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Biomedical subjects

M V Bilenko

Publications and source records attributed to M V Bilenko.

At least 37 records · Page 2Linked to original sources
PubMed1988

[Protective effect of antioxidant ionol in total ischemia of the heart].

The effect of antioxidant ionol in total myocardial ischemia during 30 and 60 min, t = 20 degrees C and 37 degrees C was studied in 60 Wistar rats. The models of isolated perfused myocardium by Langendorf, Neely and that of heterotopic transplantation of myocardium to the rat peritoneal vessels were used. It has been shown that pretreatment of ionol (240 mg/kg before 24 h of ischemia) was accompanied by improvement of myocardial contractile and diastolic functions.

Animals↗
PubMed1988

[Effect of ischemia and reperfusion of the rat brain on lipid peroxidation and the protective effect of antioxidants].

The experiments have been performed on 179 Wistar rats to examine the changes in the brain level of lipid peroxidation products upon 5-, 15-, 30- and 60-min ischemia and 5-, 20- and 60-min reperfusion and to study the protective effect of antioxidants. It has been found that ischemia is accompanied by the accumulation of lipid peroxidation products. The content increases by an average of 138-213% of the initial level. Brain reperfusion after 30-min ischemia was accompanied by an increase or maintenance of a high level of lipid peroxidation products. Ionol injection was accompanied by an increase in the survival of rats and prevented the accumulation of lipid peroxidation products after brain ischemia and reperfusion.

Animals↗
PubMed1987

[Effect of phospholipids of different compositions on coronary vessel tonus and myocardial contractility].

In experiments on perfused isolated Wistar rat hearts and frog myocardial strips it has been shown that the injection of egg phospholipid liposomes in the perfusion solution leads to a decrease in the volume velocity of the coronary perfusion and to worsening of the contractile myocardial function. Negative inotropic effect of phospholipids on the perfused heart may be linked not only with the decrease in the coronary perfusion but also with their direct inhibitory action on the contractile ability of myocardiocytes.

Animals↗
PubMed1986

[Disordered functioning of the superoxide radical-superoxide dismutase system in rat liver ischemia].

The rate of O2 radical generation in microsomal membranes (VO2), the activity of cytosol superoxide dismutase (Cu, ZnSOD) and mitochondrial superoxide dismutase (MnSOD), and the activity of xanthine oxidizing system (XO) after a two-hour ischemia following a 24-hour reoxygenation of the rat liver were investigated. The high value of VO2, as compared to Cu, ZnSOD activity, may result in regulation disorders in O2-SOD system during ischemia. During reoxygenation, xanthine oxidizing system in combination with lowered Cu, ZnSOD activity may substantially contribute to the disturbance.

Animals↗
PubMed1985

[Protection of long-term ischemic kidneys from the damages of reoxygenation by using the temporary inhalation of a gas hypoxic mixture].

Experiments were carried out on 240 August and Wistar rats. It was shown that renal reperfusion after 2 h of ischemia, performed following 24-hour inhalation by the animals of a gas hypoxic mixture (GHM) with 10 to 12% O2, increased the survival rate of the rats and accelerated the resynthesis of adenine nucleotides by the kidneys as compared with analogous characteristics during reperfusion paralleled by inhalation of air or oxygen. The protective effect of GHM inhalation on renal function and metabolism was approximately the same as the protective action of high doses (240 mg/kg) of the antioxidant ionol. The experiments confirm the role of lipid peroxidation in the pathogenesis of reoxygenation injuries and the protective effect of GHM inhalation in the early period of reperfusion.

Adenine Nucleotides↗
PubMed1984

[Dynamics and pathogenesis of ischemic contracture of the heart].

In experiments on 34 dogs, the authors studied myocardial rigidity, ATP levels and Ca2+-accumulating function of the membranes of the sarcoplasmic reticulum (SR) in the external (subepicardial) and internal (subendocardial) layers of the myocardium at 1 and 2 h of total ischemia at 37 degrees C and also 30 min after cardiac reperfusion by heterotopic transplantation. It was revealed that contracture changes in ischemia first affect the internal and then the external layer of the myocardium which corresponds to the initial and completed phases of ischemic contracture (IC) of the heart, correspondingly. IC of the heart is irreversible and in cases of total contracture of all layers of the myocardium (the completed phase) the heart loses contractile function. Changes in the contractility in the external and internal layers of the myocardium show a stronger inverse correlation with the capacity of SR membranes to absorb Ca2+ rather than with ATP levels in the tissues which indicates an essential role of the Ca2+ accumulating function of SR in the pathogenesis of IC.

Adenosine Triphosphate↗
PubMed1983

[Use of antioxidants to prevent damage during acute ischemia and reperfusion of the kidneys].

