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23 records – page 1 of 3.

[Acute myocardial ischemia-reperfusion injury: role of nitric oxide system]

https://arctichealth.org/en/permalink/ahliterature53337
Source
Fiziol Zh. 2004;50(2):34-42
Publication Type
Article
Date
2004
Author
O O Moibenko
M Ia Iuz'kiv
L V Tumanovs'ka
A V Kotsiuruba
Author Affiliation
A.A. Bogomoletz Institute of Physiology, National Academy of Sciences of Ukraine, Kiev.
Source
Fiziol Zh. 2004;50(2):34-42
Date
2004
Language
Ukrainian
Publication Type
Article
Keywords
Acute Disease
Animals
Arginine - pharmacology
Coronary Circulation - drug effects - physiology
Coronary Vessels - metabolism
Disease Models, Animal
Dogs
English Abstract
Enzyme Inhibitors - pharmacology
Male
Myocardial Reperfusion Injury - enzymology - metabolism - physiopathology
Nitric Oxide - biosynthesis - physiology
Nitric Oxide Synthase - antagonists & inhibitors
Nitroarginine - pharmacology
Abstract
In experiments on the closed-chest dogs it was shown that NOS inhibition resulted in the significant alterations of hemodynamic indices (coronary and peripheral vascular resistance, cardiac output and heart rate) under local myocardial ischemia/reperfusion in comparison with control experiments. At the first time it was shown that NOS inhibition activated the autophagic destruction of cardiomyocytes in the ischemic myocardium and could reduce an area of functionally active myocardium. L-arginine administration attenuated cardio- and hemodynamic disturbances, that substantially improved the course of ischemia/reperfusion, diminished the ultrastructural changes in myocardium and prevented development of autophagic programmed cell death.
PubMed ID
15174204 View in PubMed
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[Allelic polymorphism of endothelial NO-synthase (T(-786)-->C) promoter gene as risk factor of acute coronary syndrome]

https://arctichealth.org/en/permalink/ahliterature53180
Source
Fiziol Zh. 2005;51(1):72-6
Publication Type
Article
Date
2005
Author
V Ie Dosenko
V Iu Zahorii
Ia M Lutai
O M Parkhomenko
O O Moibenko
Source
Fiziol Zh. 2005;51(1):72-6
Date
2005
Language
Ukrainian
Publication Type
Article
Keywords
Acute Disease
Adult
Aged
Aged, 80 and over
Alleles
Coronary Disease - enzymology - epidemiology - genetics
English Abstract
Female
Genetic Predisposition to Disease
Genetic Screening
Humans
Male
Middle Aged
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type III
Polymerase Chain Reaction
Polymorphism, Restriction Fragment Length
Promoter Regions (Genetics)
Risk factors
Ukraine - epidemiology
Abstract
Frequency of promoter endothelial NO-synthase gene allelic polymorphism by using polymerase chain reaction and restriction fragment length polymorphism (RFLP-PCR) was determined in 221 patients with acute coronary syndrome (ACS) and in 83 almost healthy subjects. Data obtained indicate that different promoter allelic variant frequency differs significantly in patients with ACS and in control group. Correlation of normal homozygotes (T/T), heterozygotes (T/C) and pathologic homozygotes (C/C) was 48%, 36% and 16% respectively in patients, and in control it was 48%, 46%, 6% (P
PubMed ID
15801202 View in PubMed
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[ATP-sensitive potassium channels and changes in their functional activity during streptozocin-induced diabetes mellitus]

