[The phenomenon of ischaemic postconditioning of the heart. Analysis of clinical data]. / Fenomen ishemicheskogo postkonditsionirovaniia serdtsa. Analiz klinicheskikh dannykh.

Data concerning the effectiveness of ischaemic postconditioning (IPost) in treatment of acute ST-segment elevation myocardial infarction (STEMI) are controversial. The authors of the majority of studies have reported an anti-apoptotic and infarct reducing effect of IPost. There is evidence that IPost reduces the microvascular obstruction zone, increases coronary flow reserve, and improves the pumping functions of the heart. At the same time, there are publications reporting that IPost does not influence the course of acute STEMI. It was established that IPost protects the heart from reperfusion injury occurring after cold cardioplegia in patients with tetralogy of Fallot.

[Delta-opioid receptor activation prevents appearance of irreversible damages of cardiomyocytes and exacerbates myocardial contractility dysfunction during ischemia and reperfusion].

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.

[The effect of dalargin and des-Tyr-dalargin on the functional state of intact and ischemized-reperfused myocardium]. / Vliianie dalargina i dez-tir-dalargina na funktsional'noe sostoianie intaktnogo serdtsa i miokarda podvergnutogo vozdeistviiu ishemii-reperfuzii.

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.

[Antiarrhythmic and cardioprotective effect of stimulation of delta1-opiate receptors in myocardial ischemia and reperfusion]. / Antiaritmicheskii i kardioprotektornyi éffekt stimuliatsii delta1-opiatnykh retseptorov v usloviiakh ishemii i reperfuzii miokarda.

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.