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V F Sagach

Publications and source records attributed to V F Sagach.

At least 19 recordsLinked to original sources
PubMed2003

Age-related changes in electrical reactions of rat aorta endothelium elicited by acetylcholine and ATP.

Age-related changes in some electrophysiological parameters of the endothelium in isolated rat aorta were studied. In comparison with young rats (6 months), resting potential of the endothelium in aged rats (24-26 months) was significantly higher and varied in a wider range. The electrical responses of intact endothelium of isolated aorta to acetylcholine were typical and regular in young rats, while in aged rats these responses were irregular and atypical. It is hypothesized that atypical electrical responses of the endothelium to acetylcholine and ATP in aged animals result from functional clustering associated with disturbances in electrical contacts between endotheliocytes. We hypothesize that the age-related decrease in NO production is related to disturbances of electrical properties of endothelial membrane.

Acetylcholine↗
PubMed2003

[Comparative evaluation of cardiac hemodynamics and endothelium-dependent reactive hyperemia in people with arterial hypertension living in high-altitude and plain areas].

AIM: To reveal the specific features of cardiac hemodynamics and endothelial function in high-altitude native dwellers with arterial hypertension (AH). MATERIALS AND METHODS: 90 native dwellers from high-altitude and plain areas, who had Stages I and II AH, were examined. To assess cardiac contractility, central and peripheral hemodynamics, the authors used electrocardiography, echocardiography, tetrapolar impedance rheoplethysmography. The functional status of the endothelium was evaluated by the reproduction of endothelium-dependent reactive hyperthermia in the antebrachial vessels. RESULTS: The patients with Stages I and II AH who live in high-altitude area have been found to have less pronounced peripheral vasocontriction due to the less suppression of pump and contractile functions of the heart. Total peripheral resistance in high-altitude dwellers with Stage II AH is practically similar to that in plain inhabitants with Stage I AH. The extended vasodilator reserve in high-altitude inhabitants with AH is also shown by the data obtained in the reproduction of reactive hyperemia in the antebrachial vessels. A less marked decrease in this vascular reaction in patients with AH who live in high-altitude areas may be due to additional production and/or release of nitric oxide in order to increase the vasodilator reserve in moderate hypoxia. CONCLUSION: The course of AH in high-altitude dwellers is marked by less suppression of cardiac pump and contractile functions and less peripheral vasoconstriction. This may be accounted for by compensatory activation of endothelial vasodilator mechanisms aimed at preserving adequate tissue perfusion and at optimally providing the body with oxygen in moderate hypoxia.

Acclimatization↗
PubMed2002

Stress fibres-a Ca2+ -independent store for annexins?

Annexins belong to a family of lipid-binding proteins that are implicated in membrane organization. Several members are capable of binding to actin and, in smooth muscle cells, annexin 6 is known to form a Ca(2+)-dependent, plasmalemmal complex with actin filaments. Annexins can also associate with F-actin containing stress fibres within cultured smooth muscle cells or fibroblasts in a Ca(2+)-independent manner. Depolymerization of stress-fibre systems with cytochalasin D leads to the translocation of actin-bound annexin 2 from the cytoplasm to the plasma membrane at high intracellular levels of Ca(2+). This type of Ca(2+)-dependent annexin mobility is observed only in cells of mesenchymal phenotype, which have a well-developed stress-fibre system; not in epithelial cells.

Annexin A2↗
PubMed2002

Fos and nitric oxide synthase in rat brain with chronic mesostriatal dopamine deficiency: effects of nitroglycerin and hypoxia.

We found sustained proto-oncogene c-fos expression in neurons of the lateral and medial neostriatum and suppression of this expression in nitric oxide synthase (NOS)-containing cells within the islands of Calleja after lesions of the dopaminergic mesostriatal system induced by 6-hydroxydopamine. Systemic administration of nitroglycerin (NTG) or mild hypoxia resulted in a decreased of c-fos expression in the dorsolateral part of the denervated neostriatum. However, in other brain structures NTG or mild hypoxia evoked sustained c-fos expression in NOS-containing neurons and in the sources catecholaminergic projections involved in the control of cardiovascular function. We propose that the administration of NTG, an NO donor, or hypoxia partially attenuate the consequences of an excessively increased glutamate level in the denervated neostriatum which are manifest in high level of c-fos expression.

Animals↗
PubMed2001

[Electrical properties of intact rabbit aortic endothelium].

