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I.v. administration of the delta-opioid (OR) receptors' agonists DSLET or DTLET prevented creatine kinase leakage from the rat isolated heart in oxidative stress damage and abolished an increase in myocardial levels of conjugated diens and malondialdehyde. The agonists also prevented a stress-induced augmentation of the superoxide dismutase (SOD) activity. All protective effects of delta-receptor stimulation was completely abolished by the delta OR antagonist ICI 174,864. The data obtained suggest that the cardioprotective effect of the delta OR stimulation in vivo is not mediated via direct cardiac delta OR activation but, probably, rather via some unknown indirect circulating humoral factor(s).  相似文献   
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Journal of Evolutionary Biochemistry and Physiology - The paper continues the cycle of studies on the evolutionary link between the mechanisms of stress response formation and cognitive functions...  相似文献   
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The association of polymorphism T-786C of the endothelial NO-synthase gene NOS3 with the functional state of the left ventricle (LV) was studied among residents of the West Siberian region with ischemic heart disease (IHD), including that combined with diabetes mellitus type 2 (DMT2). Carriers of genotype–786TT had the greatest ejection fraction of the left ventricle in the group of patients without DMT2 (p = 0.012). This dependence was not revealed in the group of patients with IHD combined with DMT2. In the group with genotype–786TC, the frequency of left ventricular hypertrophy was higher among patients with DMT2 than patients without it (p = 0.025). There was no association between NOS3T–786C polymorphism and the severity of functional class of heart failure in both the groups.  相似文献   
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Preliminary intravenous injection of -opiate receptor (OR) agonists DSLET (0.1 mg/kg) or DTLET (0.1 mg/kg) increased tolerance of isolated perfused myocardium to damage by oxidative stress simulated in vivo with FeSO4 + ascorbic acid. This manifested itself by a decreased level of creatine phosphokinase (CPK) in the perfusate flowing out of the heart during the oxidative exposure. The preliminary systemic injection of -agonists DAMGO (0.1 mg/kg) or DALDA (0.1 mg/kg) failed to affect the release of CPK from the myocardium. The cardioprotective effect of the -agonist DSLET was completely abolished by preliminary intravenous injection of the -OR antagonist ICI 174,864 (2.5 mg/kg). The intravenous injection of the NO-synthase inhibitor L-NAME (50 mg/kg) also completely abolished the cardioprotective effect of -OR stimulation. The preliminary injection of DSLET but not of DAMGO prevented an increase in the level of diene conjugates and a decrease in the activity of superoxide dismutase (SOD) in the isolated myocardium tissue. Thus, the in vivo stimulation of -OR increased the tolerance of the heart to oxidative stress through activation of NO-synthase and SOD.  相似文献   
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