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Maslov LN Platonov AA Lasukova TV Lishmanov IuB Oeltgen P Nagase H Podoksenov IuK Podoksenov AIu 《Patologicheskaia fiziologiia i èksperimental'naia terapiia》2006,(4):13-17
It is shown that prestimulation of cardiac delta-opioid receptors (OR) by selective agonists (DPDPE and TAN-67) decreases creatine kinase levels in the coronary effluent of isolated rat heart during 45-min global ischemia and 30-min reperfusion. This effect was completely abolished by pretreatment with a delta-antagonist naltrindole or a non-selective agonist naloxone. It was found that preactivation of cardiac delta-OR exacerbates reperfusion contractility dysfunction of the heart. This effect was also eliminated by opioid receptor antagonists. It is suggested that stimulation of cardiac delta-OR prevents irreversible cardiac cell damage but exacerbates contractility dysfunction during ischemia and reperfusion in vitro. 相似文献
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Lasukova TV Krylatov AV Maslov LN Lishmanov IuB Gross GJ Podoksenov IuK Podoksenov AIu 《Patologicheskaia fiziologiia i èksperimental'naia terapiia》2004,(3):12-15
Pretreatment with intravenous peptide delta1-opioid receptor (OR) agonist DPDPE (0.5 mg/kg) decreases the incidence of occlusion (10 min) and reperfusion (10 min) arrhythmias in rats. The agonist of delta2-OR DSLET has no effect on arrhythmias in coronary artery occlusion and reperfusion. Pretreatment with selective delta-antagonists ICI 174,864 (2.5 mg/kg) eliminates an antiarrhythmic effect of DPDPE. The addition of DPDPE to the perfusion solution in a final concentration of 0.1 mg/l and/or 0.5 mg/l fifteen min before ischemia also decreases the incidence of reperfusion arrhythmias in a concentration-dependent manner. The addition of DPDPE to the perfusion solution in a final concentration of 0.1 mg/l decreases creatine kinase levels in the coronary sinus effluent. However, DPDPE has no cardioprotective effect in a concentration of 0.5 mg/l or after intravenous administration. It is suggested that antiarrhythmic and cardioprotective effects of DPDPE during reperfusion may be due to stimulation of cardiac delta1-receptors. 相似文献
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Maslov LN Krylatov AV Lishmanov AIu Podoksenov IuK Solenkova NV Bogomaz SA Tam SW Gross GJ 《Eksperimental'naia i klinicheskaia farmakologiia》2001,64(6):27-30
Preliminary administration of the delta 1-opioid receptor (delta 1-OR) peptide agonist DPDPE (0.5 mg/kg, i.v.) decreased the incidence of occlusion (10 min) and reperfusion (10 min) arrhythmias in rats. The delta 2-OR agonist DSLET did not affect arrhythmias upon the coronary artery occlusion and reperfusion. Pretreatment with the selective delta-antagonists ICI 174,864 (2.5 mg/kg) or TIPP[psi] (0.5 mg/kg) completely eliminated the antiarrhythmic effect of DPDPE. Uncapable of crossing the blood brain barrier, the nonselective OR antagonist naloxone methiodide (5 mg/kg) also abolished this effect. At the same time, hexametonium (10 mg/kg) did not antagonize the antiarrhythmic effect of DPDPE. Pretreatment with the KATP channel blocker glibenclamide (0.3 mg/kg) completely eliminated the protective effect of the delta 1-OR stimulation. It was concluded that the delta 1-OR stimulation prevents the ischemic and reperfusion arrhythmias by means of the KATP channel activation. 相似文献
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Maslov LN Khaliulin IG Podoksenov IuK 《Patologicheskaia fiziologiia i èksperimental'naia terapiia》2012,(1):67-72
The literature data testify the there is an early and delayed hypothermic preconditioning of brain. Neuroprotective effect of early hypothermic preconditioning is a result of activation of adenosine A1 receptors, KATP-channels. Ras protein and predetermined by a decrease in the synthesis of NO*. The infarct-sparing effect of delayed hypothermic preconditioning of brain is depended upon protein synthesis de novo. The presented data demonstrate that hypothermic preconditioning prevents cardiomyocyte necrosis in response to ischemia-reperfusion, improves pump function of the heart during reperfusion period, exerts an antiarrhythmic effect. The hypothermic preconditioning exerts more pronounced cardioprotective effect than ischemic preconditioning. The protective impact of hypothermic preconditioning is depended upon activation of protein kinase C, AMP-activated protein kinase (AMPK) and inhibition of MPT pore. The reactive oxygen species are triggers and mediators of hypothermic preconditioning of heart. 相似文献
