Skip header and navigation

Refine By

186 records – page 1 of 19.

ABC of nutrition. Reducing the risk of coronary heart disease.

https://arctichealth.org/en/permalink/ahliterature238564
Source
Br Med J (Clin Res Ed). 1985 Jul 6;291(6487):34-7
Publication Type
Article
Date
Jul-6-1985
Author
A S Truswell
Source
Br Med J (Clin Res Ed). 1985 Jul 6;291(6487):34-7
Date
Jul-6-1985
Language
English
Publication Type
Article
Keywords
Arteriosclerosis - diet therapy - etiology
Cholesterol, Dietary - adverse effects
Coronary Disease - diet therapy - epidemiology - prevention & control
Diet
Finland
Humans
Magnesium - metabolism
Myocardium - metabolism
Potassium - metabolism
Risk
Smoking
Thrombosis - diet therapy
Notes
Cites: Am J Clin Nutr. 1979 Nov;32(11):2193-7495535
Cites: J Neurol Neurosurg Psychiatry. 1985 Feb;48(2):97-1003884742
Cites: Br Med J (Clin Res Ed). 1984 Sep 1;289(6444):509-106432164
Cites: Lancet. 1983 Dec 24-31;2(8365-66):1457-96140548
PubMed ID
3926055 View in PubMed
Less detail

Acetate-induced changes in cardiac energy metabolism and hemodynamics in the rat.

https://arctichealth.org/en/permalink/ahliterature12462
Source
Basic Res Cardiol. 1988 Jul-Aug;83(4):431-44
Publication Type
Article
Author
K T Kiviluoma
M. Karhunen
T. Lapinlampi
K J Peuhkurinen
I E Hassinen
Author Affiliation
Department of Medical Biochemistry, University of Oulu, Finland.
Source
Basic Res Cardiol. 1988 Jul-Aug;83(4):431-44
Language
English
Publication Type
Article
Keywords
Acetic Acid
Acetic Acids - pharmacology
Adenosine - metabolism
Animals
Cardiac Output - drug effects
Epinephrine - blood
Heart - drug effects - physiology
Heart Rate - drug effects
Hemodynamic Processes
In Vitro
Myocardium - metabolism
Oxygen Consumption - drug effects
Phosphorylation
Rats
Rats, Inbred Strains
Time Factors
Abstract
The hemodynamic and metabolic effects of acetate were studied in rats in vivo and in the isolated perfused heart. Hemodynamic parameters, myocardial phosphagens, inorganic phosphate, and adenosine were measured in vivo. Acetate uptake, coronary flow, O2 consumption, parameters of the cellular energy state, and hypoxanthine compounds and their washout were measured in heart perfusion experiments. Heart rate (HR), cardiac output, and the peak derivative of the left ventricular pressure rise (dP/dtmax) increased significantly during acetate infusion in vivo, but mean arterial pressure, systolic arterial pressure, and systemic vascular resistance decreased. Heart muscle ATP concentrations decreased after 7 min of acetate infusion. In vivo cardiac work load (HR.(peak left ventricular pressure] showed a positive correlation with tissue adenosine concentration and a negative correlation with phosphorylation potential. Acetate uptake in the perfused hearts was about 2.5 mumol/min per gram wet weight. Acetate perfusion increased O2 consumption and coronary flow concomitantly with a decrease in tissue ATP concentration. Tissue AMP and perfusate effluent adenosine concentration and adenosine output increased significantly, perfusate adenosine showing a non-linear positive correlation with coronary flow. The results demonstrate that acetate induces considerable changes in hemodynamics and metabolism in the heart.
PubMed ID
3190660 View in PubMed
Less detail

Activation of oxygen-responsive pathways is associated with altered protein metabolism in Arctic char exposed to hypoxia.

