[Association of a polymorphic marker C825T of the beta(3) subunit of G-protein with myocardial hypertrophy in patients with hypertensive disease]. / Izuchenie assotsiatsii polimorfnogo markera C825T gena beta 3-sub"edinitsy G-belka s gipertrofiei miokarda levogo zheludochka u bol'nykh gipertonicheskoi bolezn'iu.

AIM: To elucidate association of a polymorphic marker C825T of the beta(3)-subunit of G-protein with myocardial hypertrophy in hypertension. MATERIAL AND METHODS: Alleles of polymorphic marker C825T of the CNB3 gene were identified by polymerase chain reaction with subsequent cleavage of the product by BseDI restrictase in 135 patients with hypertensive disease (essential hypertension). Left ventricular mass was determined by echocardiography. RESULTS: Patients with and without left ventricular hypertrophy had similar frequencies of T allele of the gene studied. Moreover patients with CC, CT and TT genotypes had similar left ventricular mass index (122.3+/-29.8, 118.8+/-29.9, and 115.2+/-18.3 g/m(2), respectively). CONCLUSION: No association exists between polymorphic marker C825T of the CNB3 gene and left ventricular hypertrophy in patients with essential hypertension.

[The modulating effect of endothelial relaxing factor on the reactivity of the myocardium and of arterial vascular strips]. / Moduliuiuchyi vplyv endotelial'noho relaksuiuchoho faktora na reaktyvnist' miokarda ta arterial'nykh sudynnykh smuzhok.

Under successive coperfusion of the arterial vascular rings and right atrial trabecula an examination of effects of endothelium-derived NO on reactions of vessel and myocardial trabecula recipient has been done. During arterial rings contraction a relaxing factor was released into solution. By means of chemical de-endothelialization, NO-synthase inhibition and L-arginine the role of endothelium as a source of modulated substances and the role of NO as a main dilated substance for recipient preparations were shown. The direct effect of endothelium-derived NO on a tension and reactivity of myocardial trabecula has been demonstrated.

[The role of the endothelium and of biologically active substances of endothelial origin in regulating blood circulation and cardiac activity]. / Rol' endoteliiu ta biolohichno aktyvnykh rechovyn endotelial'noho pokhodzhennia v rehuliatsiï krovoobihu i diial'nosti sertsia.

The role of endothelium and its biologically active derivatives in the central and local control of circulation is under consideration. Molecular and cellular mechanisms of the activation of the endothelium-dependent responses of different functional significance are being discussed, as well as the state of endothelial responses in the development and compensation of pathological processes in the cardiovascular system.

Participation of gamma-aminobutyric acid in the negative feedback mechanisms of the hypothalamohypophyseotesticular complex.

It is known that gamma-aminobutyric acid (GABA) participates in the regulation of the secretion of many adenohypophyseal hormones [2, 9]. In addition, GABAergic mechanisms may be involved in the regulation of testosterone-dependent aggressive [5] and sexual [8] behavior. A substantial number of studies suggest that GABA and its receptors are capable of participating in the regulation of the secretions of luteinizing hormone (LH). However, its role in this process is not entirely clear, since according to the data of various authors, GABA exerts both inhibitory and activating influences on the secretion of LH [3, 12]. Still less is known of the role of GABA and its receptors in the regulation of the secretion of LH by the negative feedback mechanism, which has been studied in bilaterally castrated rats [3]. However, such a model offers the possibility of investigating only a separate link of this mechanism which regulates the hypothalamohypophyseotesticular complex (HHTC). With regard to the study of the neurochemical regulation of the integral negative feedback system, the use of unilaterally castrated rats is more appropriate for this purpose. In such animals the compensation of the insufficiency of androgens is determined by negative feedback stimulation, and not by the administration of exogenous steroids. In addition, the level of testosterone in the peripheral blood more adequately reflects the state of this mechanism than the level of the gonadotropins [7]. However, the role of GABA and its receptors in the regulation of the integral negative feedback mechanism of the HHTC, so far as we know, remains entirely unstudied. This was in fact the purpose of the present study.

[The role of the eicosanoids in the development of a postischemic shock reaction]. / Rol' eikozanoïdiv u rozvytku postishemichnoï shokovoï reaktsiï.

The role of eicosanoids as one of the main shock mediators was demonstrated in experiments anesthetized dogs with modeled postischemic shock using premedication with indometacin and/or quercetin. Preliminary administration of the eicosanoid biosynthesis inhibitors has prevented reperfusion hemodynamics disturbances during 3 hours after the beginning of an extremity reperfusion. The presented results confirm vascular endothelium injury in the investigated areas, which caused disbalance in the necessity-flow balance in working organs. Therefore, a damage in the endotheliocytes function is the first and, probably, a leading factor in development of the postischemic disturbances of circulation.

