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V Iu Polumiskov

Publications and source records attributed to V Iu Polumiskov.

At least 19 recordsLinked to original sources
PubMed2005

[Effect of mexicor on oxidative stress in acute myocardial infarction].

Mexicor (5% solution and capsules) was used in 40 of 80 conventionally treated patients with acute myocardial infarction. The drug was given intravenously for 5 days, than intramuscularly (6-9 mg/kg) for 9 days and orally (0.1 mg t.i.d.) thereafter until discharge. Severity of oxidative stress was evaluated by K coefficient. Calculation of this coefficient required data on degree of oxidation of lipids in blood serum, serum levels of diene conjugates, malonic dialdehyde, alpha-tocopherol and ceruloplasmin. These parameters as well as activity of superoxide dismutase, glutathione peroxidase and catalase in erythrocytes were measured at admission, on days 2, 3, 7, 14 and at discharge. Mexicor treated compared with untreated (n=40) patients were characterized by diminished severity of oxidative stress at the account of lower levels of lipid peroxidation products and augmented compensatory potential of the endogenous antioxidant system.

Administration, Oral↗
PubMed2000

[Urapidil effects on oxidative stress in hypertensive crises].

Urapidil effects on oxidant stress were studied in 36 patients with hypertension stage I-III running with crises. Acute hypertensive crisis was managed by intravenous injections of urapidil (20-50 mg) for 5 min. After that for a week they received urapidil monotherapy followed by combined treatment for another week (quinapril--25 mg/day or ramipril--5-10 mg/day in combination with hypothiaside--25 mg/day; lokren--20 mg/day or atenolol--50-100 mg/day and diltiazem--180-360 mg/day) to stabilize arterial pressure finally. Oxidant stress was estimated by lipid peroxidation (LPO) and state of antioxidant system (AOS). Catabolism and anabolism were evaluated by blood levels of hydrocortisone and insulin. LPO, AOS, the blood hormones were measured before management of hypertensive crisis, immediately after it and 1, 3, 7 and 14 days after. Before the crisis treatment LPO was found high. Urapidil administration reduced levels of hydrocortisone, dienic conjugates, lipid peroxidation, oxidant stress rate (OSR). Later, LPO and OSR slowly increased. It is concluded on validity of the antioxidants use in hypertensive patients with crises.

Acute Disease↗
PubMed1996

[The efficacy of emoxipin and neoton in unstable stenocardia].

55 patients with unstable angina pectoris (group 1) received conventional treatment and neoton infusions (30 g/day for 3 days). Emoxipin was injected intramuscularly to 20 patients of group 2 (3 mg/kg for 20 days) and intravenously to 38 patients of group 3 (10 mg/kg). Control group consisted of 100 patients. Stabilization occurred in 89.2, 80 and 86.8% of group 1, 2 and 3 patients, respectively, versus 78% in controls. Holter ECG monitoring provided evidence on decline of myocardial ischemia for group 1 patients. Diene conjugates in group 1 decreased by 37%, ceruloplasmin level was higher by 30% compared to controls. Respective indices for emoxipin reached 52 and 37%, respectively. It is concluded that emoxipin and neoton produced a beneficial effect on unstable angina pectoris through correction of lipid peroxidation.

Angina, Unstable↗
PubMed1990

[Antioxidant emoxipin: its effect on the formation of a necrotic focus and reparative processes in myocardial infarction].

The effect of the water soluble antioxidant emoxipin given intravenously in a dose of 10 mg/kg for 5 days, then intramuscularly 1 mg/kg for 15 days. Comparison with the values found in the control group of patients with myocardial infarction revealed that emoxipin contributed to limitation of the size of a necrotic focus and accelerated reparative processes, whose result was a lower incidence of circulatory failure. One of the main mechanisms responsible for beneficial effects of emoxipin on the clinical course of myocardial infarction consists in normalization of lipid peroxidation and parameters of the antioxidative status.

Adult↗
PubMed1990

[Emoxipin in reperfusion of ischemic myocardium in dogs: effects on infarct size and plasma creatine kinase activity].

