Effects of activation of μ-, κ<Subscript>1</Subscript>-, δ<Subscript>1</Subscript>-, δ<Subscript>2</Subscript>-, and ORL<Subscript>1</Subscript>-receptors on heart resistance to the pathogenic action of delayed ischemia and reperfusion

Different subtypes of opioid receptors (OR) were activated in rats in vivo to study the activation effect on the heart’s resistance to ischemia and reperfusion. It has been established that administration of deltorphin II, a selective δ₂-OR agonist, lowered the infarct size/area at risk index (IS/AAR) by 23%. Naltrexone, naloxone methiodide (an OR inhibitor not penetrating the blood-brain barrier (BBB)), and naltriben (δ₂-antagonist) eliminated the cardioprotective effect of deltorphin II, while BNTX (a δ₁-antagonist) produced no effect on the cardioprotective action of the δ₂-agonist. The infarct-reducing effect of deltorphin II was eliminated by administration of chelerythrine (a protein kinase C (PKC) inhibitor), glibenclamide (a K_ATP-channels inhibitor), and 5-hydroxydecanoate (a mitochondrial K_ATP-channel blocker). Administration of other opioids did not reduce the IS/AAR index. It has been established that all the deltorphins manifest antiarrhythmic potency. Other opioids do not produce any effect on the incidence of arrhythmia occurrences. The antiarrhythmic effect of deltorphin II was eliminated by preliminary administration of naltrexone, naloxone methiodide, and naltriben, but BNTX did not affect the δ₂-agonist’s anti-arrhythmic effect. The preliminary administration of chelerythrine, a PKC inhibitor, eliminated the δ₂ agonist’s antiarrhythmic action. However, glibenclamide and 5-hydroxydecanoate did not alter the antiarrhythmic effect by deltorphin II. Therefore, activation of the peripheral δ₂-ORs reduces the infarct size and prevents the onset of arrhythmias. The antiarrhythmic effect of the δ₂-OR stimulation is mediated by activating PKC and opening the mitochondrial K_ATP-channels. PKC participates in the antiarrhythmic effect of the δ₂-OR activation, but this effect does not depend on the condition of K_ATP-channels.     

Heart resistance against stress-induced damages

Activation of peripheral-opioid receptors diminished stress-induced heart damage whereas stimulation of central-opioid receptors enhanced it. Peripheral-opioid receptors do not take part in pathogenesis of the "stress cardiomyopathy". The prostanoid system and processes of lipid peroxidation participate in realisation of cardioprotective effects associated with peripheral-opioid receptors.     

The use of a method for the quantitative determination of HIV-1 RNA for assessing the severity and prognosis of the development of the disease

The informatory role of a new marker of HIV infection, characterizing the content of HIV-1 RNA in the biological fluids of the patient's body, is evaluated. The quantitative determination of HIV-1 RNA, carried out in a single assay, was made in the blood of 25 HIV-infected patients. These studies confirmed that the determination of the level of RNA in the plasma (viral load) was a reliable criterion indicating the severity and progress of the disease. The viral load of more than 100,000 copies/ml was a sign prognosticating the future pronounced progress of the disease in spite of moderate clinical manifestations and relatively high values of CD4 cells in the patient's blood at the moment of testing.     

Role of δ1 Opiate Receptors in Regulation of Contractility in Isolated Rat Heart during Normal Oxygenation and Ischemia/Reperfusion

The experiments with the isolated rat heart demonstrated a significant decrease in reperfusion-induced damage of cardiomyocytes upon adding the selective ₁ receptor agonist DPDPE (0.1 mg/l) to the perfusion solution. On the contrary, no cardioprotective effect was observed for 0.5 mg/l concentration of the peptide or after its intravenous injection. Stimulation of the cardiac ₁ opioid receptors by intravenous injection of 0.5 mg/kg DPDPE or its addition to the perfusion solution decreased myocardial contractility both under conditions of normal oxygenation and during reperfusion. Thus, the cardioprotective and negative inotropic effect of DPDPE is mediated by activation of the cardiac ₁ opioid receptors.     

The synthesis of cationic glycerolipid acetals containing aliphatic and heterocyclic bases

1,3-Dioxolane series cationic lipids containing residues of aliphatic or heterocyclic nitrogenous bases were synthesized. The bases were attached to the glycerol backbone either directly (piperazine) or via a spacer group through a thioether bond.     

Electron microscopy of Mycobacterium leprae passed in laboratory animals

The ultrastructure of M. leprae was studied in the process of its intraplantar passage from man to mice (passages 1-8). Changes in the morphology of M. leprae, observed in the course of 3 passages, were established. From the phase of dormant forms (passage 1) the bacteria became adapted to the new host by passage 3, which was confirmed by the absence of differences in the ultrastructure of cells by passages 3-8. The possibilities of the phenotypic variability of M. leprae in the process of in vivo passage should be taken into consideration when they are used for the production of specific biopreparations, experimental modeling and the screening of antileprous preparations.     

Delta-opiate receptors and heart resistance to arrhythmogenic factors

Stimulation of peripheral delta-opioid receptors exerted no effect on arrhythmias, whereas that central delta 1- and delta 2-receptor activation decrease the heart susceptibility to arrhythmogenic action of epinephrine. Pre-treatment with the delta-opioid receptor antagonist ICI 174 prevented the antiarrhythmic effect of the central delta-receptors stimulation. The findings suggest that the heart decreased vulnerability to epinephrine-induced arrhythmias following the central delta-receptors stimulation is mediated by an enhanced vagal activity.