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N A Medvedeva

Publications and source records attributed to N A Medvedeva.

At least 19 recordsLinked to original sources
PubMed2001

[Secretory function of the endothelium as a factor of vascular tone regulation in the norm and in cardiovascular pathology].

Endothelin-1 and nitric oxide are the most potent factors of the endothelium-derived substances. The factors play opposite roles in regulation of cardiovascular system, and their interaction underlies the balance of vasoconstrictor and vasodilator influences on vascular tone under normal conditions. In our experiments, changes in endothelin-1 blood concentration were associated with affected production of endogenous nitric oxide. The altered interrelationships between the endothelium-derived vasoactive substances may precede pathological shifts in the cardiovascular system.

Animals↗
PubMed2000

Chronic administration of interferon-a decreases blood pressure and heart rate in rats.

We studied the effects of interferon-alpha on rat cardiovascular system. Intravenous administration of intron-A in a dose of 100,000 IU/kg for 3 days led to a permanent and statistically significant decrease in blood pressure (on days 2 and 3) and reduction in heart rate. These effects were not associated with changes in baroreflex regulation of the cardiovascular system.

Animals↗
PubMed2000

Vasorelaxant and antiplatelet activity of 4,7-dimethyl-1,2, 5-oxadiazolo[3,4-d]pyridazine 1,5,6-trioxide: role of soluble guanylate cyclase, nitric oxide and thiols.

1. Certain heterocyclic N-oxides are vasodilators and inhibitors of platelet aggregation. The pharmacological activity of the furoxan derivative condensed with pyridazine di-N-oxide 4,7-dimethyl-1,2, 5-oxadiazolo[3,4-d]pyridazine 1,5,6-trioxide (FPTO) and the corresponding furazan (FPDO) was studied. 2. FPTO reacted with thiols generating nitrite (NO), S-nitrosoglutathione and hydroxylamine (nitroxyl) and converted oxyHb to metHb. FPDO did not generate detectable amounts of NO-like species but reacted with thiols and oxyHb. 3. FPTO and FPDO haem-dependently stimulated the activity of soluble guanylate cyclase (sGC) and this stimulation was inhibited by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) and by 0.1 mM dithiothreitol. 4. FPTO relaxed noradrenaline-precontracted aortic rings and its concentration-response curve was biphasic (pIC(50)=9. 03+/-0.13 and 5.85+/-0.06). FPDO was significantly less potent vasodilator (pIC(50)=5.19+/-0.14). The vasorelaxant activity of FPTO and FPDO was inhibited by ODQ. oxyHb significantly inhibited only FPTO-dependent relaxation. 5. FPTO and FPDO were equipotent inhibitors of ADP-induced platelet aggregation (IC(50)=0.63+/-0.15 and 0.49+/-0. 05 microM, respectively). The antiplatelet activity of FPTO (but not FPDO) was partially suppressed by oxyHb. The antiaggregatory effects of FPTO and FPDO were only partially blocked by sGC inhibitors. 6. FPTO and FPDO (10 - 20 microM) significantly increased cyclic GMP levels in aortic rings and platelets and this increase was blocked by ODQ. 7. Thus, FPTO can generate NO and, like FPDO, reacts with thiols and haem. The vasorelaxant activity of FPTO and FPDO is sGC-dependent and a predominant role is played by NO at FPTO concentrations below 1 microM. On the contrary, inhibition of platelet aggregation is only partially related to sGC activation.

Animals↗
PubMed2000

Altered endothelin-dependent regulation of blood pressure and vascular tone in stress-sensitive august rats.

The endothelin (ET) system was studied in August rats, with genetically determined high sensitivity to stress, and in control Wistar rats. Radioimmunoassay revealed a significant difference in plasma endothelin-1 (ET-1) levels of August vs Wistar rats (7.1 fmol/ml vs 50.0 fmol/ml). Immobilization of the animals increased these values up to 11.0 fmol/ml and 65.2 fmol/ml, respectively. Elevation of ET-1 was associated with an increase in blood pressure, which was similar in both strains, whereas the heart rate increase was diminished in the stress-sensitive rats. The mixed endothelin-A/endothelin-B- (ET(A)/ET(B)) receptor antagonist PD142893 suppressed stress-induced elevation of blood pressure in August, but not in Wistar rats. In both strains, heart rate responses to stress were insensitive to the ET receptor blockade. Aortic rings of August rats displayed diminished sensitivity to the vasoconstrictor action of ET-1 vs that of Wistar rats (EC50 = 22.1 nM vs 6.3 nM, respectively). In noradrenaline-precontracted tail arteries, 50 nM ET-1 elicited further constriction without any vasodilator effects. ET-1-induced increase in perfusion pressure was greater in tail arteries of Wistar rats. Thus, endogenous ET-1 can play a strain-dependent role in the stress-induced responses of haemodynamics and the alterations in endothelin-dependent regulation may be responsible for the differences in vascular reactivity of Wistar and August rats.

Animals↗
PubMed2000

Active immunization against endothelin-1 is associated with a decrease in plasma endothelin-1 and changes in vascular reactivity.