The effects of synthetic antioxidant emoxypine on infarct size and plasma creatine kinase (CK) activity was studied on open-chest anesthetized dogs with 180-min myocardial ischemia followed by reperfusion. Emoxypine (10 and 40 mg/kg) was injected intravenously, beginning since 120th min of coronary artery occlusion. Emoxypine (10 mg/kg) resulted in infarct size limitation and reduction in plasma CK activity. An increase in dose of emoxypine to 40 mg/kg largely attenuated its protective effect on infarct size. CK activity during post-ischemic reperfusion was even higher in emoxypine (40 mg/kg) group compared with control. Augmented CK leakage from irreversibly injured myocardium to plasma under these experimental conditions may be owing to preservation of microvascular integrity and improving of drainage of infarcted tissue exerted by emoxypine.

Animals↗
PubMed1989

[The pathogenesis of heart rupture in myocardial infarct].

Examination of 166 patients with primary transmural myocardial infarction (MI) of the anterior site has shown that the blood of MI patients (n = 34) complicated by cardiorrhexis manifests the maximal increase of the stress reaction components, lipid peroxidation products and an appreciable lowering of the content of adaptogens. It is emphasized that the development of the maladaptation syndrome underlies the pathogenesis of cardiorrhexis during MI as the result of the failure of the compensatory-adaptive potentialities of the body in response to the excessive stress reaction. It has been discovered that the high rise of the ST segment on the ECG and pronounced arterial hypoxemia are informative indicators mirroring the high probability of cardiorrhexis occurrence in MI patients. A scheme of cardiorrhexis pathogenesis in MI patients is offered.

Adaptation, Physiological↗
PubMed1989

[Effects of transcranial electrostimulation of the opioid systems on reparative processes in patients with myocardial infarct].

Sixty three patients with primary excessive myocardial infarction (MI) were examined. Transcranial electric stimulation (TES) was demonstrated to contribute to more rapid formation of a postinfarction scar, development of compensatory hypertrophy of the preserved myocardium, and improvement of cardiac contractility. TES-induced activation of the endogenous opioid system was found to be one of the mechanisms responsible for stimulation of reparative processes in patients with MI. Introduction of TES into the multimodality therapy for MI improves the clinical picture of the disease, promoting diminution of circulatory failure signs and relapses of angina-associated pains and favoring decrease in the long-term course of MI and frequency of cardiac arrhythmias.

Arrhythmias, Cardiac↗
PubMed1989

[Lipid peroxidation and the major factors of its activation in patients with myocardial infarction].

A dynamic study of 97 patients with primary macrofocal myocardial infarction (MI) has demonstrated that activated lipid peroxidation (LPO) is an important pathogenetic element of MI, with LPO level reflecting major stages of the disease and its complications. In acute MI, LPO activation depends on the magnitude of the stress syndrome and the severity of arterial hypoxia and is mediated by gas exchange disorders in the pulmonary circulation network. The passage of LPO products from ischemized myocardium to systemic circulation is also of significance. In the scarring phase, LPO activation is due to circulatory hypoxia associated with reduced cardiac contractility. The markedness of leucocytic response is an important factor of MI-associated LPO activation. The extent of LPO disorders is largely limited by the antioxidant system of the body.

Adult↗
PubMed1988

[Diagnosis and prevention of myocardial reperfusion injury in experimental myocardial infarction].

In an experimental study in 69 dogs with the occluded anterior descending branch of the left coronary artery, dibunol, an antioxidant, and isoptin, a Ca2+ antagonist reduced myocardial infarction area, prolonged survival time and brought down mortality rate, in spite of an increase in reperfusion-related arrhythmias. The value of various electrocardiographic parameters for the diagnosis of ischemized-myocardium reperfusion and the severity of reperfusion-related heart damage in relation to the type of preventive medication, as compared to postmortem findings, are discussed.

Animals↗
PubMed1988

[Stimulation of reparative processes in myocardial infarction: comparative evaluation of the effects of piracetam and inosine].