Prophylactic injection of the natural antioxidant alpha-tocopherol and synthetic antioxidants ionol, diludin and 6-mercurascan prevented the development of lesions during acute renal ischemia and subsequent reperfusion. Ionol proved more effective on intraperitoneal injection than on intragastric route of administration. It has been demonstrated that antiischemic effect of ionol is related to its ability to exhibit the process of lipid peroxidation.

Animals↗
PubMed1983

[Protective action of antioxidants and microsomal monooxygenase inducers in ischemic and reoxygenation damage to the liver].

One-hour ischemia followed by rat liver reoxygenation brings about the accumulation of endogenous products of lipid peroxidation (LPO) and deterioration of the monooxygenase system (the drop of cytochrome P-450 content, amidopyrine N-demethylase and NADP X H cytochrome reductase activity). Application of the antioxidant ionol inhibited LPO and protected the monooxygenase system from reoxygenation but not from ischemic injuries. Phenobarbital alone and combined with ionol did not protect the monooxygenase system from ischemic and reoxygenation injuries but provided the retention of high absolute indicators of the system. Ionol and its combination with phenobarbital also increased the survival of rats with ischemized liver.

Animals↗
PubMed1982

[Effect of lipid peroxidation products on vascular tonus].

A total of 126 experiments on the model of perfusion of isolated rabbit ear vessels were made to study the effect of primary (hydroperoxides - HP) and secondary products (SP) of phospholipid peroxidation (phosphatidyl ethanolamine - PEA), hydroperoxides of fatty acids (arachidonic acid - AA), as well as that of non-modified PEA and AA on the vascular tone. PEA in doses of 0.1 and 10 mumole produced a distinct vasodilator effect in 63 and 70% of cases, respectively. Unlike PEA, HP of PEA in doses of 0.01 and 0.1 mumole had a vasoconstrictive effect, which was manifested by a fall of the volumetric perfusion rate in 71 and 53% of cases, respectively. The SP of PEA also produced a vasoconstrictive action, but the effect was not dose-dependent. Study into the effects of AA and HP of AA revealed no distinct unidirectional action on the vascular tone. On the basis of the preliminary data the authors suggest that the effect of lipid peroxidation products on barrier properties of the sarcoplasmic reticulum membranes lies at the basis of their action on the vascular tone.

Animals↗
PubMed1981

[Lipid peroxidation and damage to the mixed function oxidase system in membranes of the endoplasmic reticulum in the presence of liver ischemia].

The content of endogenous lipid peroxidation products and variations in mixed function oxygenases were examined in liver microsomes of rats exposed to thermal ischemia of varying duration (15, 30, 60 and 120 min). The development of ischemic injury was accompanied by the accumulation of lipid hydroperoxides and Schiff's base, by the lowering of the content of cytochrome P-450 and diminution of the activity of NADPH-cytochrome P-450 reductase. The maximum changes were demonstrated 2 hours after ischemia. The presence of a reverse correlation between the content of lipid peroxidation products and the content of cytochrome P-450 was recorded.

Animals↗
PubMed1980

[Intensification of peroxidation and changes in lipid composition in ischemic liver homogenates and subcellular fractions].

Lipid peroxidation (hydroperoxides and antioxidant activity) and lipid composition in liver homogenates and in its mitochondrial, microsomal and nuclear fractions were studied after 15--120 minutes of liver warm ischemia. Pronounced enhancement of lipid peroxidation during ischemia was seen in all subcellular fractions, particularly in the mitochondrial one. The results are consistent with low resistance of the liver and specifically its mitochondria to ischemia. Activation of lipid peroxidation corresponded with changes in the lipid composition. Decrease in the level of total and readily oxidizable lipids (cardiolipin) and accumulation of poorly oxidizable phospholipids (sphingomyelin) and highly toxic lysophosphatides were recorded. The evidence obtained suggests a role for lipid peroxidation in the pathogenesis of ischemic injuries to the liver.

Animals↗
PubMed1979

[Disruption of the Ca++ transport enzyme system in sarcoplasmic reticulum membranes upon exposure to phospholipid hydroperoxides and fatty acid hydroperoxides].

It was shown that when injected into a suspension of sarcoplasmic reticulum (SR) vesicles phosphatidyl ethanol-amine hydroperoxide (HP) slightly activated Ca++-dependent ATPase and increased the permeability of SR membranes for Ca++ during the enzyme function. Linoleic acid HP had no effect on the parameters of the enzymatic Ca++- transporting system (activity of Ca++-dependent ATPase, Ca/ATP ratio, rate of Ca++ efflux) in the SR membranes due to its insufficient incorporation into the SR fragments. It is concluded that among the primary molecular products of lipid peroxidation (free fatty acid HP, phospholipid HP) induced both in vitro (by the Fe++ + ascorbate system) and in vivo (ischemia, E-avitaminosis), only the phospholipid HPs were modifiers of Ca++ transport in the SR membranes.

Animals↗