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Biomedical subjects

Iu B Lishmanov

Publications and source records attributed to Iu B Lishmanov.

At least 19 recordsLinked to original sources
PubMed2004

Scintigraphic evaluation of myocardial and cerebral blood flow in patients with a history of coronary artery bypass grafting.

This paper deals with a comparative scintigraphic evaluation of the changes that occur in coronary and cerebral circulation in patients with coronary artery disease (CAD) after coronary artery bypass grafting (CABG) under conditions of cardiopulmonary bypass (CPB) or beating heart. Twenty-nine CAD patients who underwent CPB were examined. Of these, 14 patients were operated on using CPB (the first group) and 15 patients on the beating heart using the myocardial "stabilizer" Octopus (the 2nd group). The patient groups matched in terms of the age, sex, the clinical and angiographic factors. Perfusion scintigraphy of the heart and brain by means of single-photon emission computed tomography (SPECT) and the neurologic evaluation were performed twice in all the patients: before and 2-4 weeks after CABG. The second group patients demonstrated a significant lowering of the mean magnitude of stable defects (SD) of myocardial perfusion. The lowering or disappearance of SD was observed in a greater percentage of cases versus the first group. All the patients were found to have areas of hypokinesis in the SD projection. Also, the second group showed a significant rise of the mean magnitude of left ventricle ejection fraction. Operations with CPB were associated with a 5% decrease of cerebral blood flow in the frontal and temporal lobes of the right hemisphere. No significant deterioration of brain perfusion was observed in patients (on the whole in the group) operated on without heart arrest. It is noteworthy that there was a significant improvement of the average group indicators of cerebral perfusion in the right occipital and posterior segments of the temporal lobes. The changes in cerebral perfusion were in agreement with the course of changes in the cognitive status. Thus, CABG on the resting heart in CAD patients favours a more remarkable restoration of perfusion and contractility of the hibernated myocardium versus revascularization performed under CPB and exerts, as a result, a beneficial effect on cerebral circulation and the neuropsychological status of the patients.

Adult↗
PubMed2004

Central hemodynamic and cognitive function in the short- and long-term periods after coronary bypass grafting.

The aim of the present work was to study cerebral hemodynamics and cognitive function in patients suffering from coronary artery disease (CAD) in the short- and long-term periods after coronary bypass grafting (CBG). The study accrued 65 patients who underwent myocardial revascularization using cardiopulmonary bypass (43 persons) and without heart interruption (22 persons). In 21 cases, CBG using cardiopulmonary bypass with a purpose of preventing cerebral events was supplemented by administration of instenon manufactured by the Nycomed Company, Perfusion tomoscintigraphy of the brain and neuropsychological testing were provided to all the patients prior to CBG, 14 days and 6 months following surgery. CBG coupled with preventive administration of instenon or beating heart operation allow to appreciably minimize the risk of disorders of cerebral hemodynamics and cognitive function in the long-term postoperative period.

Brain↗
PubMed2003

[Pharmacological prevention of cerebrovascular complications in cardiac patients after coronary artery bypass surgery].

The aim of the study was to evaluate cognitive functions and cerebral perfusion in cardiac patients following coronary artery bypass graft surgery (CABG) and to investigate a potential of pharmacological prevention of neurocognitive deficit and cerebral perfusion disorders. Forty patients undergone CABG with cardiopulmonary bypass (CPB) were included in the study. For prevention of cerebral perfusion impairments and cognitive deficit, instenon ("Nycomed") was administered to 18 of the patients. The results revealed that the use of instenon allowed reducing a negative effect of CABG with CPB on neuropsychological state of the patients, thus preventing cerebral perfusion disturbances during surgery intervention.

Benzamides↗
PubMed2003

[Role of ORL1 receptors in the regulation of cardiac resistance to arrhythmogenic effects ].

It has been found that intravenous administration of nociceptin (0.4 mg/kg) prevents development of aconitine-induced arrhythmias but has no effect on the incidence of occlusion, reperfusion, CaCl2-induced arrhythmias, and exacerbates epinephrine-evoked dysrhythmias. Pretreatment with hexamethonium, atropine, guanethidine and naloxone did not abolish the arrhythmic effect of nociceptin. Intracerebroventricular infusion of orphanin FQ was shown to increase cardiac tolerance of arrhythmogenic influence of aconitine, but this effect is completely abolished by hexamethonium administration. It has been suggested that stimulation of both central and peripheral ORL1 receptors increases cardiac resistance against arrhythmogenic effect of aconitine via different mechanisms.