https://arctichealth.org/en/permalink/ahliterature9530
Source
Fiziol Zh. 2003;49(6):22-30
Publication Type
Article
Date
2003
Author
R B Strutyns'kyi
O O Moibenko
S M Pyvovar
V Ie Dosenko
L M Iahupol's'kyi
Author Affiliation
A.A. Bogomoletz Institute of Physiology, National Academy of Science of Ukraine, Kiev.
Source
Fiziol Zh. 2003;49(6):22-30
Date
2003
Language
Ukrainian
Publication Type
Article
Keywords
Adenosine Triphosphate - metabolism
Angiotensin II - pharmacology
Animals
Aorta, Thoracic - drug effects - metabolism
Comparative Study
Diabetes Mellitus, Experimental - metabolism
Endothelium, Vascular - drug effects - metabolism
English Abstract
Male
Muscle, Smooth, Vascular - drug effects
Norepinephrine - pharmacology
Potassium - pharmacology
Potassium Channels - drug effects
Rats
Rats, Wistar
Vasoconstriction - drug effects
Vasoconstrictor Agents - pharmacology
Abstract
Attenuation in the vasodilatory effects of a new synthesized opener of ATP-sensitive K' channels on isolated aorta strips of rat has been shown under experimental (streptozocin-induced) diabetes mellitus. The level of that attenuation depended on the nature of initial vasoconstriction. The most pronounced decrease--43.34% as compared to the control responses in healthy rats, we observed after norepinephrine-induced vasoconstriction. Following preliminary angiothensin-induced vasoconstriction and potassium depolarization, attenuation in vasoconstriction was 20.37% and 22.4%, respectively. Norepinephrine inhibited vasodilator effects of phlocalin in the aorta of diabetic rats much more significantly, as compared to those after potassium depolarization. Inhibitory effects of angiothensin II in rats with diabetes mellitus did not differ from those in the control rats. At the same time, constrictory responses to biological active agents were preserved and they did not differ from those in control rats. We suggest that impairment in vascular reactivity under diabetes mellitus, at least in part, depends on the changes in the functioning of ATP-sensitive potassium channels.
PubMed ID
14965034 View in PubMed
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[Cardioprotective effect of heme oxygenase-1 induction by hemin on the isolated rat heart during ischemia--reperfusion]

https://arctichealth.org/en/permalink/ahliterature53401
Source
Fiziol Zh. 2003;49(6):14-21
Publication Type
Article
Date
2003
Author
T V Kukoba
O O Moibenko
A V Kotsioruba
Source
Fiziol Zh. 2003;49(6):14-21
Date
2003
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Blood pressure
Coronary Circulation
Creatine Kinase - metabolism
English Abstract
Gene Expression Regulation, Enzymologic
Heart - physiopathology
Heme Oxygenase (Decyclizing) - metabolism
Heme Oxygenase-1
Hemin - metabolism
In Vitro
Male
Myocardial Ischemia - enzymology - physiopathology
Myocardial Reperfusion Injury - enzymology - metabolism - physiopathology - prevention & control
Rats
Reactive Oxygen Species - metabolism
Time Factors
Ventricular Dysfunction, Left - physiopathology
Ventricular Pressure
Abstract
The aim of the study was to determine the role of both an inducible isoform of heme oxygenase (HO-1) and products of heme catabolism (carbon monoxide (CO), cardiac bilirubin and Fe2+) in protecting myocardium against post-ischemic myocardial dysfunction. Rat hearts were isolated and perfused according to the Langendorff technique to evaluate the recovery of myocardial function after total ischemia (20 min) and reperfusion (40 min) and production of reactive oxygen forms at a reperfusion phase. Ischemia/reperfusion caused impairment in myocardial function: left ventricular developing pressure (LVDP) was shown to be decreased, while end-diastolic pressure (EDP) and both coronary perfusion pressure and coronary resistance increased. Free oxygen radicals were generated at the reperfusion phase which led to injuries to cardiomyocytes and creatine kinase efflux into perfusate. We have found that upregulation of HO-1 by preliminary (24 h before ischemia) injections of 25 mg/kg hemin (i.p.) resulted in improving the myocardial function due to increasing the enzyme activity and forming the cardial bilirubine, while generation of reactive oxygen forms was inhibited, as well as the contents of creatine kinase reduced. As a result, impairment in cardiomyocytes diminished, and coronary vessels dilated to improve the functional parametres of the heart work.
PubMed ID
14965033 View in PubMed
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[Cardioprotective effects of activation of ATP-sensitive potassium channels in experiments in vivo: influence on blood biochemical parameters following ischemia-reperfusion of the myocardium]