The ionic nature of membrane potential and electrical reactions to vasodilators and vasoconstrictors of intact endothelium of rabbit aorta have been investigated. It has been shown that K+ and Na+, but not Cl- permeability form membrane resting potential. The endothelium was hyperpolarized by ACh. ATP produced the triphasic reaction of short small depolarization, hyperpolarization followed by depolarization. Both noradrenalin and serotonin evoked depolarization.

Acetylcholine↗
PubMed1997

Basal release of nitric oxide augments the Frank-Starling response in the isolated heart.

BACKGROUND: The Frank-Starling response contributes to the regulation of cardiac output. The major underlying subcellular mechanism is a length-dependent change in myofilament responsiveness to Ca2+. Recent studies indicate that nitric oxide decreases myofilament responsiveness to Ca2+ and modulates myocardial relaxation and left ventricular (LV) diastolic function. We therefore investigated the interaction between nitric oxide and the Frank-Starling response. METHODS AND RESULTS: Isolated ejecting guinea pig hearts (constant afterload and heart rate) were studied before and after interventions. Elevation of filling pressure from 10 to 20 cm H2O increased cardiac output, LV end-diastolic pressure (LVEDP), and peak LV pressure (LVPmax). In the presence of N(G)-monomethyl-L-arginine (L-NMMA, 10 micromol/L; n=10) or free hemoglobin (1 micromol/L; n=8), preload-induced increases in cardiac output were significantly attenuated but baseline cardiac output was unaffected. The effects of L-NMMA were inhibited in the presence of excess L-arginine (100 micromol/L; n=6). These changes were not attributable to alterations in coronary flow. Prostaglandin F2alpha (0.01 micromol/L; n=6), which reduced coronary flow, failed to alter the cardiac output response to preload elevation. The exogenous nitric oxide donor sodium nitroprusside (1 micromol/L; n=6) reduced cardiac output at the lowest preload but not at higher preloads. LVEDP was elevated after L-NMMA and hemoglobin but reduced after sodium nitroprusside. CONCLUSIONS: Basal intracardiac production of nitric oxide significantly augments preload-induced rises in cardiac output in the isolated ejecting guinea pig heart. The mechanism appears to be unrelated to changes in coronary flow and may involve direct effects of nitric oxide on myocardial diastolic and/or systolic function.

Animals↗
PubMed1995

Length-tension dependence in vascular smooth muscle: possible participation of endothelin.

The results of experiments with isolated strips of rat portal vein, and of 'sandwich' experiments involving strips of the portal vein or aorta, revealed the involvement of endothelin in the development of myogenic reactions of the vascular smooth muscle, observed on distension of the vascular wall. Released by the endothelial cells, endothelin is capable of stimulating the contraction of these muscles.

Animals↗
PubMed1994

[The role of nitric oxide in the development of reactive hyperemia in the coronary bed].

De-endothelialization of the coronary vessels induced a 3-4-fold decrease in the level of hyperemia in anesthetised dogs. Infusion of L-arginine augmented the reactive hyperemia and the endothelium-dependent relaxation in response to acetylcholine administration. The reactive hyperemia seems to be wholly depending on the endothelium, being conditioned by the effect of endothelium-derived nitric oxide.

Acetylcholine↗
PubMed1993

Phospholipid vesicles (liposomes) restore endothelium-dependent cholinergic relaxation in thoracic aorta from spontaneously hypertensive rats.

OBJECTIVE: The present study was designed to examine, using isolated preparations of thoracic aorta, the effects of artificial phosphatidylcholine vesicles (liposomes) on vascular endothelium-dependent responses in spontaneously hypertensive rats (SHR) compared with those in Wistar-Kyoto (WKY) normotensive rats. DESIGN: Phosphatidylcholine liposomes, which possess the ability to repair the plasma membrane of living cells, were used in these experiments. METHODS: Liposomes were prepared from egg phosphatidylcholine. A suspension of lipid was subjected to ultrasound treatment at 20 degrees C at a frequency of 44 kHz for 45 s. The contraction of vascular smooth muscle was recorded using a force-displacement transducer coupled with a physiograph. RESULTS: It was shown that aortic smooth muscle from SHR demonstrated a loss of endothelium-dependent relaxation in acetylcholine (10(-6) mol/l) compared with WKY rat aortic smooth muscle. Liposomes in a concentration of 100-125 micrograms/ml restored these endothelium-dependent responses more effectively than L-arginine (10(-5) to 10(-4) mol/l), which is known to be a precursor of endothelium-derived relaxing factor (EDRF). This effect was not observed in denuded aortic rings, and liposomes lost their ability of repairing endothelium-dependent vascular relaxant responses in the presence of methylene blue (5 x 10(-5) mol/l), which inhibits soluble guanylyl cyclase activation by nitric oxide (NO), and N omega-nitro-L-arginine (L-NNA, 5 x 10(-5) to 10(-4) mol/l), a potent and selective inhibitor of NO synthase. CONCLUSION: The present results suggest that the loss of vascular endothelium-dependent responses in SHR may be, at least partly, due to endothelial cells membrane damage, and that the phosphatidylcholine liposomes can repair the function of endothelial cells and restore synthesis or release, or both, of EDRF in hypertension.

