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24 records – page 1 of 3.

[Adaptation of the myocardium to decreased coronary flow]

https://arctichealth.org/en/permalink/ahliterature54934
Source
Duodecim. 1994;110(8):777-9
Publication Type
Article
Date
1994
Author
K. Ylitalo
K. Peuhkurinen
Author Affiliation
Sisätautien klinikka, Oulu.
Source
Duodecim. 1994;110(8):777-9
Date
1994
Language
Finnish
Publication Type
Article
Keywords
Humans
Myocardial Ischemia - diagnosis - physiopathology
Myocardial Stunning
Myocardium - metabolism - pathology
Necrosis
PubMed ID
8586035 View in PubMed
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Aging influences multiple indices of oxidative stress in the heart of the Fischer 344/NNia x Brown Norway/BiNia rat.

https://arctichealth.org/en/permalink/ahliterature83665
Source
Redox Rep. 2007;12(4):167-80
Publication Type
Article
Date
2007
Author
Asano Shinichi
Rice Kevin M
Kakarla Sunil
Katta Anjaiah
Desai Devashish H
Walker Ernest M
Wehner Paulette
Blough Eric R
Author Affiliation
Department of Biological Sciences, Marshall University, Huntington, West Virginia 25755-1090, USA.
Source
Redox Rep. 2007;12(4):167-80
Date
2007
Language
English
Publication Type
Article
Keywords
Aging - physiology
Aldehydes - metabolism
Analysis of Variance
Animals
Blood Pressure - physiology
Female
Heart - physiopathology
Heat-Shock Proteins - metabolism
Immunoblotting
Immunohistochemistry
Male
Microscopy, Fluorescence
Mitogen-Activated Protein Kinases - metabolism
Myocardium - metabolism - pathology
Oxidative Stress
Phosphorylation
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Inbred BN
Rats, Inbred F344
Reactive Oxygen Species - metabolism
Regression Analysis
Signal Transduction - physiology
Superoxides - metabolism
Tyrosine - analogs & derivatives - metabolism
Abstract
We report the influence of aging on multiple markers of oxidative-nitrosative stress in the heart of adult (6-month), aged (30-month) and very aged (36-month) Fischer 344/NNiaHSd x Brown Norway/BiNia (F344/NXBN) rats. Compared to adult (6-month) hearts, indices of oxidative (superoxide anion [O2*-], 4-hydroxy-2-nonenal [4-HNE]) and nitrosative (protein nitrotyrosylation) stress were 34.1 +/- 28.1%, 186 +/- 28.1% and 94 +/- 5.8% higher, respectively, in 36-month hearts and these findings were highly correlated with increases in left ventricular wall thickness (r > 0.669; r > 0.710 and P
PubMed ID
17705987 View in PubMed
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[Anti-arrhythmic effect of the sigma-receptor blocker DuP 734 in ischemia and myocardial reperfusion]