Exogenous endothelin-1 (ET-1) or high concentrations of the peptide in pathological conditions have marked effects on vascular reactivity. In order to evaluate the role of endogenous ET-1 we investigated responsiveness of conduit (aorta) and of resistant-like (tail artery) vessels in ET-1-deficient rats. Elimination of circulating ET-1 was achieved by active immunization of Wistar rats with a peptide-haemocyanin conjugate (anti-ET-1 group), leading to a marked reduction in plasma level of the peptide in comparison with that of vehicle-treated animals (control group): 1.9 fmol/ml vs 4.9 fmol/ml, respectively. The immunization was associated with a slight elevation of mean arterial pressure, whereas heart rate remained unchanged. In the anti-ET-1 group rings of isolated aorta displayed reduced sensitivity to ET-1: EC50 = 6.57 nM vs 2.95 nM in the control group. Tail arteries of the ET-1-deficient rats showed diminished responses to ET-1, the maximal rise in perfusion pressure: +5.2 mmHg vs +13.6 mmHg in the control group. After immunization, rings of isolated aorta displayed no changes in endothelium-dependent relaxation to acetylcholine (Ach, EC50 = 0.20 microM vs 0.35 microM in the control group), whereas experiments on perfused tail artery showed a twofold reduction in Ach effects. Thus, depletion of circulating ET-1 induces slight changes in haemodynamics associated with altered vessel responsiveness to vasoactive substances.

Acetylcholine↗
PubMed2000

[Hemostatic changes during the treatment of acute promyelocytic leukemia with all-transretinoic acid].

AIM: To study hemostasis in ATRA treatment of acute promyelocytic leukemia (APL). MATERIAL AND METHODS: Hemostasis was studied in 8 newly admitted APL patients treated with ATRA. All of them had hemorrhages, thrombocytopenia 5-15 x 10(9)/l at diagnosis, laboratory signs of the DIC syndrome at induction therapy. RESULTS: Hemorrhage arresting was seen on the ATRA therapy day 14 to 30. Duration of thrombocytopenia under 20 x 10(9)/l was 5.8 +/- 1.8 days. After 7 days of ATRA therapy coagulation tests improved with some hypercoagulation tendency. Subsequent condition of hemostasis was considered as normo/hypercoagulation accompanied by constant thrombin persistence (in the presence of FDP) and depression of hageman-dependent fibrinolysis even in remission. A case of ileofemoral thrombosis followed by fatal thromboembolism of the pulmonary artery is reported. CONCLUSION: It is suggested to use heparin, especially low molecular weight heparin when there are signs of hypercoagulation in APL patients.

Adolescent↗
PubMed1999

Evidence for an antihypertensive factor from the adrenal medulla of SHR modulating neurogenic vasoconstriction.

The aim of this study is to investigate some vasoactive properties of the blood of spontaneously hypertensive rats (SHR). Isolated segments of rat tail arteries obtained from normotensive rats (Wistar-Kyoto (WKY) and Wistar) were perfused with blood from conscious donor rats (WKY, Wistar or SHR). Alterations of the neurogenic constrictor responses (NCR) of the isolated segments evoked by electrical stimulation were studied. The amplitude of NCR of the isolated arteries was studied during perfusion with blood according to the perfusion scheme WKY1(1)-SHR1(2)-WKY1(3) and WKY1(1)-WKY2(2)-WKY1(3). The release of 3H-noradrenaline ([3H]-NA) from vascular sympathetic fibres was measured. The influence of adrenal demedullation on NCR was estimated. We have shown that NCR of isolated arteries decreased by 28.3 +/- 7.9% (P < 0.05 vs. WKY1(1)) during perfusion with blood from SHR (scheme WKY1(1)-SHR1(2)-WKY1(3)). In these experiments, release of [3H]-NA from sympathetic fibres of the artery segments decreased by 39.9 +/- 9.6% during the perfusion with blood from SHR vs. WKY1(1) (P < 0.05). Adrenal demedullation prevented the decrease of NCR during perfusion of the arteries with blood from SHR. In conclusion, the blood of SHR has some antihypertensive factor(s), which causes decrease of NCR in the tail artery from normotensive rats. This decline is accompanied by the decrease of release in [3H]-NA from the transmural sympathetic fibres and is abolished after adrenal demedullation of blood donor rats.

Adrenal Medulla↗
PubMed1998

Chronopharmacological dependence of antihypertensive effects of the imidazoline-like drugs in stroke-prone spontaneously hypertensive rats.

In the present study we investigated the chronopharmacological dependence of dose-dependent hypotensive and cardiochronotropic effects of the imidazoline-like drugs (clonidine, rilmenidine and moxonidine) in stroke-prone spontaneously hypertensive rats (SHR-SP), using radio-telemetric system (Data Sciences, USA). The 24-h blood pressure, heart rate and locomotor activity profiles showed peak values during the rats' active phase during the night period. The degree of hypotensive and bradycardic effects of all drugs were most evident at this time and occurred in the absence of a change in locomotor activity. These studies show that clonidine, rilmenidine and moxonidine decrease blood pressure and heart rate in a time-dependent manner in SHR-SP. It was demonstrated that the degree and duration of hypotensive action of imidazoline-like drugs vary with the time of drug administration.

Animals↗
PubMed1998

Influence of sino-aortic barodenervation on the cardiovascular effects of imidazoline-like drugs.

Earlier findings have shown that hypotensive effects of centrally acting drugs, such as clonidine, are enhanced in animals after denervation of arterial baroreceptors. The purpose of this study was to investigate the dynamic of changes in arterial pressure, heart rate and hypotensive effects of clonidine, rilmenidine and moxonidine in Wistar rats after sino-aortic denervation (SAD) using radio-telemetry. SAD was followed by significant elevation of arterial pressure lability (the standard deviation of the mean arterial pressure), while the baseline mean arterial pressure (MAP) and heart rate in barodenervated rats (12 days after SAD) was similar to intact rats. The hypotension produced by clonidine, rilmenidine and moxonidine was much greater in SAD rats than in intact rats. The study suggests that baroreflex mechanisms are not only important for maintaining levels of blood pressure in the very short term, but also for buffering the effects of centrally acting antihypertensive drugs.

Animals↗