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Biomedical subjects

G G Nahas

Publications and source records attributed to G G Nahas.

At least 19 recordsLinked to original sources
PubMed1991

Catecholamines, cocaine toxicity, and their antidotes in the rat.

Acute lethal cocaine intoxication in the rat induces significant increases of plasma dopamine, norepinephrine, and epinephrine concentrations associated with cardiac functional and morphologic changes. Nitrendipine (a calcium channel antagonist) administered 5 min following cocaine administration lowers catecholamine concentration and restores cardiovascular function to normal, while preventing lethality, and so does enalaprilat (an enzyme-converting inhibitor) administration with diazepam. Cocaine cardiac toxicity in the rat appears to be associated with a significant stimulation of the sympathoadrenal and a sustained elevated plasma concentration of epinephrine. The renin angiotensin system also appears to be activated.

Analysis of Variance↗
PubMed1990

Interactions of nimodipine and cocaine on endogenous catecholamines in the squirrel monkey.

The effects of nimodipine on the cocaine-induced alterations in blood pressure, heart rate, and plasma catecholamines were studied in the squirrel monkey. Cocaine in intravenously administered doses of 0.5, 1, and 2 mg/kg produced significant increases in blood pressure and significant decreases in heart rate. These cardiovascular changes were associated with transient episodes of arrhythmias and with significant increases in plasma concentrations of dopamine, epinephrine, and norepinephrine. Nimodipine, 1 micrograms/kg/min for 5 min administered intravenously 5 min after cocaine, corrects the cardiovascular and plasma catecholamine concentration changes induced by this alkaloid. The same dose of nimodipine administered 5 min before cocaine prevents elevations of blood pressure. Plasma catecholamine increments are also prevented except for the highest dose of cocaine. Cardiovascular changes induced by cocaine administration in the squirrel monkey are temporally associated with significant increments in plasma catecholamines. Administration of nimodipine prevents or minimizes these endocrine and physiologic changes.

Animals↗
PubMed1990

The experimental use of cocaine in human subjects.

Continuation of the practice of experimental administration of cocaine to cocaine-addicted volunteers has been recommended by some investigators. The author's view is that the risk of experimental use of cocaine outweighs its benefits and that this practice should not be pursued. The author describes the damaging effects of cocaine on the cardiovascular system, particularly its ability to induce myocardial band necrosis, and the unique reinforcing properties of the drug. The legal and ethical issues raised by the experimental use of cocaine are also discussed.

Cocaine↗
PubMed1986

In vivo inhibition of enterocyte metabolism by delta 9-tetrahydrocannabinol.

Mice were given 10 to 100 mg/kg by stomach tube of delta 9-tetrahydrocannabinol (THC) in a single dose or for 4 consecutive days. [3H]Thymidine or [3H]glucosamine was given 3 or 24 hr before sacrifice. Enterocytes were isolated, and the incorporation of radioactivity into the acid insoluble fraction was measured. THC significantly inhibits in a dose-related fashion (from 10 to 90%) in vivo enterocyte metabolism. This inhibition is found in all enterocytes whatever their position in the intestinal tract; it is also independent of the state of differentiation of enterocytes. After a single ingestion of THC, crypt cells which synthesize DNA incorporate 37 to 45% less thymidine, and villus cells, which synthesize important amounts of glycoproteins, incorporate 15 to 39% less glucosamine. After 4 days of THC administration, the inhibition of thymidine incorporation is even more significant (up to 88%).

Analysis of Variance↗
PubMed1981

A pharmacological classification of drugs of abuse.

This paper questions the validity of the distinction between "psychic" and "physical" dependence in relation to drug addiction. The author describes the action of dependence-producing or addictive drugs on the brain at the neuronal and structural level as well as the alterations of arousal, awareness, impairment of sleep, memory, psychomotor performance and sensory perception which are symptomatic of neuropsychological toxicity. Addictive drugs are consumed for the primary pleasurable reward that they produce as a result of their effects on the pleasure reward mechanisms of the brain. These pleasurable sensations will act as reinforcers for repeated administration when the drug effects have worn off and induce a compulsive drug-oriented behaviour. The tolerance, which develops to addictive drugs and the occurrence of withdrawal symptoms, are added reinforcers. The author therefore proposes a pharmacological classification of the most commonly used addictive drugs based on these foregoing effects which may be quantified to a large extent.

Animals↗