https://arctichealth.org/en/permalink/ahliterature53976
Source
Eksp Klin Farmakol. 2000 Nov-Dec;63(6):24-7
Publication Type
Article
Author
Iu B Lishmanov
L N Maslov
A V Krylatov
S A Afanas'ev
V Iu Timofeev
P. Gilligan
S V Tam
Author Affiliation
Laboratory of Experimental Cardiology, Institute of Cardiology, Tomsk Scientific Center, Siberian Division, Russian Academy of Medical Sciences, ul. Shevchenko 24, Tomsk, 634050 Russia.
Source
Eksp Klin Farmakol. 2000 Nov-Dec;63(6):24-7
Language
Russian
Publication Type
Article
Keywords
Action Potentials
Animals
Anti-Arrhythmia Agents - pharmacology
Arrhythmia - etiology - physiopathology - prevention & control
Arterial Occlusive Diseases - complications
Coronary Disease - complications
Electrocardiography
English Abstract
In Vitro
Microelectrodes
Myocardial Infarction - etiology - pathology
Myocardial Reperfusion Injury - etiology - physiopathology - prevention & control
Myocardium - metabolism - pathology
Narcotic Antagonists - pharmacology
Piperidines - pharmacology
Rats
Rats, Wistar
Receptors, sigma - antagonists & inhibitors - metabolism
Sclerosis - prevention & control
Abstract
It has been found that in vivo pretreatment of rats with the sigma receptor antagonist DuP 734 (1 mg/kg) resulted in an increase in the heart tolerance to ischemic and reperfusion arrhythmias both in vivo and ex vivo. Administration of DuP 734 (1 mg/liter) directly in the perfusion solution of isolated rat heart 10 min before total ischemia also promoted a decrease in the incidence of reperfusion arrhythmias. The normoxic perfusion of isolated rat heart at a dose of 1 mg/liter had no effect on the action potential. It was concluded that antiarrhythmic effect of DuP 734 might depend on the decrease in the Ca2+ overload but not on K+ and Na+ channel blockade.
PubMed ID
11202505 View in PubMed
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[Cardioprotective action of coenzyme Q in conditions of its endogenous synthesis activation in cardiac ischemia-reperfusion in old rats]

https://arctichealth.org/en/permalink/ahliterature98841
Source
Fiziol Zh. 2009;55(4):58-63
Publication Type
Article
Date
2009
Author
S V Timoshchuk
H L Vavilova
N A Strutyns'ka
S A Talanov
D M Petukhov
O B Kuchmenko
H V Donchenko
V F Sahach
Source
Fiziol Zh. 2009;55(4):58-63
Date
2009
Language
Ukrainian
Publication Type
Article
Keywords
Aging - drug effects - metabolism - pathology
Animals
Cardiotonic Agents - pharmacology
Coronary Circulation - drug effects
Heart - drug effects
Heart Function Tests
Male
Methionine - pharmacology
Myocardial Reperfusion
Myocardial Reperfusion Injury - metabolism - pathology - prevention & control
Myocardium - metabolism - pathology
Parabens - pharmacology
Rats
Rats, Wistar
Ubiquinone - biosynthesis - physiology
alpha-Tocopherol - pharmacology
Abstract
The changes of functional state isolated by Lanhendorf old rat hearts with low content of ubiqinone--coenzyme Q (CoQ) under activation of it endogenous synthesis through administration of precursors--4-hydroxybenzoic acid, methionine and modulator vitamin E were studied. The activation of ubiqinone biosynthesis contribute to cardioprotective effect due to reduce the degree of the ischemia-reperfusion injury in old rat heart, namely the restoration of myocardial contractile function and coronary flow as well as decrease the end diastolic pressure and oxygen cost of the heart compared with control group of the animals during ischemia-reperfusion. Thus the results allow to conclude that the activation of KoQ biosynthesis under administration of it precursors has protective effect in the development of the heart postreperfusion damages in aging.
PubMed ID
19827631 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 in the rhythmoinotropic dependence of the myocardium in rats with postinfarction cardiosclerosis after beta1-adrenoreceptor blocking.

https://arctichealth.org/en/permalink/ahliterature95217
Source
Bull Exp Biol Med. 2009 Mar;147(3):371-4
Publication Type
Article
Date
Mar-2009
Author
Kondratyeva D S
Afanasyev S A
Ligacheva N A
Popov S V
Krivolapov S N
Author Affiliation
Institute of Cardiology, Tomsk Research Center, Siberian Division of the Russian Academy of Medical Sciences, Russia. dina@cardio.tsu.ru
Source
Bull Exp Biol Med. 2009 Mar;147(3):371-4
Date
Mar-2009
Language
English
Publication Type
Article
Keywords
Adrenergic beta-Antagonists - pharmacology
Animals
Bisoprolol - pharmacology
Calcium - metabolism
Heart Ventricles - pathology
Male
Myocardial Infarction - complications
Myocardium - metabolism - pathology
Myocytes, Cardiac - drug effects - metabolism
Papillary Muscles - drug effects - metabolism
Rats
Rats, Wistar
Sarcoplasmic Reticulum - drug effects - metabolism
Abstract
The rhythmoinotropic dependence of the papillary muscles was studied in rats with postinfarction cardiosclerosis after blocking of beta(1)-adrenoreceptors by concor (7 mg/kg daily). The development of postinfarction cardiosclerosis led to a reduction of the postextrasystolic potentiation and of potentiation induced by periods of rest. Preliminary blocking of beta(1)-adrenoreceptors stimulated the postextrasystolic contractions and contractions after periods of rest in the myocardium of rats with postinfarction cardiosclerosis. These results suggest that blocking of beta(1)-adrenoreceptors promotes an improvement of calcium-accumulating function of the cardiomyocyte sarcoplasmatic reticulum in the myocardium of rats with postinfarction cardiosclerosis.
PubMed ID
19529864 View in PubMed
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Differential protein expression during aging in ventricular myocardium of Fischer 344 x Brown Norway hybrid rats.

