cardiovascular-agents and Alcoholism

Topics: Alcoholism; Animals; Cardiomyopathies; Cardiovascular Agents; Diagnosis, Differential; Free Radicals; Humans; Muscle Proteins; Prognosis; Temperance

The growing interest for research addressing the interactions between drug and alcohol metabolisms is not unrelated to the increasing prevalence of alcoholism and associated drug additions. Most physicians are now aware of the increased therapeutic risk in alcoholics, but the intimate mechanism of this interaction is usually unknown. On the whole, while many studies address the problems related to drug-alcohol interactions, those on the interactions between chronic alcoholism and cirrhosis are scarce or imprecise.

Topics: Alcoholism; Anti-Bacterial Agents; Anti-Inflammatory Agents; Anticoagulants; Antitubercular Agents; Cardiovascular Agents; Drug Interactions; Humans; Hypoglycemic Agents; Liver Cirrhosis, Alcoholic; Pharmaceutical Preparations; Psychotropic Drugs

Mildronate is an antiischemic drug. It inhibits carnitine biosynthesis (suppresses beta-oxidation of fatty acid) The aim of the study was to establish how Mildronate influences the concentration of L-carnitine in blood and in some tissues in rats with various stages chronic consumption of alcohol. 28 white rats instead of drinking water were taking 15 % ethanol. In the group A the rats were on the three-week alcohol consumption, in the group B--after 3 weeks of alcohol consumption on a background of alcohol they were taking the mildronate, group C--four-week alcohol consumption; D--after 4 weeks of alcohol consumption only mildronate was administered. The concentration of L-carnitine in the group A was as follows: in the liver 136.11+/-2.44; in heart 74.3+/-3.15; in brain 60.44+/-5.21; in blood 45.8+/-2.32. In the group B: in liver 115.7+/-4.69; in heart 72.11+/-4.23; in brain 59.23+/-2.44; in blood 62.5+/-1.99. In the group C: in liver 107.71+/-1.43; in heart 52.57+/-0.95; in brain 71.5+/-1.08; in blood 38.8+/-2.32. And in group D: in liver 106.94+/-1.81; in heart 42.04+/-0.88; in brain 56.84+/-2.75; in blood 2.37+/-0.69 (nmol/l). During the chronic use of alcohol the decrease of concentration of L-carnitine is marked. The level of L-carnitine is reduced under influence of alcohol, but at the same time it suppressed also all steps of metabolism of the cells. Mildronate not only suppresses carnitine-dependent oxidation, but also switches metabolism to more favorable aerobic glycolysis. Under the influence of mildronate general condition of the body is improved both during complete acceptance of alcohol, and on the background of continuation of consumption of alcohol.

Topics: Alcoholism; Animals; Cardiovascular Agents; Carnitine; Ethanol; Male; Methylhydrazines; Rats; Rats, Inbred Strains; Tissue Distribution

Chronic alcohol consumption elicits an increase in catecholamine release, which may be detrimental to heart function. Adenosine attenuates adrenergic stimulation via an adenosine receptor-mediated antiadrenergic action. This study investigated the effect of ethanol on adenosine antiadrenergic actions and adenosine release in the rat heart.. Rats were pair-fed a liquid diet with or without ethanol for 4 weeks or 8 months. Hearts were isolated for determination of contractile function, and coronary effluents were collected for adenosine content. Dose-response relationships for phenylisopropyladenosine (PIA) were determined for hearts adrenergically stimulated by isoproterenol. Experiments were also conducted with normal hearts with or without ethanol (25 mM) administered acutely. The effect of PIA on adenylyl cyclase activities of adrenergic-stimulated crude membrane preparations obtained from alcoholic and nonalcoholic hearts was determined.. Acute ethanol reduced basal adenosine release by 39%, but it did not significantly decrease adenosine release during adrenergic stimulation. In hearts chronically treated with ethanol for 4 weeks, adenosine release values before and during adrenergic stimulation were significantly reduced from control values. After 8 months of ethanol, adenosine release was similar with or without adrenergic stimulation. PIA 50% inhibiting concentration (IC50) values for contractile function were reduced from pair-fed control values. Acute ethanol did not significantly change the PIA IC50 value. Chronic ethanol reduced the PIA IC50 for adenylyl cyclase by 96%.. Chronic ethanol treatment increases the antiadrenergic action of adenosine by mechanisms that seem independent of changes in adenosine concentration. Therefore, adenosine-induced cardioprotection against increased catecholamine stimulation is enhanced by ethanol.

Topics: Adenosine; Adenylyl Cyclases; Adrenergic Antagonists; Alcoholism; Animals; Cardiovascular Agents; Central Nervous System Depressants; Drug Synergism; Echocardiography; Ethanol; Heart; In Vitro Techniques; Inosine; Male; Myocardial Contraction; Myocardium; Purines; Rats; Rats, Sprague-Dawley

Topics: Alcoholism; Cardiovascular Agents; Methocarbamol; Muscle Relaxants, Central

Topics: Alcoholism; Alkaloids; Cardiovascular Agents; Hypnotics and Sedatives; Muscle Relaxants, Central; Parasympatholytics; Rauwolfia

Topics: Alcoholism; Cardiovascular Agents; Muscarinic Antagonists; Muscle Relaxants, Central

Topics: Alcoholism; Cardiovascular Agents; Humans; Mental Disorders; Muscle Relaxants, Central