https://arctichealth.org/en/permalink/ahliterature99073
Source
Fiziol Zh. 2009;55(6):12-9
Publication Type
Article
Date
2009
Author
R B Strutyns'kyi
A V Kotsiuruba
O P Neshcheret
A M Shysh
R A Rovenets'
O O Moibenko
Source
Fiziol Zh. 2009;55(6):12-9
Date
2009
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Antioxidants - metabolism
Cardiotonic Agents - administration & dosage - pharmacology - therapeutic use
Disease Models, Animal
Dogs
Free Radicals - blood
Hemodynamics - drug effects
KATP Channels - metabolism
Myocardial Infarction - pathology - prevention & control
Myocardial Reperfusion Injury - blood - metabolism - pathology - physiopathology
Phosphorus - blood
Pinacidil - administration & dosage - analogs & derivatives - pharmacology - therapeutic use
Uric Acid - blood
Abstract
In experiments on the anaesthetized dogs with modeling of experimental ischemia (90 min) and reperfusion (180 min), the participation of biochemical processes in the cardioprotective effect of the preischemic activation of ATP-sensitive potassium (KATP) channels caused by intravenous introduction of flokalin, a new fluorine-containing opener of these channels was shown. Flokalin was introduced in a dose 0.1 mg/kg of animal body weight which practically did not change the parameters of hemodynamic in normoxia. Thus, the experiments investigating the influence offlokalin on changes of biochemical parameters of arterial blood during ischemia-reperfusion of myocardium showed certain features of ischemia-reperfusion syndrome development during stimulation of K(ATP) channels. The analysis of biochemical parameters of blood showed that flokalin suppressed free radical reactions and had antioxidant properties: reduced quantity of H2O2 and NO3- (the last can interpreted as a reduction in peroxynitrites formation), prevented the decline of catalase and superoxide dismutase activity. Practically constant content of low-molecular nitrosothiols in blood during all duration of experiment and increase of NO2-level during reperfusion may indicate on intact functions of the NO system and protective influence of flokalin during ischemia-reperfusion of myocardium. Practically unchanged content of inorganic phosphorus and uric acid in blood during ischemia- reperfusion under conditions of preischemic introduction of flokalin indicates the prevention of ATP degradation and fomation of both superoxide anion by xanthinoxidase and peroxynitrite by it interaction with nitric oxide. All mentioned properties of flokalin related to the changes of biochemical parameters of arterial blood, together with the changes of parameters of hemodynamics, result in diminishment of infarct size of myocardium after ischemia-reperfusion by 37% versus control experiments. K(ATP) channels, flokalin, ischemia-reperfusion, free radikaly, NO system.
PubMed ID
20201384 View in PubMed
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[Cardioprotective effects of flokalin in experiments in vivo: influence on hemodynamic and myocardial lesions in ischemia-reperfusion]

https://arctichealth.org/en/permalink/ahliterature98283
Source
Fiziol Zh. 2009;55(5):9-16
Publication Type
Article
Date
2009
Author
R B Strutyns'kyi
O P Neshcheret
L V Tumanovs'ka
R A Rovenets'
O O Moibenko
Source
Fiziol Zh. 2009;55(5):9-16
Date
2009
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Blood Pressure - drug effects
Cardiac Output - drug effects
Cardiotonic Agents - administration & dosage - therapeutic use
Disease Models, Animal
Dogs
Heart Rate - drug effects
Hemodynamics - drug effects
KATP Channels - metabolism
Myocardial Contraction - drug effects
Myocardial Infarction - metabolism - pathology - physiopathology - prevention & control
Myocardial Reperfusion Injury - metabolism - pathology - physiopathology - prevention & control
Myocardium - metabolism - pathology
Necrosis
Pinacidil - administration & dosage - analogs & derivatives - therapeutic use
Abstract
In experiments on anaesthetized dogs with modeling of experimental ischemia (90 min) and reperfusion (180 min) the cardioprotective influence of the preischemic activation of ATP-sensitive potassium (K(ATP)) channels by intravenous introduction of flokalin, a new fluorine-containing opener of these channels was shown. Flokalin was introduced in dose 0.1 mg/kg of animal body weight which practically did not change the parameters of hemodynamic in conditions of normoxia. Thus, the experiments performed about flokalin influence on changes of cardiohemodynamic during ischemia-reperfusion of myocardium showed certain features of ischemia-reperfusion syndrome development under conditions of K(ATP) channels activity stimulation. In our opinion, positive influence offlokalin can be explained by moderate decrease of blood pressure that decreases loading of the damaged heart and allows to preserve cardiac emission in the first period of ischemia. Also, these positive effects can be explained by prevention of the increase of coronal vessel resistance and relative preservation of myocardium contractility indexes by flokalin in the period of reperfusion. All protective properties of flokalin showed above result in diminishing of infarct size of myocardium after ischemia-reperfusion on 37% versus control experiments.
PubMed ID
20095379 View in PubMed
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[Changes of nitric oxide system during acute myocardial ischemic reperfusion]