https://arctichealth.org/en/permalink/ahliterature92622
Source
Exp Gerontol. 2008 Oct;43(10):909-18
Publication Type
Article
Date
Oct-2008
Author
Richardson M R
Lai X.
Mason S B
Miller S J
Witzmann F A
Author Affiliation
Department of Cellular & Integrative Physiology, Indiana University School of Medicine, Biotechnology Research & Training Center, Indianapolis, IN 46202, USA.
Source
Exp Gerontol. 2008 Oct;43(10):909-18
Date
Oct-2008
Language
English
Publication Type
Article
Keywords
Aging - genetics - physiology
Animals
Apoptosis - genetics - physiology
Fibrosis
Gene Expression - genetics
Heart Valve Diseases - pathology - physiopathology
Heart Ventricles - pathology - physiopathology
Myocardium - metabolism - pathology
Rats
Rats, Inbred BN
Abstract
The aging heart undergoes well characterized structural changes associated with functional decline, though the underlying mechanisms are not understood. The aim of this study was to determine to what extent ventricular myocardial protein expression was altered with age and which proteins underwent protein nitration. Fischer 344 x Brown Norway F1 hybrid (FBN) rats of four age groups were used, 4, 12, 24, and 34 months. Differential protein expression was determined by 2-DE and proteins were identified by peptide mass fingerprinting. Altered protein nitration with age was assessed by immunoblotting. Over 1000 protein spots per sample were detected, and 255 were found to be differentially expressed when all aged groups were compared to young rats (4 months) (p0.05). A strong positive correlation between differential protein expression and increasing age (p=0.03, R(2)=0.997) indicated a progressive, rather than abrupt, change with age. Of 46 differentially expressed proteins identified, seventeen have roles in apoptosis, ten in hypertrophy, seven in fibrosis, and three in diastolic dysfunction, aging-associated processes previously reported in both human and FBN rat heart. Protein expression alterations detected here could have beneficial effects on cardiac function; thus, our data indicate a largely adaptive change in protein expression during aging. In contrast, differential protein nitration increased abruptly, rather than progressively, at 24 months of age. Altogether, the results suggest that differential myocardial protein expression occurs in a progressive manner during aging, and that a proteomic-based approach is an effective method for the identification of potential therapeutic targets to mitigate aging-related myocardial dysfunction.
PubMed ID
18682286 View in PubMed
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Effect of in vivo and in vitro stimulation of delta1-opioid receptors on myocardial resistance to arrhythmogenic action of ischemia and reperfusion.

