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427 records – page 1 of 43.

5-HT(1A) receptor antagonist p-MPPI attenuates acute ethanol effects in mice and rats.

https://arctichealth.org/en/permalink/ahliterature9998
Source
Neurosci Lett. 2002 Mar 29;322(1):1-4
Publication Type
Article
Date
Mar-29-2002
Author
Nina K Popova
Elena A Ivanova
Author Affiliation
Institute of Cytology and Genetics, Siberian Branch of Russian Academy of Sciences, Lavrentyeva 10, 630090 Novosibirsk, Russia. npopova@bionet.nsc.ru
Source
Neurosci Lett. 2002 Mar 29;322(1):1-4
Date
Mar-29-2002
Language
English
Publication Type
Article
Keywords
Acute Disease
Alcohol-Induced Disorders, Nervous System - drug therapy - metabolism - physiopathology
Aminopyridines - pharmacology
Animals
Brain - drug effects - metabolism - physiopathology
Dose-Response Relationship, Drug
Drug Interactions - physiology
Drug Tolerance - physiology
Ethanol - pharmacology
Hypothermia - chemically induced - drug therapy - physiopathology
Male
Mice
Mice, Inbred C3H
Neurons - drug effects - metabolism
Piperazines - pharmacology
Rats
Rats, Wistar
Receptors, Serotonin - drug effects - metabolism
Receptors, Serotonin, 5-HT1
Research Support, Non-U.S. Gov't
Serotonin - metabolism
Serotonin Antagonists - pharmacology
Sleep - drug effects - physiology
Startle Reaction - drug effects - physiology
Abstract
The effect of a selective 5-HT(1A) antagonist, 4-(2'-methoxy-)phenyl-1-[2'-(N-2"-pyridinyl)-p-iodobenzamino-]ethyl-piperazine (p-MPPI), on acute ethanol-induced hypothermia, sleep and suppression of acoustic startle reflex in C3H/He mice and Wistar rats was studied. Administration of p-MPPI at the doses of 0.4, 0.7 and 1.0 mg/kg reduced in a dose-dependent manner the ethanol-induced hypothermia and the sleep time and attenuated the ethanol-induced decrease of acoustic startle reflex magnitude in mice. Similar p-MPPI (0.4 mg/kg) effects on ethanol-induced sleep and hypothermia were obtained in rats. It was concluded that 5-HT(1A) receptors were involved in the mechanisms of the ethanol-induced hypothermia and sleep, and that 5-HT(1A) antagonist increased acute ethanol tolerance.
PubMed ID
11958829 View in PubMed
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7-Alkoxyquinoline O-dealkylation by microsomes from human liver and placenta.

https://arctichealth.org/en/permalink/ahliterature64902
Source
Br J Clin Pharmacol. 1992 Nov;34(5):415-20
Publication Type
Article
Date
Nov-1992
Author
J. Hakkola
J. Mäenpää
R T Mayer
S S Park
H V Gelboin
O. Pelkonen
Author Affiliation
Department of Pharmacology and Toxicology, University of Oulu, Finland.
Source
Br J Clin Pharmacol. 1992 Nov;34(5):415-20
Date
Nov-1992
Language
English
Publication Type
Article
Keywords
Animals
Antibodies, Monoclonal - diagnostic use
Benzyl Compounds - metabolism
Cytochrome P-450 Enzyme System - antagonists & inhibitors - metabolism
Dealkylation
Female
Humans
In Vitro
Male
Mice
Mice, Inbred Strains
Microsomes - enzymology - metabolism
Microsomes, Liver - enzymology - metabolism
Placenta - enzymology - metabolism
Pregnancy
Quinolines - metabolism
Rats
Rats, Wistar
Research Support, Non-U.S. Gov't
Smoking - metabolism
Abstract
1. The O-dealkylation of seven 7-alkoxyquinoline derivatives by human hepatic and placental microsomes and the effect of maternal cigarette smoking on placental 7-alkoxyquinoline metabolism was studied. 2. None of several monoclonal antibodies to isoenzymes of cytochrome P450 had a clear effect on metabolism of the compounds by liver microsomes. 3. Maternal cigarette smoking induced the O-dealkylation of all of the 7-alkoxyquinoline derivatives, being greatest for 7-butoxy- and 7-benzyloxyquinoline. 4. Placental 7-alkoxyquinoline metabolism induced by smoking was partially inhibited by the monoclonal antibody 1-7-1 raised against 3-methylcholanthrene-induced rat liver P450. 5. None of the 7-alkoxyquinoline O-dealkylations could be assigned specifically to any known P450 isoenzyme in human liver or placenta.
PubMed ID
1467136 View in PubMed
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[Acid-base equilibrium and nitrogen metabolism in rats in a state of artificial hibernation]