https://arctichealth.org/en/permalink/ahliterature53904
Source
Fiziol Zh. 2000;46(6):3-11
Publication Type
Article
Date
2000
Author
O O Moibenko
M Ia Iuz'kiv
A V Kotsiuruba
O M Bukhanevych
L V Tumanovs'ka
Author Affiliation
A.A. Bogomoletz Institute of Physiology, National Academy of Science of Ukraine, Kiev.
Source
Fiziol Zh. 2000;46(6):3-11
Date
2000
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Arginine - metabolism
Disease Models, Animal
Dogs
English Abstract
Myocardial Ischemia - blood - metabolism - urine
Myocardial Reperfusion
Nitric Oxide - metabolism
Abstract
The reciprocal changes of NOS and arginase activity during acute myocardial ischaemia (90 min) and reperfusion (180 min) was shown in experiments on chest-closed dogs with spontaneous breathing. NOS activity in the ischemia injured myocardial decreased on 60% while arginase activity increased on 487%. Levels of both alternative pathways of L-arginine metabolism altered reciprocally too. NO2(-)-level was reduced on 57%, and urea level increased on 665%. The same changes were in arterial blood, started from 10 min of ischemia. These changes can play an important role for development of acute ischaemia treatment.
PubMed ID
11424561 View in PubMed
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[Coronary vascular reaction in non-ischemic myocardium during experimental acute ischemia reperfusion]

https://arctichealth.org/en/permalink/ahliterature53490
Source
Fiziol Zh. 2003;49(4):14-23
Publication Type
Article
Date
2003
Author
O O Moibenko
M Ia Iuz'kiv
V I Azarov
Author Affiliation
A.A. Bogomoletz Institute of Physioligy, Kiev.
Source
Fiziol Zh. 2003;49(4):14-23
Date
2003
Language
Ukrainian
Publication Type
Article
Keywords
Acute Disease
Animals
Coronary Circulation - physiology
Coronary Vessels - physiology
Disease Models, Animal
Dogs
Electrocardiography
English Abstract
Myocardial Reperfusion Injury - metabolism - physiopathology
Myocardium - metabolism
Nitric Oxide - antagonists & inhibitors - biosynthesis
Nitroarginine - pharmacology
Vasodilation - physiology
Abstract
The aim of this study was to investigate coronary vascular responses, particularly NO-dependent, in the non-ischemic miocardium during local acute myocardial ischemia/reperfusion. The experiments were performed on the dogs with closed chest. Occlusion of a branch of the coronary artery resulted in a dilatation of the coronary vessels within the intact part of the myocardium. Neither inhibition of prostanoid production and KATP-channels, nor administration of atropine sulfate and dissection of the vagus nerve altered coronary dilatation within the non-ischemic myocardium. Whereas inhibition of NOS by L-NNA (50 mg/kg) completely changed it after coronary occlusion, furthermore coronary resistance temporally increased. Thus, the most reliable mechanism of that response was NO-dependent.
PubMed ID
14509923 View in PubMed
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[Disorders of myocardial contractile function and the mechanisms of their compensation in ischemic heart disease in man]

