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Biomedical subjects

V F Sagach

Publications and source records attributed to V F Sagach.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Prevention of postischemic lesions of the myocardium using liposomes].

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.

Animals↗
PubMed1991

Nitric oxide influences ventrolateral medullary mechanisms of vasomotor control in the cat.

In acute experiments on cats changes in the background sympathetic activity in the renal nerve, chosen as a model of vaso-constrictor nerve, together with arterial pressure shifts have been found following injections of nitric oxide (NO) containing drugs into the ventrolateral medulla. This is the first report of evidence that both sodium nitroprusside, which produces NO spontaneously and thus mimics endothelium-derived relaxing factor (EDRF), and L-arginine, being a precursor for NO, as well as L-NG-monomethyl-L-arginine (L-NMMA) which inhibits synthesis of NO, induce remarkable changes in the background activity of the renal nerve and systemic arterial pressure (SAP) level shifts, following unilateral injections of drugs examined into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla. These sites are essential for the maintenance of arterial pressure level and vascular tone control. Injections of NO-containing drugs in the RVLM induce attenuation of the renal nerve sympathetic activity and lower the SAP level, while injections in the CVLM reverse these effects. After previous application of Methylene blue on the ventral medullary surface we failed to induce any of the effects following NO injections in the sites examined. Our results raise the possibility that NO influences mechanisms of the neurogenic vasomotor control, realized by neurons within the RVLM and the CVLM via activation of the guanylate cyclase.

Animals↗
PubMed1991

On the mechanism of the involvement of endothelium in reactive hyperemia.

Experiments on anesthetized dogs and on vascular test-preparations demonstrated that reactive hyperemia (RH) was accompanied by the appearance of vasodilator in the blood, and that the level increased with the duration of occlusion of the artery. Removal of the endothelium of the part of the vascular bed studied using saponin, decreased the RH and relaxation of a test-preparation. A rise of pressure in the vascular bed, and a decrease in the deformability of the endothelium resulting from pretreatment with dimerized glutaraldehyde, affected both the hyperemia and the reaction of the vascular preparation in a similar way. It was concluded that the RH resulted from the secretion of vasoactive substances by the endothelium in response to a fall in intravascular pressure.

Animals↗
PubMed1991

Pooling of blood in postischemic shock is modulated by platelet-activating factor (PAF).

In experiments on dogs, i.v. administration of platelet-activating factor (PAF) (500 ng/kg) was shown to induce hypotension which, apart from decreased myocardial contractility, was characterized by blood pooling in veins (82.6 +/- 6.8 mL/kg). This was accompanied by restriction of venous return to the heart and reduction of cardiac output (CO). During postischemic shock the cardio- and hemodynamic disturbances were similar to those induced by i.v. administration of PAF. In the postischemic shock model, preliminary blockage of PAF receptors with the PAF receptor antagonist BN 52021 (6 mg/kg, i.v.) significantly decreased the amount of blood pooled in shock from 38.7 +/- 5 to 18.3 +/- 2 mL/kg (p less than 0.01). Simultaneously, the reduction of CO and blood pressure, induced by reperfusion of the continuously ischemized tissues of a rear limb, was less significant in pretreated vs. the nontreated group. The data suggest that PAF may be involved in postischemic blood pooling and that PAF antagonists could be used to correct postischemic cardio- and hemodynamic disturbances.

Animals↗
PubMed1991

Chemosensitive ventrolateral medulla in the cat: the fine structure and GABA-induced cardiovascular effects.