https://arctichealth.org/en/permalink/ahliterature57286
Source
Ukr Biokhim Zh. 1995 Jul-Aug;67(4):67-75
Publication Type
Article
Author
S D Mel'nychuk
S P Rohovs'kyi
D O Mel'nychuk
Source
Ukr Biokhim Zh. 1995 Jul-Aug;67(4):67-75
Language
Ukrainian
Publication Type
Article
Keywords
Acid-Base Equilibrium - physiology
Animals
Anoxia - metabolism
Arginase - metabolism
Bicarbonates - blood
Carbon Dioxide - blood
English Abstract
Glutamate Dehydrogenase - metabolism
Glutaminase - metabolism
Hypothermia, Induced
Male
Nitrogen - metabolism
Rats
Rats, Wistar
Abstract
Experiments on rats have shown an important role of hypercapnia in the development of condition of artificial hibernation in combination with influence of hypothermia, hypoxia and hypercapnia. It is proved that the joint action of hypothermia, hypoxia and hypercapnia has induced development of respiratory acidosis and hibernation in animals, while removal of the hypercapnia effect has induced development of acute metabolic acidosis and death of animals. It has been found that animals in the state of artificial hibernation have considerable changes in concentrations of main electrolytes (Na+, K+, Ca+, Mg2+, phosphates, Cl-) and metabolites (NH3, glutamine, urea) in blood as well as in activity of enzymes (glutamaldehydrogenase, glutaminase, arginase) in tissues of the liver and kidneys.
PubMed ID
8553476 View in PubMed
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[A comparative evaluation of the effect of different types of sapropel on dynamic liver function in intact rats and in the modelling of toxic hepatitis]

https://arctichealth.org/en/permalink/ahliterature56727
Source
Vopr Kurortol Fizioter Lech Fiz Kult. 1998 Mar-Apr;(2):37-8
Publication Type
Article
Author
D I Kuz'menko
G N Sidorenko
E F Levitskii
B I Laptev
E I Dzhuraeva
Source
Vopr Kurortol Fizioter Lech Fiz Kult. 1998 Mar-Apr;(2):37-8
Language
Russian
Publication Type
Article
Keywords
Animals
Benzopyrans - pharmacology - therapeutic use
Carbon Tetrachloride Poisoning - metabolism - rehabilitation
Comparative Study
Disease Models, Animal
English Abstract
Hepatitis, Toxic - metabolism - rehabilitation
Humic Substances - pharmacology - therapeutic use
Lipid Peroxidation - drug effects
Liver - drug effects - metabolism
Mud Therapy
Rats
Rats, Wistar
Reference Values
Seasons
Siberia
Abstract
A course of silicic sapropel applications compared to calcareous sapropel induced a reversible fall of total lipid concentration in blood serum of intact rats. Sapropels of different kinds and of the same kind but obtained from different depths of the same deposit varied by their ability to correct hepatic function in rats with toxic hepatitis. The highest benefit was registered in application of carbonate sapropels taken from the depth of 1.5-2.5 m.
PubMed ID
9643147 View in PubMed
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Activation of constitutive androstane receptor under the effect of hepatocarcinogenic aminoazo dyes in mouse and rat liver.

https://arctichealth.org/en/permalink/ahliterature86237
Source
Bull Exp Biol Med. 2007 Sep;144(3):338-41
Publication Type
Article
Date
Sep-2007
Author
Pakharukova M Y
Smetanina M A
Kaledin V I
Kobzev V F
Romanova I V
Merkulova T I
Author Affiliation
Institute of Cytology and Genetics, Siberian Division of Russian Academy of Sciences, Novosibirsk. pmaria@yandex.ru
Source
Bull Exp Biol Med. 2007 Sep;144(3):338-41
Date
Sep-2007
Language
English
Publication Type
Article
Keywords
Animals
Coloring Agents - metabolism
Humans
Ligands
Liver Neoplasms - chemically induced
Male
Methyldimethylaminoazobenzene - metabolism
Mice
Rats
Rats, Wistar
Receptors, Cytoplasmic and Nuclear - genetics - metabolism
Transcription Factors - genetics - metabolism
o-Aminoazotoluene - metabolism
Abstract
Selective increase of DNA-binding activity of constitutive androstane receptor was detected in rat and mouse liver in response to aminoazo dyes exhibiting hepatocarcinogenic activity for these species (ortho-aminoazotoluene for mice and 3'-methyl-4-dimethylaminobenzene for rats). Competition of azo dyes with 3H-5alpha-androst-16-ene-3alpha-ol (a well-known ligand of constitutive androstane receptor) for binding to liver cell cytosol proteins was studied. Ortho-aminoazotoluene and 3'-methyl-4-dimethylaminobenzene were better competitors for cytosol proteins from mouse and rat liver, respectively.
PubMed ID
18457031 View in PubMed
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Activation of kappa-opioid receptor as a method for prevention of ischemic and reperfusion arrhythmias: role of protein kinase C and K(ATP) channels.