https://arctichealth.org/en/permalink/ahliterature308255
Source
J Exp Biol. 2019 11 21; 222(Pt 22):
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
11-21-2019
Author
Alicia A Cassidy
Simon G Lamarre
Author Affiliation
Département de Biologie, Université de Moncton, Moncton, NB, Canada, E1A 3E9 alicia.cassidy@dfo-mpo.gc.ca.
Source
J Exp Biol. 2019 11 21; 222(Pt 22):
Date
11-21-2019
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Animals
Autophagy
Basic Helix-Loop-Helix Transcription Factors - metabolism
Hypoxia - metabolism
Myocardium - metabolism
Oxygen - metabolism
Protein Biosynthesis - physiology
Proteolysis
Signal Transduction
TOR Serine-Threonine Kinases - metabolism
Trout - metabolism
Unfolded Protein Response - physiology
Abstract
Fish exposed to fluctuating oxygen concentrations often alter their metabolism and/or behaviour to survive. Hypoxia tolerance is typically associated with the ability to reduce energy demand by supressing metabolic processes such as protein synthesis. Arctic char is amongst the most sensitive salmonid to hypoxia, and typically engage in avoidance behaviour when faced with lack of oxygen. We hypothesized that a sensitive species will still have the ability (albeit reduced) to regulate molecular mechanisms during hypoxia. We investigated the tissue-specific response of protein metabolism during hypoxia. Little is known about protein degradation pathways during hypoxia in fish and we predict that protein degradation pathways are differentially regulated and play a role in the hypoxia response. We also studied the regulation of oxygen-responsive cellular signalling pathways [hypoxia inducible factor (HIF), unfolded protein response (UPR) and mTOR pathways] since most of what we know comes from studies on cancerous mammalian cell lines. Arctic char were exposed to cumulative graded hypoxia trials for 3 h at four air saturation levels (100%, 50%, 30% and 15%). The rate of protein synthesis was measured using a flooding dose technique, whereas protein degradation and signalling pathways were assessed by measuring transcripts and phosphorylation of target proteins. Protein synthesis decreased in all tissues measured (liver, muscle, gill, digestive system) except for the heart. Salmonid hearts have preferential access to oxygen through a well-developed coronary artery, therefore the heart is likely to be the last tissue to become hypoxic. Autophagy markers were upregulated in the liver, whereas protein degradation markers were downregulated in the heart during hypoxia. Further work is needed to determine the effects of a decrease in protein degradation on a hypoxic salmonid heart. Our study showed that protein metabolism in Arctic char is altered in a tissue-specific fashion during graded hypoxia, which is in accordance with the responses of the three major hypoxia-sensitive pathways (HIF, UPR and mTOR). The activation pattern of these pathways and the cellular processes that are under their control varies greatly among tissues, sometimes even going in the opposite direction. This study provides new insights on the effects of hypoxia on protein metabolism. Adjustment of these cellular processes is likely to contribute to shifting the fish phenotype into a more hypoxia-tolerant one, if more than one hypoxia event were to occur. Our results warrant studying these adjustments in fish exposed to long-term and diel cycling hypoxia.
PubMed ID
31704904 View in PubMed
Less detail

Activation of peripheral delta2 opioid receptors increases cardiac tolerance to ischemia/reperfusion injury Involvement of protein kinase C, NO-synthase, KATP channels and the autonomic nervous system.

https://arctichealth.org/en/permalink/ahliterature89863
Source
Life Sci. 2009 May 8;84(19-20):657-63
Publication Type
Article
Date
May-8-2009
Author
Maslov Leonid N
Lishmanov Yury B
Oeltgen Peter R
Barzakh Eva I
Krylatov Andrey V
Govindaswami Meera
Brown Stephen A
Author Affiliation
Laboratory of Experimental Cardiology, Research Institute of Cardiology, Siberian Branch, Russian Academy of Medical Sciences, Tomsk, Russia. :maslov@cardio.tsu.ru
Source
Life Sci. 2009 May 8;84(19-20):657-63
Date
May-8-2009
Language
English
Publication Type
Article
Keywords
Animals
Anti-Arrhythmia Agents - metabolism
Arrhythmias, Cardiac - metabolism
Autonomic Nervous System - metabolism
Benzophenanthridines - metabolism
Cardiotonic Agents - metabolism
Decanoic Acids - metabolism
Glyburide - metabolism
Hydroxy Acids - metabolism
Hypoglycemic Agents - metabolism
KATP Channels - metabolism
Male
Myocardial Reperfusion Injury - metabolism - pathology
Myocardium - metabolism
Nitric Oxide Synthase - metabolism
Oligopeptides - metabolism
Protein Kinase C - metabolism
Rats
Rats, Wistar
Receptors, Opioid, delta - antagonists & inhibitors - metabolism
Abstract
AIMS: This study aims to investigate the role of peripheral delta(2) opioid receptors in cardiac tolerance to ischemia/reperfusion injury and to examine the contribution of PKC, TK, K(ATP) channels and the autonomic nervous system in delta(2) cardioprotection. MAIN METHODS: Deltorphin II and various inhibitors were administered in vivo prior to coronary artery occlusion and reperfusion in a rat model. The animals were monitored for the development of arrhythmias, infarct development and the effects of selected inhibitors. KEY FINDINGS: Pretreatment with peripheral and delta(2) specific opioid receptor (OR) antagonists completely abolished the cardioprotective effects of deltorphin II. In contrast, the selective delta(1) OR antagonist 7-benzylidenenaltrexone (BNTX) had no effect. The protein kinase C (PKC) inhibitor chelerythrine and the NO-synthase inhibitor L-NAME (N-nitro-L-arginine methyl ester) also reversed both deltorphin II effects. The nonselective ATP-sensitive K+ (K(ATP)) channel inhibitor glibenclamide and the selective mitochondrial K(ATP) channel inhibitor 5-hydroxydecanoic acid only abolished the infarct-sparing effect of deltorphin II. Inhibition of tyrosine kinase (TK) with genistein, the ganglion blocker hexamethonium and the depletion of endogenous catecholamine storage with guanethidine reversed the antiarrhythmic action of deltorphin II but did not change its infarct-sparing action. SIGNIFICANCE: The cardioprotective mechanism of deltorphin II is mediated via stimulation of peripheral delta(2) opioid receptors. PKC and NOS are involved in both its infarct-sparing and antiarrhythmic effects. Infarct-sparing is dependent upon mitochondrial K(ATP) channel activation while the antiarrhythmic effect is dependent upon TK activation. Endogenous catecholamine depletion reduced antiarrhythmic effects but did not alter the infarct-sparing effect of deltorphin II.
PubMed ID
19245818 View in PubMed
Less detail