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Lasukova TV Maslov LN Lishmanov IuB Ovchinnikov MV Bespalova ZhD Podoksenov IuK Podoksenov AIu 《Eksperimental'naia i klinicheskaia farmakologiia》2004,67(4):21-25
Experiments on isolated perfused rat heart showed that dalargin, an antagonist of mu- and delta-opioid receptors, favors a decrease in the parameters of contractility of intact myocardium, while not influencing the pumping function (systolic and diastolic contractility) of reperfused myocardium. At the same time, des-Tyr-dalargin (the non-opioid analog of dalargin) suppresses the contractility of both the intact heart and the isolated myocardium subjected to global ischemia and reperfusion. Both dalargin and des-Tyr-dalargin reduced the incidence of reperfusion-induced arrhythmia, but did not affect the coronary flow before ischemia and after restoration of the coronary flow. It is suggested that the effect of dalargin is related to activation of the cardiac delta-opioid receptors, while the inotropic action of des-Tyr-dalargin involves other receptor mechanisms. 相似文献
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Lasukova TV Maslov LN Podoksenov YK Podoksenov AY Platonov AA Ovchinnikov MV Bespalova ZhD 《Bulletin of experimental biology and medicine》2004,137(1):27-30
Experiments on isolated perfused rat heart showed that nonselective micro- and delta-opiate receptor agonist dalargin decreased contractility of the intact heart, but had no effect on pump function of the ischemic myocardium. Dalargin analogue des-Tyr-dalargin not binding to opiate receptors decreased contractility of intact myocardium and isolated heart exposed to 45-min total ischemia. We hypothesize that the influence of dalargin is related to activation of cardiac delta-opiate receptors, while the inotropic effect of des-Tyr-dalargin is mediated by other receptors. 相似文献
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Nikolay O. Kamenshchikov Irina A. Mandel Yuriy K. Podoksenov Yulia S. Svirko Vladimir V. Lomivorotov Sergey L. Mikheev Boris N. Kozlov Vladimir M. Shipulin Aleksandra A. Nenakhova Yana J. Anfinogenova 《The Journal of thoracic and cardiovascular surgery》2019,157(6):2328-2336.e1
ObjectivesThe aim of this pilot study was to elucidate the effects of exogenous nitric oxide (NO) supply to the extracorporeal circulation circuit for cardioprotection against ischemia–reperfusion injury during coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB).MethodsA total of 60 patients with coronary artery disease scheduled for CABG with CPB were enrolled in a prospective randomized study. Patients were allocated randomly to receive treatment according to standard or modified CPB protocol where 40-ppm NO was added to the CPB circuit during cardiac surgery. The primary endpoint was the measurement of cardiac troponin I (cTnI). The secondary end points consisted in the measurements of creatine kinase-muscle/brain fraction (CK-MB) and vasoactive inotropic score (VIS).ResultsNO delivered into the CPB circuit had a cardioprotective effect. The level of cTnI was significantly lower in NO-treated group compared with the control group 6 hours after surgery: 1.79 ± 0.39 ng/mL versus 2.41 ± 0.55 ng/mL, respectively (P = .001). The CK-MB value was significantly lower in NO-treated group compared with the control group 24 hours after surgery: 47.69 ± 8.08 U/L versus 62.25 ± 9.78 U/L, respectively (P = .001); and the VIS was significantly lower in the NO-treated group 6 hours after the intervention.ConclusionsNO supply to the CPB circuit during CABG exerted a cardioprotective effect and was associated with lower levels of VIS and cardiospecific blood markers cTnI and CK-MB. 相似文献