Acetylcholine↗
PubMed1993

[Cardiodynamics and cardiac pump function in hyperthermia].

Disorders of myocardial pumping function were shown in experimental dogs under hyperthermia. End-systolic, end-diastolic and stroke volume were decreased under those conditions. The effectiveness of Frank-Starling mechanism was reduced in severe hyperthermia.

Animals↗
PubMed1993

[Cardiodynamics and cardiac pump function in hyperthermia].

Breaking of myocardial pumping function was shown in experiments in anesthesized dogs under hyperthermia. The end-systolic, end-diastolic and stroke volume was decreased under those conditions. The effectiveness of Frank-Starling mechanism was reduced in severe hyperthermia.

Animals↗
PubMed1992

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.

Animals↗
PubMed1992

Involvement of endothelium in vasodilating effects of vintoperol.

Experiments were performed on vessels of the femoral vascular bed of anesthetized dogs and on isolated rings of the rat pulmonary artery, vena cava, and thoracic aorta. Vintoperol was administered intra-arterially (0.01, 0.1, and 0.3 mg/kg/min for 10 min) or added in vitro (10(-4) M). De-endothelialization by saponin (0.5 mg/ml for 5 min) of intact vascular beds or mechanical endothelium removal in rings decreased vasodilation or relaxation by 50-60% vs. control. In de-endothelialized vascular beds, vintoperol (0.3 mg/kg/min) increased blood flow by 18 +/- 5% but 47 +/- 4% under control conditions (p < 0.05). Methylene blue (10 mg/kg) reduced the increment of blood flow to vintoperol from 47 +/- 4 to 24 +/- 4% (p < 0.05). After de-endothelialization of the isolated pulmonary artery, relaxation of precontracted segments was reduced (21 +/- 4% vs. 56 +/- 5% under control conditions; p < 0.05). Vintoperol-induced relaxation of vascular rings was also inhibited by gossypol (2 x 10(-5) M) or methylene blue (5 x 10(-5) M); the level of inhibition (50-100%) or methylene blue (5 x 10(-5) M); the level of inhibition (50-100%) depended on the duration of exposure to the inhibitors. In conclusion, relaxation to vintoperol must be mediated by the release of endothelium-derived nitric oxide.

Animals↗
PubMed1992

Functional hyperemia of skeletal muscle: role of endothelium.

The role of the endothelium and endothelium-derived vasoactive factors in the development of skeletal muscle functional hyperemia was studied. Experiments were performed in anesthetized dogs. Functional hyperemia of isometrically contracted gastrocnemius muscle was produced by direct electric stimulation. Five series of experiments were conducted to investigate the effect of (a) de-endothelialization of gastrocnemius vessels, (b) inhibition of prostanoids biosynthesis by indomethacin, (c) inhibition by gossipol of lipoxygenase, which mediates biosynthesis of endothelium-derived relaxing factor (EDRF), (d) inhibition of cGMP formation by methylene blue, and (e) stimulation of EDRF biosynthesis of L-arginine. The gastrocnemius muscle work was accompanied by an increase in blood flow by 6.8 +/- 0.6 ml/min/N (8 Hz) and by 2.5 +/- 0.2 ml/min/N) (40 Hz). Chemical deendothelialization of gastrocnemius vessels decreased functional hyperemia, and blood flow increased by only 1.2 +/- 0.3 ml/min/N (8 Hz) and by 0.5 +/- 0.1 ml/min/N (40 Hz). Cyclooxygenase inhibition by indomethacin had no significant effect on functional hyperemia, whereas methylene blue and gossipol inhibited functional hyperemia by 4.2- and 6.6-fold, respectively, and L-arginine significantly elevated blood flow by 12.6 +/- 1.4 ml/min/N (8 Hz) and by 3.5 +/- 0.2 ml/min/N (40 Hz) during skeletal muscle work. Thus, it can be concluded that the endothelium plays an important role in functional hyperemia of skeletal muscle, probably through the release of EDRF.

Animals↗