[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
Less detail

Adaptive or maladaptive response to adenoviral adrenomedullin gene transfer is context-dependent in the heart.

https://arctichealth.org/en/permalink/ahliterature92802
Source
J Gene Med. 2008 Aug;10(8):867-77
Publication Type
Article
Date
Aug-2008
Author
Leskinen Hanna
Rauma-Pinola Tanja
Szokodi István
Kerkelä Risto
Pikkarainen Sampsa
Uusimaa Paavo
Hautala Timo
Vuolteenaho Olli
Ruskoaho Heikki
Author Affiliation
Institute of Biomedicine, Department of Pharmacology and Toxicology, Biocentre Oulu, University of Oulu, Oulu, Finland.
Source
J Gene Med. 2008 Aug;10(8):867-77
Date
Aug-2008
Language
English
Publication Type
Article
Keywords
Adenoviridae - drug effects
Adrenomedullin - metabolism - pharmacology
Animals
Gene Transfer Techniques
Heart - drug effects - physiology - physiopathology
Heart Ventricles - drug effects
Hypertrophy, Left Ventricular - metabolism - physiopathology
Male
Myocardial Infarction - physiopathology
Myocardium - metabolism
RNA, Messenger - metabolism
Rats
Rats, Sprague-Dawley
Systole - drug effects
Ventricular Function, Left - drug effects
Abstract
BACKGROUND: Adrenomedullin (AM) is a potent vasodilator and natriuretic peptide produced in the heart, but controversy persists regarding its cardiac effects. We explored the potential role of AM on cardiac function and remodeling by direct recombinant adenoviral AM gene delivery into the anterior wall of the left ventricle (LV). METHODS: AM was overexpressed in healthy rat hearts and in hearts during the remodeling process in response to pressure overload and myocardial infarction. The AM effects were analysed with echocardiography and in an isolated perfused rat heart preparation. The expression of AM and the activation of underlying signaling pathways were also investigated. RESULTS: AM mRNA increased by 20.9-fold (p
PubMed ID
18615773 View in PubMed
Less detail

Adrenomedullin gene expression in the rat heart is stimulated by acute pressure overload: blunted effect in experimental hypertension.

https://arctichealth.org/en/permalink/ahliterature54511
Source
Endocrinology. 1997 Jun;138(6):2636-9
Publication Type
Article
Date
Jun-1997
Author
H. Romppanen
M. Marttila
J. Magga
O. Vuolteenaho
P. Kinnunen
I. Szokodi
H. Ruskoaho
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Endocrinology. 1997 Jun;138(6):2636-9
Date
Jun-1997
Language
English
Publication Type
Article
Keywords
Animals
Argipressin - pharmacology
Atrial Natriuretic Factor - biosynthesis
Blood Pressure - drug effects
Heart - physiology - physiopathology
Heart Failure, Congestive - metabolism
Heart Ventricles
Humans
Hypertension - metabolism - physiopathology
Male
Myocardium - metabolism
Natriuretic Peptide, Brain
Peptide Biosynthesis
Peptides
RNA, Messenger - biosynthesis
Rats
Rats, Inbred Strains
Rats, Sprague-Dawley
Research Support, Non-U.S. Gov't
Time Factors
Transcription, Genetic - drug effects
Abstract
The levels of adrenomedullin (ADM), a newly discovered vasodilating and natriuretic peptide, are elevated in plasma and ventricular myocardium in human congestive heart failure suggesting that cardiac synthesis may contribute to the plasma concentrations of ADM. To examine the time course of induction and mechanisms regulating cardiac ADM gene expression, we determined the effect of acute and short-term cardiac overload on ventricular ADM mRNA and immunoreactive ADM (ir-ADM) levels in conscious rats. Acute pressure overload was produced by infusion of arginine8-vasopressin (AVP, 0.05 microg/kg/min, i.v.) for 2 h into 12-week-old hypertensive TGR(mREN-2)27 rats and normotensive Sprague-Dawley (SD) rats. Hypertension and marked left ventricular hypertrophy were associated with 2.2-times higher ir-ADM levels in the left ventricular epicardial layer (178 +/- 36 vs. 81 +/- 23 fmol/g, P
PubMed ID
9165059 View in PubMed
Less detail