Role of eicosanoids in the postischemic shock development.

Using premedication with indomethacin and/or quercetin, the role of the eicosanoids as one of the main shock mediators has been demonstrated in anesthetized dogs using a model of postischemic shock. Hemodynamic disturbances were correlated with an increment in eicosanoids blood levels both in time and value courses. The results testify to the vascular endothelium injury in all investigated regions. This event might be a starting point of the disturbances in balance between a necessity and real flow in working organs under shock-like states. Therefore, a damage in endotheliocytes function is the first and may be a leading factor in the development of postischemic disturbances of circulation. Pretreatment with the inhibitors of eicosanoids biosynthesis prevented the reperfusion-evoked hemodynamic disturbances.

[The participation of adrenoreceptors in regulating dominant behavior and gonadal endocrine function in male mice of different genotypes]. / Uchastie adrenoretseptorov v reguliatsii dominantnogo povedeniia i éndokrinnoi funktsii gonad u samtsov myshei raznykh genotipov.

Dominant behaviour and testosterone level were investigated after adrenoreceptor (AR) blocking drugs injections in PT and CBA/Lac mice predisposed, correspondingly, to dominant and subordinate behaviour in a population and their hybrids F1. Phentolamine (alpha-AR blocker, 1 mg/kg) or obsidan (beta-AR blocker, 1 mg/kg) injections resulted in a loss of the dominant rank of CBA/Lac mice and did not affect the PT mice behaviour. Higher doses (2 and 5 mg/kg) were also ineffective. Simultaneous phentolamine and obsidan injections (1 mg/kg) caused a dominant phenotype inversion, decrease of aggression and testosterone level in PT mice. F1 inherited an ability to dominate in a population and a sensitivity of AR form PT inbred strain. Their behaviour and endocrine characteristics after injections of AR-blockers were close to those of PT mice.

[Prevention of postischemic lesions of the myocardium using liposomes]. / Preduprezhdenie postishemicheskikh povrezhdenii miokarda s pomoshch'iu liposom.

The experiments on dogs showed that 60-min blood flow restriction in the left coronary artery branch resulted in pumping and contractile heart dysfunctions. The removal of the blood flow barrier caused reinforcement of the above dysfunctions. The administration of 50 mg/kg liposome prior to reperfusion improved pumping and contractile heart functions and allowed maintenance of stable hemodynamics during the reperfusion.

Endothelium-dependent effects of platelet-activating factor in the coronary circulation.

In experiments on anesthetized dogs, the effect of intracoronary administration of different doses of platelet-activating factor (PAF) has been investigated. One of the branches of the left coronary artery was catheterized via the main carotid artery. The coronary artery was autoperfused with blood from the subclavian artery. Intracoronary administration of small doses of PAF (100 and 200 ng/kg) caused a dose-dependent decrease in coronary resistance (CR) and an increase in coronary blood flow (CF). When 200 ng/kg of PAF was used, these changes were 30 and 34% vs. control, respectively. Dose increase to 300 ng/kg led to a biphasic reaction. Intracoronary administration of larger PAF doses produced opposite effects, i.e., increase in CR and decrease in CF. Chemical de-endothelialization by saponin (5 mg/5 ml, 1.5-2 min) transformed coronary dilation to small doses of PAF to constriction. The CR rose from 2.8 +/- 0.3 to 5.6 +/- 0.9 mm Hg/ml/min (p < 0.01) and CF dropped two-fold. The PAF receptor antagonists BN 52021 (6 mg/kg) and WEB 2086 (3 mg/kg) completely abolished PAF-induced coronary reactions. Hence, PAF-induced vasodilation of the canine coronary circulation is endothelium dependent.

[The role of prostaglandins in the development of cardio- and hemodynamic disorders in postischemic shock]. / Rol' prostaglandinov v razvitii narushenii kardio- i gemodinamiki pri postishemicheskom shoke.

Experiments on anaesthetized dogs have shown, that reperfusion of ischemized tissues is accompanied by significant increase in thromboxane A2 (Tx A2) and prostacyclin (PG I2) blood level and by development of pronounced cardiovascular insufficiency. Preliminary blockade of prostaglandins biosynthesis prevent an increase of TbA2 and PG12 blood level, postreperfusion disturbances of central and regional circulation develop later and are less pronounced. Therefore, endogenic prostaglandins take part in the development of post ischemic shock reaction, influencing chiefly the venous vessels and blood return to heart.