https://arctichealth.org/en/permalink/ahliterature84987
Source
Bull Exp Biol Med. 2007 Feb;143(2):187-90
Publication Type
Article
Date
Feb-2007
Author
Lishmanov A Yu
Maslov L N
Lasukova T V
Crawford D.
Wong T M
Author Affiliation
Institute of Cardiology, Tomsk Research Center, Siberian Division of the Russian Academy of Medical Sciences.
Source
Bull Exp Biol Med. 2007 Feb;143(2):187-90
Date
Feb-2007
Language
English
Publication Type
Article
Keywords
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer - administration & dosage - pharmacology
Alkaloids - administration & dosage - pharmacology
Animals
Anti-Arrhythmia Agents - administration & dosage - pharmacology
Arrhythmias, Cardiac - etiology - physiopathology - prevention & control
Benzophenanthridines - administration & dosage - pharmacology
Glyburide - administration & dosage - pharmacology
Male
Myocardial Reperfusion Injury - complications
Naltrexone - administration & dosage - analogs & derivatives - pharmacology
Oxymorphone - administration & dosage - pharmacology
Potassium Channels - physiology
Protein Kinase C - antagonists & inhibitors - metabolism
Rats
Rats, Wistar
Receptors, Opioid, kappa - agonists - antagonists & inhibitors - physiology
Abstract
Intravenous pretreatment with kappa-opioid receptor antagonist (-)-U-50,488 (1 mg/kg) improved heart resistance to the arrhythmogenic effect of coronary occlusion and reperfusion. Selective kappa1-opioid receptor antagonist norbinaltorphimine and nonselective blocker of peripheral opioid receptors methylnaloxone abolished this antiarrhythmic effect. Preliminary blockade of protein kinase C with chelerythrine or inhibition of ATP-dependent K+ channels (K(ATP) channels) with glybenclamide abolished the antiarrhythmic effect of kappa-opioid receptor activation. Selective inhibitor of sarcolemmal K(ATP) channels did not modulate the kappa-opioid receptor-mediated increase in cardiac electrical stability. Our results suggest that protein kinase C and mitochondrial K(ATP) channels play an important role in the antiarrhythmic effect associated with activation of peripheral kappa-opioid receptors.
PubMed ID
17970197 View in PubMed
Less detail

Activation of mu-opiate receptors as a factor of regulation of heart resistance to ischemia-reperfusion and oxidative stress.

https://arctichealth.org/en/permalink/ahliterature53983
Source
Bull Exp Biol Med. 2000 Aug;130(8):752-5
Publication Type
Article
Date
Aug-2000
Author
T V Lasukova
T Y Rebrova
S V Tam
Author Affiliation
Laboratory of Experimental Cardiology, Institute of Cardiology, Siberian Division of the Russian Academy of Medical Sciences, Tomsk.
Source
Bull Exp Biol Med. 2000 Aug;130(8):752-5
Date
Aug-2000
Language
English
Publication Type
Article
Keywords
Animals
Enkephalin, Ala(2)-MePhe(4)-Gly(5)- - pharmacology
In Vitro
Male
Myocardial Contraction - drug effects - physiology
Myocardial Reperfusion Injury - etiology - physiopathology - prevention & control
Oxidative Stress
Rats
Rats, Wistar
Receptors, Opioid, mu - agonists - physiology
Abstract
Intravenous injection of the selective mu-opiate receptor agonist DAMGO (0.1 mg/kg, 15 min before isolation of the heart) improved resistance of isolated perfused rat heart to ischemia (45 min) and reperfusion (60 min) damages. In vivo administration of DAMGO prevented reperfusion-induced damages to cardiomyocytes and decreased the content of conjugated dienes in the myocardium during ischemia-reperfusion in vitro. Furthermore, stimulation of mu-opiate receptors promoted recovery of myocardial contractility during reoxygenation, but had no effect on heart resistance to free radical-induced damages during perfusion of isolated heart with a solution containing Fe2+ and ascorbic acid.
PubMed ID
11177234 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
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Activation of type II cannabinoid receptors improves myocardial tolerance to arrhythmogenic effects of coronary occlusion and reperfusion.

