每年出版 4 期
ISSN 打印: 2155-014X
ISSN 在线: 2155-0158
Cardioprotective Effects of ATP-Sensitive Potassium Channels Activation in Experiments in Vivo: Influence on Biochemical Parameters of Blood Following Ischemia-Reperfusion of Myocardium
摘要
In experiments on the anesthetized dogs with modeling of experimental ischemia (90 min) and reperfusion (180 min), participation of biochemical processes in the cardioprotective effect of the preischemic activation of ATP-sensitive potassium (KATP) channels caused by intravenous introduction of flocalin, a new fluorine-containing opener of these channels was shown. Flocalin was introduced in a dose of 0.1 mg/kg of animal body weight which practically did nit change parameters of hemodynamic under normoxia. Thus, experiments on the influence of flocalin on changes of biochemical parameters of arterial blood during ischemia-reperfusion of myocardium revealed certain features of ischemia-reperfusion syndrome development under stimulation of KATP channels. Analysis of blood biochemical parameters revealed that flocalin suppressed free radicals reactions and manifested anti-oxidative properties: reduced quantity of H2O2 and NO3− (the latter can be interpreted as a reduction in peroxini-trite formation), prevented the decline of catalase and superoxide dismutase activity. Practically constant content of low-molecular nitrosothiols in blood during the whole experiment and increase in the level of NO2− during the reperfusion can be indicative of intact functions of the NO system and protective influence of flocalin during the ischemia-reperfusion of myocardium. Practically the unchanged content of inorganic phosphorus and uric acid in blood during ischemia-reperfusion under conditions of preischemic introduction of flocalin indicates that there is a prevention of ATP degradation and formation of both superoxide anion by xantinoxidase and peroxinitrite by its interaction with nitric oxide. All the mentioned properties of flocalin, related with the changes in biochemical parameters of arterial blood, together with the changes in hemodynamic parameters, result in decrease of infarct size in myocardium after ischemia-reperfusion by 37% versus control experiments.
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