https://arctichealth.org/en/permalink/ahliterature53619
Source
Bull Exp Biol Med. 2002 Oct;134(4):359-62
Publication Type
Article
Date
Oct-2002
Author
T V Lasukova
A V Krylatov
L N Maslov
Yu B Lishmanov
G J Gross
G B Stefano
Author Affiliation
Laboratory of Experimental Cardiology, Institute of Cardiology, Tomsk Research Center, Siberian Division of the Russian Academy of Medical Sciences, Russia.
Source
Bull Exp Biol Med. 2002 Oct;134(4):359-62
Date
Oct-2002
Language
English
Publication Type
Article
Keywords
Animals
Anti-Arrhythmia Agents - pharmacology
Arrhythmia - etiology - metabolism - physiopathology - prevention & control
Comparative Study
Dose-Response Relationship, Drug
Enkephalin, D-Penicillamine (2,5)- - pharmacology
Enkephalin, Leucine - analogs & derivatives - pharmacology
In Vitro
Myocardial Ischemia - complications - metabolism
Myocardial Reperfusion Injury - etiology - prevention & control
Myocardium - metabolism - pathology
Narcotic Antagonists - pharmacology
Oligopeptides - pharmacology
Rats
Rats, Wistar
Receptors, Opioid, delta - agonists - metabolism
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Abstract
Preliminary intravenous injection of peptide agonist of delta1-opioid receptors DPDPE (0.5 mg/kg) decreased the incidence of occlusion (10 min) and reperfusion (10 min) arrhythmias in rats. By contrast, delta2-opioid receptor agonist DSLET produced no effect on the incidence of arrhythmias provoked by coronary occlusion and reperfusion. Preliminary injection of selective delta-receptor antagonist ICI 174,864 (2.5 mg/kg) or TIPP[y] (0.5 mg/kg) completely abolished the antiarrhythmic effect of DPDPE. Stimulation of cardiac delta1-opioid receptors with DPDPE added to perfusion saline in concentrations of 0.1 and 0.5 mg/liter decreased the incidence of reperfusion arrhythmias. Addition of DPDPE to perfusion saline in a concentration of 0.1 mg/liter prevented reoxygenation destruction of cardiomyocytes. By contrast, no cardioprotective effect of this peptide was observed at a concentration of 0.5 mg/liter in perfusion saline or when it was injected intravenously. It is concluded that the cardioprotective and antiarrhythmic effects of DPDPE are caused by activation of cardiac delta1-opioid receptors.
PubMed ID
12533759 View in PubMed
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Effect of ischemic postconditioning on infarct size in patients with ST-elevation myocardial infarction treated by primary PCI results of the POSTEMI (POstconditioning in ST-Elevation Myocardial Infarction) randomized trial.

https://arctichealth.org/en/permalink/ahliterature258278
Source
J Am Heart Assoc. 2014;3(2):e000679
Publication Type
Article
Date
2014
Author
Shanmuganathan Limalanathan
Geir Ø Andersen
Nils-Einar Kløw
Michael Abdelnoor
Pavel Hoffmann
Jan Eritsland
Author Affiliation
Center for Heart Failure Research, University of Oslo, Oslo, Norway.
Source
J Am Heart Assoc. 2014;3(2):e000679
Date
2014
Language
English
Publication Type
Article
Keywords
Aged
Balloon Occlusion
Biological Markers - blood
Coronary Circulation
Female
Humans
Ischemic Postconditioning - methods
Linear Models
Magnetic Resonance Imaging
Male
Middle Aged
Multivariate Analysis
Myocardial Infarction - blood - diagnosis - physiopathology - therapy
Myocardium - metabolism - pathology
Necrosis
Norway
Percutaneous Coronary Intervention - adverse effects - instrumentation
Prospective Studies
Risk factors
Stents
Stroke Volume
Time Factors
Treatment Outcome
Troponin T - blood
Ventricular Function, Left
Abstract
Reduction of infarct size by ischemic postconditioning (IPost) has been reported in smaller proof-of-concept clinical studies, but has not been confirmed in other smaller studies. The principle needs to be evaluated in larger groups of ST-elevation myocardial infarction (STEMI) patients before being implemented in clinical practice. This study assessed the effect of ischemic postcoditioning (IPost) on infarct size in patients with STEMI treated by primary percutaneous coronary intervention (PCI).
Patients with first-time STEMI,
Notes
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PubMed ID
24760962 View in PubMed
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24 records – page 1 of 3.