https://arctichealth.org/en/permalink/ahliterature53855
Source
Bull Exp Biol Med. 2001 Jun;131(6):523-5
Publication Type
Article
Date
Jun-2001
Author
A V Krylatov
D S Ugdyzhekova
N A Bernatskaya
L N Maslov
R. Mekhoulam
R G Pertwee
G B Stephano
Author Affiliation
Institute of Cardiology, Tomsk Scientific Center, Siberian Division of Russian Academy of Medical Sciences.
Source
Bull Exp Biol Med. 2001 Jun;131(6):523-5
Date
Jun-2001
Language
English
Publication Type
Article
Keywords
Animals
Anti-Arrhythmia Agents - pharmacology - therapeutic use
Cannabinoids - pharmacology - therapeutic use
Coronary Disease - physiopathology
Heart - physiopathology
Myocardial Reperfusion
Myocardial Reperfusion Injury - drug therapy - physiopathology
Rats
Rats, Wistar
Receptors, Cannabinoid
Receptors, Drug - agonists - physiology
Research Support, Non-U.S. Gov't
Tetrahydrocannabinol - analogs & derivatives - pharmacology - therapeutic use
Abstract
Preliminary intravenous injection of cannabinoid receptor agonist HU-210 (0.05 mg/kg) reduced the incidence of ventricular arrhythmias during 10-min coronary occlusion and 10-min reperfusion in chloralose-anesthetized rats. Preliminary injection of type I cannabinoid receptor antagonist SR 141716A (3 mg/kg) had no effect on the antiarrhythmic effect of HU-210, while type II cannabinoid receptor antagonist SR 144528 (1 mg/kg) completely abolished the effect of HU-210. Preconditioning with glibenclamide (0.3 mg/kg), an inhibitor of ATP-dependent K(+)-channels, did not affect the antiarrhythmic activity of HU-210. These findings suggest that antiarrhythmic effect of HU-210 is mediated through activation of type II cannabinoid receptors rather than activation of K(+)-channels.
PubMed ID
11586395 View in PubMed
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[Activities of the liver microsome reductases in adult and aged rats during stress]

https://arctichealth.org/en/permalink/ahliterature10009
Source
Vopr Med Khim. 2001 Nov-Dec;47(6):599-604
Publication Type
Article
Author
N P Rud'ko
V V Davydov
Author Affiliation
State Medical University, Mayakowsky av., 26, Zaporozhye, 69035, Ukraine.
Source
Vopr Med Khim. 2001 Nov-Dec;47(6):599-604
Language
Russian
Publication Type
Article
Keywords
Aging - metabolism
Animals
Comparative Study
English Abstract
Hydrogen Peroxide - pharmacology
Immobilization
Male
Microsomes, Liver - enzymology
Quinone Reductases - metabolism
Rats
Rats, Wistar
Sodium Dodecyl Sulfate - pharmacology
Stress, Psychological - enzymology
Urea - pharmacology
Abstract
The influence of 0.01% sodium dodecyl sulphate, 1.5 and 6.0 M urea and 0.03 M hydrogen peroxide to the NAD(P)H: 2,6 dichlorphenolindophenol reductase activity in livers of adult and old Wistar rats during immobilizing stress was interested. Obtained results indicate that the NADPH--dependent reductase is more resistant to modulating effect of sodium dodecyl sulphate, hydrogen peroxide and urea than NADH-dependent enzyme. The significant decrease of NADH: 2.6 dichlorphenolindophenol reductase sensitivity to the action of all studied modulators occurs in old rats. The similar changes appears in the adult rats liver during stress. The old rats immobilization is accompanied by a decrease of this enzyme activity and the reduction of the influence of all studied modulators to NADH: 2.6 dichlorphenolindophenol reductase as compared with adult ones. These changes in the activity and properties of microsomal NADH: 2,6 dichlorphenolindophenol reductase promote more pronounced decrease of the substrate hydroxylation in the liver of old rats during stress compared to adult ones.
PubMed ID
11925750 View in PubMed
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427 records – page 1 of 43.