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 cardiovascular
system. However the role of opioid receptor in myocardial infarction
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 rrtyocordial
infarction and its relation to opioid receptors. The aim of the
present work was to investigate the role of opioid receptors and ATPsensitive
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 rnyocradicd
infraction denoting that endogenous opioids have a cardioprotective effect.
Glibenclamide, an ATP sensitive potassium channel blocker, blocked
the cardioprotective effect of morphine, also separate injection of glibenclamide
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
in myocardial infraction which is nearly similar to that caused by
injection of each drug separately, this gives an evidence that opioid receptor
and k+ channels are internitely linked. |
