[Contribution of nitric oxide in the mechanisms of flow-dependent vasodilation in normo- and hypertensive rats].

The aim of this study was to evaluate the role of nitric oxide (NO) in the mechanisms of arterial distensibility and intravascular pressure stability in normotensive and spontaneously hypertensive rats. The experiments were performed on the anesthetized male Wistar, Wistar-Kyoto (WKY), and spontaneously hypertensive rats (SHR). The abdominal aorta was cannulated and perfused with variable blood flow rates with subsequent determination of major characteristics of regional vascular function.

[Effects of individual and combined administration of ethylmethylhydroxypyridine succinate and ischemic preconditioning on ischemic-reperfusive myocardial injury in rats].

It was shown previously that ethylmethylhydroxypyridine succinate (EMHPS) can produce metabolic cardioprotective action due to its antihypoxant and antioxidant properties. In the present study, the cardioprotective effects of EMHPS administered in doses 50 and 100 mg/kg alone and in combination with ischemic preconditioning have been studied on the model of ischemic-reperfusive myocardial infarction in rats. It is established that both the administration of EMHPS in a dose 50 mg/kg and the ischemic preconditioning produce significant limitation of the infarction size.

[The effects of modulation of cardiac metabolism and antioxidant state on myocardial ischemia-reperfusion injury].

The effects of mexicor (ethylmethylhydroxypyridine succinate) at doses of 50 and 100 mg/kg on myocardial infarct size, serum levels of myocardial markers, and severity of ischemia- and reperfusion-induced arrhythmias were studied in the rat model of myocardial ischemia-reperfusion injury. It was shown that pre-ischemic intravenous infusion of mexicor at a dose of 50 mg/kg resulted in significant reduction of myocardial infarct size and troponin I level. When the dose of mexicor was increased up to 100 mg/kg the infarct-limiting effect was reversed.

Resistance of the myocardium to ischemia and the efficacy of ischemic preconditioning in experimental diabetes mellitus.

Data on the influences of diabetes mellitus on the severity of ischemic damage to the myocardium are contradictory. We report here experiments using a model based on in vivo myocardial infarcts resulting from coronary occlusion to study the resistance of the myocardium in rats with alloxan-induced insulin-dependent diabetes mellitus to prolonged ischemia, along with studies of the infarct-limiting efficacy of ischemic preconditioning. The results showed that after diabetes mellitus for six weeks, the relative size of infarcts was significantly less than in controls (39.

[The role of oxygen free radicals in the mechanisms of local and distant ischemic myocardial preconditioning].

The phenomenon of ischemic preconditioning consists in increase in myocardial tolerance to ischemia after short periods of ischemia and reperfusion of the myocardium (local preconditioning) or a distant organ (distant preconditioning). This study is dedicated to the role of oxygen free radicals (OFR) in the mechanisms of preconditioning; pharmacological inhibition of OFR with N-2-mercaptopropionylglycin, a synthetic anti-oxidant, was used. Mouse experiments demonstrated a reduction in the infarction-limiting effect of local preconditioning as a result of OFR inhibiting.