Age-dependent differences in the stimulation of lipid peroxidation in the heart of rats during immobilization stress.

https://arctichealth.org/en/permalink/ahliterature9705
Source
Exp Gerontol. 2003 Jun;38(6):693-8
Publication Type
Article
Date
Jun-2003
Author
Vadim V Davydov
Vladimir N Shvets
Author Affiliation
Laboratory of Biochemistry and Endocrinology of Aging, Institute of Children and Adolescent Health Protection, Academy of Medical Science, 50-Let VLKSM av., 52A, 61153, Kharkov, Ukraine. dav@nord.vostok.net
Source
Exp Gerontol. 2003 Jun;38(6):693-8
Date
Jun-2003
Language
English
Publication Type
Article
Keywords
Aging - metabolism
Animals
Catalase - metabolism
Chemiluminescent Measurements
Epinephrine - blood
Lipid Peroxidation
Male
Myocardium - metabolism
Rats
Rats, Wistar
Restraint, Physical
Stress - metabolism
Subcellular Fractions - enzymology
Superoxide Dismutase - metabolism
Abstract
In order to investigate the possible reasons for age-related decrease in myocardium resistance to stress, we carried out a study of lipid peroxidation (LPO) stimulation features in the myocardium of adult (10-12 months) and aged (22-25 months) male Wistar rats during immobilization stress. In our studies of ascorbate-dependent LPO and induced chemiluminescence, we found that immobilization stress is accompanied by decreased efficiency in the induction of free radical processes in the heart of aged rats. An important cause of this phenomenon may be age-dependent changes in the catalytical properties of the cytosolic superoxide dismutase. The pathophysiological consequences of stress-related, age-dependent decreased efficiency of induction of free radical processes in the heart are discussed.
PubMed ID
12814805 View in PubMed
Less detail

Aged rat myocardium exhibits normal adenosine receptor-mediated bradycardia and coronary vasodilation but increased adenosine agonist-mediated cardioprotection.

https://arctichealth.org/en/permalink/ahliterature53062
Source
J Gerontol A Biol Sci Med Sci. 2005 Nov;60(11):1399-404
Publication Type
Article
Date
Nov-2005
Author
Gentian Kristo
Yukihiro Yoshimura
Byron J Keith
Robert M Mentzer
Robert D Lasley
Author Affiliation
Department of Surgery, University of Kentucky College of Medicine, 800 Rose Street, Lexington, KY 40536-0298, USA.
Source
J Gerontol A Biol Sci Med Sci. 2005 Nov;60(11):1399-404
Date
Nov-2005
Language
English
Publication Type
Article
Keywords
Aging - physiology
Animals
Bradycardia - physiopathology
Cardiotonic Agents - pharmacology
Heart - physiopathology
Imidazoles - pharmacology
In Vitro
Male
Myocardial Infarction - physiopathology
Myocardium - metabolism
Pyridines - pharmacology
Rats
Rats, Inbred F344
Receptors, Purinergic P1 - agonists - physiology
Research Support, N.I.H., Extramural
Vasodilation - physiology
Abstract
The purpose of this study was to determine whether aged myocardium exhibits decreased responsiveness to adenosine A1 and A(2a) receptor activation. Studies were conducted in adult (4-6 months) and aged (24-26 months) Fischer 344 x Brown Norway hybrid (F344 x BN) rats. Effects of the adenosine A1/A(2a) agonist AMP579 were measured in isolated hearts and in rats submitted to in vivo regional myocardial ischemia. Aged isolated hearts exhibited lower spontaneous heart rates and higher coronary resistance, as well as normal A1- and A(2a)-mediated responses. There was no difference in control infarct size between adult and aged rats; however, AMP579 treatment resulted in a 50% greater infarct size reduction in aged rats (18 +/- 4% of risk area) compared to adult rats (37 +/- 3%). These findings suggest that adenosine A1 and A(2a) receptor-mediated effects are not diminished in normal aged myocardium, and that aged hearts exhibit increased adenosine agonist-induced infarct reduction.
PubMed ID
16339325 View in PubMed
Less detail

186 records – page 1 of 19.