Aconitine↗
PubMed2003

Thallium-199 myocardial perfusion scintigraphy in the diagnosis of restenoses after balloon dilatation and stenting of the coronary arteries.

AIM: To evaluate the diagnostic importance of thallium-199 myocardial perfusion single-photon emission computed tomography (SPECT) in the recognition of coronary restenoses and stenoses de novo of varying sites after endovascular treatment of coronary artery disease (CAD). MATERIAL AND METHODS: Myocardial perfusion scintigraphy was used to examine forty-six patients presenting with CAD before, 2-3 weeks, 3-6 months and 1-2 years after balloon dilatation and/or stenting of the coronary arteries (CA). The presence, character and magnitude of perfusion defects were estimated. RESULTS: The coronary angioplasty resulted in a 76% decrease of the mean size of transient ischemic zones. The reversible defects of thallium accumulation coexisted after operation with incomplete myocardial revasculization in patients with hemodynamically significant multivessel lesions. In the long-term follow up (3-6 months and 1-2 years after endovascular treatment), aggravation of coronary insufficiency in patients with incomplete revascularization proceeded mainly due to an increase in the size of the areas marked by persistent disturbance of coronary microcirculation determined not only by acute necrotic myocardial infarction but also by transformation of transient ischemic zones to the new stable perfusion defects. As compared to the early times, the patients with verified restenoses and stenoses de novo showed in the later period (3-6 months after coronary angioplasty) a significant increase in the mean size of the transient ischemic zones, exceeding the preoperative level. In six of the eleven patients, the appearance of the new stable defects was marked after 1-2 years in the area of blood supply to the recanalized CA. Meanwhile the condition of myocardial perfusion in the group of patients without restenoses did not undergo any noticeable changes. CONCLUSION: Myocardial perfusion scintigraphy using thallium-199 chloride allows to objectively evaluate over time the results of endovascular treatment of CAD. Also, there is every probability of success of predicting restenoses and stenoses de novo.

Angina, Unstable↗
PubMed2003

[Alterations of inotropic function of isolated heart and extent of injury of cardiomyocytes after cannabinoid receptor activation during ischemia and reperfusion].

It was found that CB1- and CB2-receptor activation by intravenous administration of the selective CB-agonist HU-210 at a dose 0.1 mg/kg prompts an increase of myocardial resistance to the pathogenic action of ischemia and reperfusion in vitro. The revealed effects of HU-210 do not depend on the activation of CB-receptors in the myocardium.

Animals↗
PubMed2002

[Contribution of delta1-opioid receptors in regulation of cardiac resistance to ischemia-reperfusion].

It has been found that pretreatment with a delta 1-opioid receptor agonist, DPDPE, in dose of 0.1 mg/kg intravenously 15 min before heart isolation, prevents appearance of reperfusion, ventricular arrhythmias during total global ischemia (45 min) and reperfusion (10 min) of isolated rat heart. This effect was dose-dependent. Addition of DPDPE to the perfusion solution in a final concentration of 0.1 mg/L and/or 0.5 mg/L 15 min before ischemia also decreased the incidence of reperfusion arrhythmias in a concentration-dependent manner. Addition of DPDPE to the perfusion solution in a final concentration of 0.1 mg/L also decreased creatine kinase levels in the coronary sinus. However DPDPE had no cardio-protective effect in concentration of 0.5 mg/L or after intravenous administration. A previous intravenous injection of DPDPE in dose of 0.5 mg/kg exacerbated reperfusion-induced contractile dysfunction of isolated heart but exerted no effect in dose of 0.1 mg/kg. Previous perfusion of the rat isolated heart by DPDPE in concentration of 0.1 mg/L and 0.5 mg/L 15 min before ischemia also exacerbated myocardial contractile dysfunction during reperfusion. It is proposed that the antiarrhythmic, cardio-protective and negative inotropic effect of DPDPE during reperfusion may be due to stimulation of cardiac delta-1 receptors.

Animals↗
PubMed2002

[Clinical response to agonists of mu and beta opiate receptors in patients with ischemic heart disease: effects of D-Ala2-Leu5-Arg6-enkephalin on hemodynamics, oxygen balance and lipid spectrum of blood].