These studies were designed to provide information on both GABA influences on the neuronal structures within the rostral ventrolateral medulla (RVLM) involved in the cardiovascular control, and fine structure of the GABA-sensitive RVLM in cats. By electron microscopy, the S-type asymmetric junctions (believed to mediate excitation) as well as F-type symmetric junctions (thought to provide inhibition) were identified within the RVLM area examined. The axonal terminals thick with spherical electron-transparent synaptic vesicles, measuring about 50 nm in diameter and forming S-type synapses, were distributed within the entire area. Large numbers of axonal terminals forming the F-type synapses and filled with flattened synaptic vesicles with a longitudinal axis of around 60-80 nm were found at the site located 5-6 mm caudal to the trapezoid bodies. Both spherical electron-transparent and flattened synaptic vesicles could be found together with electron-dense vesicles averaging 80-160 nm in diameter. No axonal terminals containing only the latter type of vesicles were found within the area studied. Some axo-axo-dendritic F-S-type synapses were identified within the RVLM. Unilateral injection of GABA into the RVLM site located 2-5 mm caudal to the trapezoid bodies induced a dose-related fall in the systemic arterial pressure and inhibition of the renal nerve sympathetic activity, the most marked responses being found at the site 4-5 mm caudal to the trapezoid bodies. It also resulted in decrease of heart rate and myocardial contractility when injected into a distinct site, located 0-1.5 mm rostral to the outflow of the 12th cranial nerve roots. There was some laterality in GABA effects on heart rate and myocardial contractility following its injections into the RVLM on the left and right side. Injections of bicuculline into the GABA-sensitive RVLM site resulted in an increase in cardio-haemodynamic responses together with the enhancement of renal nerve sympathetic activity in a dose-related fashion. These results suggest that, in cats, GABA-sensitive sympathoexcitatory neuronal structures in the RVLM alter peripheral sympathetic vasomotor and cardiac nerve background activities through GABA action on the bicuculline-sensitive GABAa-receptors.

Animals↗
PubMed1991

[The participation of humoral factors released by the endothelium in the development of reactive hyperemia].

In anesthetized dogs and on test-preparations of isolated vascular rings of femoral artery used for detection of appearance of vasoactive substances in venous blood, the reactive hyperemia was accompanied by the appearance of vasodilation substances in blood, the concentration of which increased with the occlusion duration. Chemical injury of endothelium by saponin, inhibition of lipoxygenase by quercetin and guanylate cyclase by methylene blue decreased the reactive hyperemia and the relaxation of test-preparation. Cyclooxygenase inhibition by indomethacin did not affect the reactive hyperemia or release of vasoactive substances. The endothelium seems to play an important role in development of reactive hyperemia induced by endothelium-derived relaxing factor release.

Animals↗
PubMed1991

[Gaba-ergic mechanisms of regulation of the vascular tone and cardiac activity localized in the caudal ventrolateral area of the cat medulla].

Data showing that GABA (0.5-50 mumols) injections into the neuronal structures of the caudal ventrolateral medulla (CVLM) being followed with hypertensive reactions induced by enhancement of the background activities of the renal and inferior cardiac nerves are obtained in acute experiments on cats. Inhibitory cardiac influences from the CVLM are realized in asymmetric manner: neuronal structures from the left side influence the myocardial contractile activity but fail to induce the heart rate changes, while those of the right side preferentially control the heart rate. Bicuculline injections into the CVLM induce an abrupt fall in the arterial pressure level, attenuate the background activities in the peripheral sympathetic nerves, reduce the heart rate and myocardial contractile activity. These data evidence that in cats there is a tonically active inhibitory GABA-ergic input to depressor neurons within the CVLM.

Animals↗
PubMed1991

[The role of the endothelium in the development of functional hyperemia of the skeletal muscles].

Experiments on anesthesized dogs demonstrated that gastrocnemius muscle vessels working hyperemia substantially decreased after chemical destruction of endothelium by saponin, inhibition of endothelium-derived relaxing factor synthesis by gossypol and inhibition of quanylate cyclase by methylene blue. Reaction was not decreased after cyclooxygenase inhibition by indomethacin. The endothelium-derived relaxing factor predecessor--L-arginine essentially increased working hyperemia. We concluded that endothelium plays an important role in reaction of working hyperemia by endothelium-derived relaxing factor release.

Animals↗
PubMed1990

[Mechanisms involving the endothelium in reaction of reactive hyperemia].

The experiments on anesthetized dogs and on test-preparations of isolated vascular rings of femoral artery used for detection of appearance of vasoactive substances in venous blood demonstrated that the response of reactive hyperemia is accompanied by the appearance of vasodilation substances in the blood, the concentration of which taking into account the reaction of relaxation of vascular preparation, increases with the occlusion duration. Chemical inhibition of endothelium of a studied bed by saponin essentially decreases the reactive hyperemia and relaxation of test-preparation. The rise of pressure in an overlapped part of a bed and the decrease in the deformation of endothelium with the help of dimerized glutaraldehyde treatment affected the hyperemia and vascular preparation reaction in the similar way. We concluded that the reaction of reactive hyperemia is the result of the vasoactive substances secretion by endothelium in response to a decrease in intravascular pressure.

