[Role of KATP channels in the cardioprotection provided by ischemic preconditioning in anesthetized rabbits].
The effects of KATP channel opener cromaklim (Cro) and ischemic preconditioning (IP) on hemodynamics and myocardial infarct size were examined in both urethane and sodium pentobarbital anesthetized rabbit models of myocardial ischemia-reperfusion to determine whether the KATP channel was involved in the cardioprotection provided by IP. The results were as follows: (1) All hemodynamic parameters and myocardial oxygen consumption were decreased progressively during the course of ischemia (30 min)-reperfusion (180 min). (2) In the urethane anesthetized model, the myocardial infarct size of the left ventricle induced by ischemia-reperfusion was (32.3 +/- 0.8)%. Pretreatment with Cro reduced the myocardial infarct size to (23.3 +/- 2.2)%, while IP significantly reduced the infarct size to (21.6 +/- 1.8)%, which was abolished by a potent KATP channel blocker glibenclamide. (3) In the sodium pentobarbital anesthetized model, myocardial infarct size was (32.7 +/- 1.0)%. IP also reduced the myocardial infarct size to (19.7 +/- 1.5)%, which could not be blocked by cardioprotection of IP by glibenclamide. Cro failed to decrease infarct size. Such results indicated that activation of KATP channels exerted a beneficial action on ischemia-reperfused myocardium only in the urethane anesthetized rabbit.
Ding
Y F
YF
Department of Physiology, Hebei Medical University, Shijiazhuang.
He
R R
RR
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001693:Biological Transport, Active; D019806:Cromakalim / Q000494:pharmacology; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism* / Q000473:pathology; D015221:Potassium Channels / Q000378:metabolism*; D011817:Rabbits; D014665:Vasodilator Agents / Q000494:pharmacology
D015221:Potassium Channels; D014665:Vasodilator Agents; D019806:Cromakalim; D000255:Adenosine Triphosphate