https://arctichealth.org/en/permalink/ahliterature11356
Source
Fiziol Zh. 1995 Sep-Dec;41(5-6):70-9
Publication Type
Article
Author
O O Moibenko
H A Hryhorash
M V Kostylev
Source
Fiziol Zh. 1995 Sep-Dec;41(5-6):70-9
Language
Ukrainian
Publication Type
Article
Keywords
Adaptation, Physiological - drug effects
Adrenergic beta-Antagonists - therapeutic use
Adult
Aged
Comparative Study
English Abstract
Female
Heart Function Tests - drug effects
Hemodynamic Processes - drug effects - physiology
Humans
Male
Middle Aged
Myocardial Contraction - drug effects - physiology
Myocardial Ischemia - diagnosis - drug therapy - physiopathology
Propranolol - therapeutic use
Abstract
Myocardial contractile function was investigated in 84 patients with coronary diseases CD of I-IV functional classes (according to NYHA) and 17 persons with normal coronary arteries using new noninvasive method of construction LV end-systolic pressure-volume relation (ESPVR). Significant decrease of end-systolic elastance, ejection fraction, circumferential fibers shortening velocity and increase of end-systolic and end-diastolic ventricular volume was increased with patient's class number. These data correlated with the increase of total amount of lesion of coronary vessels and extension of asynergic zones. But this contractile function disturbances were not accompanied by significant changes of cardiac output and arterial pressure. When blocking beta-adrenergic receptors with anaprillin it was established that at early stages of CD the compensation of contractile function disturbances is reached via the increasing of heart adrenergic stimulation, and in the patients of III-IV classes the Frank-Starling's law becomes of great significance homo- and heterometric mechanisms efficiency reduces with CD development. These data show that ESPVR reconstruction before and after the blocking of beta-adrenergic receptors allows systolic LV function and efficiency of its regulation to be estimated.
PubMed ID
9026397 View in PubMed
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[Effect of heme oxygenase-1 expression and activity on the heart function in ischemia-reperfusion]

https://arctichealth.org/en/permalink/ahliterature53023
Source
Fiziol Zh. 2006;52(1):41-8
Publication Type
Article
Date
2006
Author
T V Kukoba
A V Kotsiuruba
O O Moibenko
Source
Fiziol Zh. 2006;52(1):41-8
Date
2006
Language
Ukrainian
Publication Type
Article
Keywords
Animals
Coronary Circulation - physiology
English Abstract
Heart - physiopathology
Heme Oxygenase (Decyclizing) - biosynthesis - metabolism
In Vitro
Male
Myocardial Ischemia - complications - metabolism - physiopathology
Myocardial Reperfusion Injury - etiology - metabolism - physiopathology
Rats
Ventricular Function - physiology
Ventricular Function, Left - physiology
Ventricular Function, Right - physiology
Abstract
The purpose of this study was to determine the protective effects of heme oxygenase-1 (HO-1) expression against postischemic myocardial dysfunction. We also investigated HO-1 expression in cardiac tissue from the left and right ventricles of myocardium. Rat hearts were isolated and perfused according to Langendorff technique to evaluate the recovery of myocardial function after 20 min of global ischemia and 40 min of reperfusion. We found that HO-1 expression was more expressed in left ventricles of myocardium in basic conditions and after ischemia/reperfusion as well as after its previous induction by hemin. Upregulation of the inducible isoform of HO-1 and increase its activity after treatment of animals with hemin 24 h before ischemia ameliorated myocardial function (raised left ventricular developed pressure, decreased end-diastolic pressure, attenuated vasoconstriction) and reduced oxydative stress in cardiac tissue during reperfusion of isolated hearts. Zinc protoporphyrin IX, an inhibitor of heme oxygenase activity, completely abolished the HO-1 expression in left ventricles of myocardium and increased postischemic myocardial dysfunction. Likewise, cardiac tissue injury was exacerbated by treatment with zinc protoporphyrin IX through significant inhibition of HO activity and increasing of hydroxyl radical production on reperfusion. The treatment of animals with hemin and following ischemia/reperfusion resulted in 5-6-times increase of HO-1 expression in the left ventricle of myocardium whereas in right ventricle only in 3-times. Our data provide strong evidence for a primary role of HO-1 in cardioprotection against reperfusion injury and show different HO-1 expression in left and right ventricles of myocardium.
PubMed ID
16553297 View in PubMed
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23 records – page 1 of 3.