Animals↗
PubMed1990

[Study of the role of the endothelium in the development of coronary vessel reactions of different etiologies].

Experiments were made in dogs under the conditions of blood autoperfusion of one of the left coronary artery branches. Chemical removal of the endothelium with saponin was shown to lead to abnormal coronary reactivity, eliminate dilatory and give rise to constrictive responses to ATP, acetylcholine, histamine. After an initial coronary dilatation, hypoxic hypoxia resulted in a pronounced increase in coronary resistance and a reduction in coronary flow in intact animals. Preliminary deendothelization of the coronary artery caused disappearance of a dilatatory phase of the reaction, acceleration and enhancement of coronary constriction in response to hypoxia.

Animals↗
PubMed1989

[Role of the endothelium in the development of reactive hyperemia].

The experiments on anesthetized dogs demonstrated that reaction of the femoral vessels reactive hyperemia essentially decreased after chemical inhibition of endothelium by saponin, inhibition of lipoxygenase by quercetin and guanylate cyclase by methylene blue. Reaction was increased after cyclooxygenase inhibition by indomethacin. We concluded that the endothelium plays an important role in reaction of reactive hyperemia by endothelium-derived relaxing factor release.

Animals↗
PubMed1988

Comparative study of morphological changes in the myocardium after different types of allergic reaction in coronary vessels.

Changes in the dog heart were studied by light and electron microscopy 1 h after production of different types of reactions of immediate hypersensitivity--anaphylactic, cytotoxic and immune complex--in the coronary vascular bed. It was shown that cytotoxic action of anticardiac antibodies produced the most significant changes. These were disturbance of coronary circulation, ischemic changes in the myocardium, structural changes in cardiomyocytes. Early destruction of glycocalyx and formation of defects in the cardiomyocyte sarcolemma revealed by an electron microscopic tracer colloidal lanthanum were most characteristic of this reaction.

Anaphylaxis↗
PubMed1988

[Effect of cyclo- and lipoxygenase blockade on the development of immunogenic shock].

In acute experiments on anesthetized dogs it was shown that simultaneous blockade of cyclo- and lipoxygenase (indomethacin and quercetin) completely prevented the development of hypotensive reaction after immune influence induced by intracoronary injection of anti-cardiac antibodies. The prevention of the development of shock reaction was caused by complete depression of pooling blood reaction in the periphery of the vascular bed with the following limitation of venous return to the heart and sharp drop in the cardiac output. Thus, metabolites of arachidonic acid dilating venous part of the vascular bed are of great importance for the development of immunogenic shock.

Animals↗
PubMed1988

[Role of vasopressin in the development of arterial hypertension and the search for ways to correct it].

The sensitivity of the vessel smooth muscles to vasopressin and their contractile responses were obviously increased in hypertensive rats, whereas the vasopressin inhibitory effect and tachyphylaxis were decreased. These changes seem to be connected with the prevalence of V1-activating over V2-inhibitory vasopressin receptors in hypertensive rats' vessel smooth muscles. Administration of lithium oxybutyrate for 4 weeks normalized central hemodynamics and decreased the sensitivity to vasopressin. The findings suggest a possible role of the inositol pathway in transmission of hormonal signal (vasopressin) to hypertensive rats' vessel smooth muscles as well as participation of vasopressin in pathogenesis of arterial hypertension and the possibility of using lithium oxybutyrate for its correction.

Animals↗
PubMed1986

[Role of leukotrienes in shock of immune origin].

In experiments on anesthetized dogs it was shown that leukotriene biosynthesis block with quercetin essentially decreased cardiac and hemodynamic disturbances following the immune heart damage (intracoronary injection of anticardiac serum). Blood pressure was reduced by half, with cardiac output and myocardial contractility also decreasing. Pretreatment with quercetin improved coronary stenosis, removing the second phase (15-60 min) of capacity vessel dilatation reaction (blood deposition).

Anaphylaxis↗