[Cardioprotective effects of flokalin in experiments in vivo: influence on hemodynamic and myocardial lesions in ischemia-reperfusion].
In experiments on anaesthetized dogs with modeling of experimental ischemia (90 min) and reperfusion (180 min) the cardioprotective influence of the preischemic activation of ATP-sensitive potassium (K(ATP)) channels by intravenous introduction of flokalin, a new fluorine-containing opener of these channels was shown. Flokalin was introduced in dose 0.1 mg/kg of animal body weight which practically did not change the parameters of hemodynamic in conditions of normoxia. Thus, the experiments performed about flokalin influence on changes of cardiohemodynamic during ischemia-reperfusion of myocardium showed certain features of ischemia-reperfusion syndrome development under conditions of K(ATP) channels activity stimulation. In our opinion, positive influence offlokalin can be explained by moderate decrease of blood pressure that decreases loading of the damaged heart and allows to preserve cardiac emission in the first period of ischemia. Also, these positive effects can be explained by prevention of the increase of coronal vessel resistance and relative preservation of myocardium contractility indexes by flokalin in the period of reperfusion. All protective properties of flokalin showed above result in diminishing of infarct size of myocardium after ischemia-reperfusion on 37% versus control experiments.
Strutyns'kyĭ
R B
RB
Neshcheret
O P
OP
Tumanovs'ka
L V
LV
Rovenets'
R A
RA
Moĭbenko
O O
OO
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D054086:KATP Channels / Q000378:metabolism*; D009200:Myocardial Contraction / Q000187:drug effects; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D020110:Pinacidil / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use
D002316:Cardiotonic Agents; D054086:KATP Channels; C559719:N-(4-difluoromethoxyphenyl)-N'-pinacolyl-N''-cyanoguanidine; D020110:Pinacidil