Effects of intravenous dalargin daily administered in a dose of 28 micrograms/kg during 7 days on hemodynamics, oxygen balance, lipid spectrum were studied in patients with coronary heart disease. The results of the treatment show that dalargin decreases incidence of anginal attacks, peripheral vascular resistance, venous tonicity, increases exercise tolerance, peripheral blood flow and venous flow. In addition, such treatment reduces oxygen consumption, levels of total cholesterol, triglycerides, low density lipoprotein cholesterol.

Adrenergic beta-Agonists↗
PubMed2001

[The role of mu- and delta-opiate receptors in resistance of the myocardium to free radical damage].

I.v. administration of the delta-opioid (OR) receptors' agonists DSLET or DTLET prevented creatine kinase leakage from the rat isolated heart in oxidative stress damage and abolished an increase in myocardial levels of conjugated diens and malondialdehyde. The agonists also prevented a stress-induced augmentation of the superoxide dismutase (SOD) activity. All protective effects of delta-receptor stimulation was completely abolished by the delta OR antagonist ICI 174,864. The data obtained suggest that the cardioprotective effect of the delta OR stimulation in vivo is not mediated via direct cardiac delta OR activation but, probably, rather via some unknown indirect circulating humoral factor(s).

Animals↗
PubMed2001

[Effect of stimulation of mu-opiate receptors on contractility of the isolated heart in normal oxygenation and during ischemia-reperfusion].

Activation of mu-opioid receptor (OR) in rats prevented development of reperfusion-induced myocardial cell damage. In contrast, direct cardiac mu-OR stimulation with the opioid receptor agonist DAMGO decreased cardiac contractility in normal oxygenation and aggravated the reperfusion-induced myocardial cell damage. The findings suggest that the cardioprotective effect of mu-OR stimulation is not mediated via cardiac mu-OR activation.

Animals↗
PubMed2001

[Role of delta opioid receptors and their ligands in the development of adaptive heart protection against arrhythmogenesis].

It has been found that stimulation of delta-1 opioid receptors by intravenous administration of DPDPE (0.5 mg/kg) decreases the incidence of ischemic and reperfusion-induced arrhythmias and also increases myocardial tolerance to the arrhythmogenic action of epinephrine in rats. Pretreatment with a selective delta-2 agonist, DSLET, had no antiarrhythmic effect. The inhibition of the enzymatic breakdown of endogenous enkephalins by intravenous administration of acetorphan decreased the incidence of epinephrine-induced arrhythmias. Pretreatment with a selective delta opioid receptor antagonist, ICI-174.868, completely abolished this antiarrhythmic effect. Adaptation of rats to repeated immobilization stress during 12 days increased myocardial tolerance to the arrhythmogenic action of coronary artery occlusion (10 min) and reperfusion (10 min). Pretreatment with a selective delta opioid receptor antagonist, TIPP(Psy), did not abolish the antiarrhythmic effect of adaptation to immobilization stress. It seems that endogenous agonists of delta opioid receptors are not involved in the antiarrhythmic effect resulting from adaptation to stress.

Adaptation, Physiological↗
PubMed2000

[Opioid system and cardiac resistance to ischemic and reperfusion injuries].

In vivo pre-treatment with the opioid receptor antagonist D,L-naloxone completely eliminated the reperfusion-induced creatine kinase (CK) leakage from the rat isolated perfused haert. The inactive isomer L-naloxone decreased the CK release by half. The (-antagonist ICI 174,864 and k-antagonist nor-binanltorphimine exerted a weaker protective effect. The (-antagonist DAMGO, the (2-agonist DSLET, the k1-agonist spiradolin, or the sigma-agonist (+)-SKF 10047, improved myocardial cell viability after ischemia/reperfusion.

Animals↗
PubMed1999

[Dependence of the pump function of the isolated rat heart on the functional activity of sigma receptors during reperfusion].

Pre-treatment of the sigma-receptor with the sigma-receptor agonist (+)-SKF 10.047 improved the reperfusion recovery of cardiac pump function. The sigma-receptor activation, among other effects, prevented the reperfusion contracture, increased pressure in the left ventricle, and improved survival of cardiomyocytes after ischemia/reperfusion. Pre-treatment with the sigma-receptor antagonist DuP 734 augmented the reperfusion systolic dysfunction of the myocardium and prevented postischemic contractures and cardiac cell lesions. Activation of the cardiac sigma-receptor seems to prompt an augmentation of tolerance to the reperfusion damage.

Animals↗