A study of 102 patients with primary macrofocal myocardial infarction, admitted to hospital within the first 6 hours after the onset of the disease, and experimental evidence obtained in 110 Wistar rats are reported. In a control group of myocardial infarction patients, collagen synthesis was depressed in the presence of the activation of free-radical lipid oxidation and circulatory hypoxia. Piracetam and inosine treatment was associated with the inhibition of free-radical lipid oxidation and a reduction of hypoxia, those being accompanied by increased collagenogenesis and accelerated postinfarction scar formation. Piracetam, as compared to inosine, had a more marked stimulating effect on the development of compensatory myocardial hypertrophy, thus contributing to rapid recovery of cardiac contractility and reducing manifestations of circulatory insufficiency.

Adult↗
PubMed1987

[Prevention of myocardial damage during reperfusion of the coronary artery in dogs using dibunol combined with verapamil].

An experimental study in 69 dogs examined the effect of isolated and combined use of dibunol and verapamil (isoptin) on the course of reperfusion of ischemized myocardium after 180 minutes' coronary occlusion. Verapamil alone had no protective effect on reperfused myocardium, whereas dibunol, and particularly its combination with verapamil, essentially limited the size of necrosis, reduced plasma CPK activity and animal mortality rate and maintained ultrastructural integrity of cardiomyocytes, which was accompanied by a decrease of plasma lipid peroxidation products and a stabilization of cardiomyocyte sarcolemma. The significance of membrane damage and uncontrolled calcium entrance into cardiomyocytes for the mechanism of myocardial damage at the recovery of coronary circulation is discussed.

Animals↗
PubMed1987

[Effect of dibunol and isoptin on the creatine kinase and myoglobin content of the blood serum in dogs undergoing postischemic coronary reperfusion].

The effect of an antioxidant dibunol and calcium antagonist verapamil on postperfusion release of myoglobin (Mb) and MB-creatine kinase (MB-CK) has been assessed in 30 dogs with experimental coronary occlusive myocardial infarction. It has been shown that reperfusion after 3-hour ischemia does not only accelerate the release of intracellular proteins, but also leads to pronounced myoglobinemia and blood enzymes. In postischemic blood flow recovery with combined dibunol and verapamil preliminary injections, an almost threefold decrease in MB-CK and Mb blood content, as compared to "reperfusion" indexes, was observed by the 10th minute of reperfusion.

Animals↗
PubMed1986

[Rate of development and the size of the necrotic focus in patients with myocardial infarct treated by intracoronary thrombolysis].

Streptokinase intracoronary thrombolytic therapy (ITT) was given to 68 of 135 patients with large-focal myocardial infarction (MI) admitted to hospital within 6 hours of the attack. Coronary flow was recovered in 31 MI patients. The size of the necrotic focus was assessed on the basis of precordial cartograms from 35 ECG leads and serial measurements of MB CPK activity. ITT achieving successful thrombolysis is conducive to rapid formation and accelerated repair of the necrotic focus in MI patients. The recovery of coronary circulation after 3 hours of infarction was accompanied by the reperfusion syndrome, i. e. rapid necrotization of the ischemized region, a considerable release of MB CPK into the circulation, complex cardiac rhythm and conductivity disorders, and signs of transient heart failure.

Adult↗
PubMed1984

[Effect of systemic thrombolytic therapy on necrotic focus formation in myocardial infarct patients].

The formation of the myocardial necrotic focus was assessed by precardial charting at 35 leads and the serial determination of CPK activity and MB fraction in 50 patients receiving the systemic thrombolytic therapy and 52 patients of the control group. Thrombolytic therapy initiated within the first 6 h of the disease was shown to facilitate the limitation of the extent of myocardial infarction through a more rapid stabilization of the necrotic focus. The calculated extent of myocardial infarction in patients treated with thrombolytic drugs was 37.4% less than in the control group. A beneficial clinical effect of thrombolytic therapy was demonstrated.

Adult↗