by isoprenalin which was blocked by naloxone signifying an opioid receptor cardioprotective action Also, injection of naloxone alone caused an increase in myocradial infraction denoting that endogenous opioids have a cardioprotective effect. Glibenclamide, an ATP sensitive potassium channel blocker, blocked the cardioprotective effect of mmphine, also separate injection of glibenv clamide caused an increase in myocardial infarction, this means that the cardioprotective effect of both exogenous and endogenous opioids is largely mediated through k+ channels. The results showed also, that combined injection of naloxone and glibenclamide caused a significant increase tn myocardial infraction which is nearly similar to that caused by injection of each drug separately. this gives an evidence that opioid receptor and 16 channels are internitely linked. |
