ABSTRACT
Coenzyme A disulfide (CoA disulfide) was pharmacologically studied. It has been found to normalize lipid and carbohydrate metabolism when given in a dose of 2 mg/kg, i.m., in diverse liver dysfunctions. It possesses an antihypoxic action under hemic and histotoxic hypoxia. When given in small doses (80-160 micrograms/kg, i.v.), CoA disulfide depresses the function of cellular hemostasis.
Subject(s)
Coenzyme A/pharmacology , Acute Disease , Animals , Carbon Tetrachloride Poisoning/drug therapy , Carbon Tetrachloride Poisoning/metabolism , Chemical and Drug Induced Liver Injury/drug therapy , Chemical and Drug Induced Liver Injury/metabolism , Coenzyme A/therapeutic use , Drug Evaluation, Preclinical , Hemostasis/drug effects , Hypoxia/drug therapy , Hypoxia/metabolism , Liver/drug effects , Liver Cirrhosis, Experimental/drug therapy , Liver Cirrhosis, Experimental/metabolism , Protein Deficiency/drug therapy , Protein Deficiency/metabolism , RatsABSTRACT
Psychotropic activity of different salts of homopantothenic acid was studied. In homopantothenic acid derivatives, the substitution of calcium ions by sodium and magnesium ions gives rise to a decrease of the sedative and potentiation of the stimulating properties.
Subject(s)
Pantothenic Acid/analogs & derivatives , Psychotropic Drugs/pharmacology , gamma-Aminobutyric Acid/analogs & derivatives , Animals , Drug Evaluation, Preclinical , Female , Lethal Dose 50 , Male , Mice , Motor Activity/drug effects , Pantothenic Acid/pharmacology , Pantothenic Acid/therapeutic use , Pantothenic Acid/toxicity , Psychotropic Drugs/therapeutic use , Psychotropic Drugs/toxicity , Seizures/drug therapy , Seizures/etiology , Sleep/drug effects , Structure-Activity Relationship , gamma-Aminobutyric Acid/pharmacology , gamma-Aminobutyric Acid/therapeutic use , gamma-Aminobutyric Acid/toxicityABSTRACT
D, L-carnitine chloride antihypoxic action was studied. Carnitine chloride (100-200 mg/kg) was found to increase mouse life expectancy under different experimental models of hypoxia both at acute and chronic administration.
Subject(s)
Carnitine/therapeutic use , Hypoxia/drug therapy , Animals , Atmosphere Exposure Chambers , Carnitine/administration & dosage , Disease Models, Animal , Dose-Response Relationship, Drug , Drug Evaluation, Preclinical , Hypoxia/chemically induced , Hypoxia/etiology , Mice , Nitroprusside , Sodium Nitrite , Time FactorsABSTRACT
The antihypoxic properties of GABA-containing vitamin derivatives (pyridoxalphosphate-GABA, picamilone, pantogam, sodium homopantothenate) as compared with GABA were studied. All agents were found to increase mouse life expectancy under hypoxia in contrast to GABA.
Subject(s)
Hypoxia/drug therapy , Vitamins/therapeutic use , gamma-Aminobutyric Acid/therapeutic use , Animals , Drug Evaluation, Preclinical , Hypoxia/chemically induced , Male , Mice , Nitroprusside , Pantothenic Acid/analogs & derivatives , Pantothenic Acid/therapeutic use , Pyridoxal Phosphate/analogs & derivatives , Pyridoxal Phosphate/therapeutic use , gamma-Aminobutyric Acid/analogs & derivativesABSTRACT
Calcium D-pantothenate (Ca D-P) and calcium D-homopantothenate (Ca D-HP) (pantogam) exhibiting antagonism in a number tests of pharmacological screening were shown to inhibit the absorption of [14C]-GABA (0.2 microM) by the rat brain cortex slices (3 mm) incubated in calcium-free medium. The effect of Ca D-HP manifests at its low concentrations (10(-6) M) and that of Ca D-P at high concentrations (10(-6) M). The data obtained are discussed in relation to the possible influence of the anion and cation components of the studied compounds.
Subject(s)
Cerebral Cortex/drug effects , Pantothenic Acid/analogs & derivatives , Pantothenic Acid/pharmacology , gamma-Aminobutyric Acid/analogs & derivatives , gamma-Aminobutyric Acid/metabolism , Absorption , Animals , Carbon Radioisotopes , Cerebral Cortex/metabolism , Culture Techniques , Dose-Response Relationship, Drug , GABA Antagonists , Male , Rats , Rats, Inbred Strains , Structure-Activity Relationship , gamma-Aminobutyric Acid/pharmacologyABSTRACT
Experiments on albino mice and rats have shown that pantogam, a derivative of pantothenic acid, potentiates the hypnotic effects of hexobarbital and barbital and enhances the effect of subthreshold doses of hexobarbital. The drug inhibits the amphetamine action in the amphetamine hyperaction test without affecting hexobarbital and amphetamine metabolism, or without increasing the blood-brain barrier permeability for these compounds and barbital. Pantogam does not influence the intensity of ethylmorphine N-demethylation in liver homogenates and the content of cytochrome P 450 and b5 in liver microsomes.
Subject(s)
Amphetamine/antagonists & inhibitors , Barbital/administration & dosage , Barbiturates/administration & dosage , Hexobarbital/administration & dosage , Hypnotics and Sedatives , Motor Activity/drug effects , Pantothenic Acid/analogs & derivatives , gamma-Aminobutyric Acid/analogs & derivatives , Animals , Blood-Brain Barrier , Dose-Response Relationship, Drug , Drug Synergism , Liver/metabolism , Mice , Pantothenic Acid/administration & dosage , RatsABSTRACT
Pyriditol (encephabol, enerobol, pyrithioxin, etc.), a disulfide derivative of pyridoxin, exerts an inhibitory effect on hexobarbital and amphetamine metabolism i vivo and on ethylmorphine N-demethylation in vitro. In the latter case the inhibition proceeds according to the mixed type of action. Pyriditol potentiates the hypnotic action of hexobarbital and barbital as well as the effects of amphetamine stereotypy. The mechanism of the potentiating of hexobarbital and amphetamine effects is of combined character and is conditioned both by the physiological properties of pyriditol and its inhibitory effect on hexobarbital and amphetamine metabolism.
Subject(s)
Amphetamine/metabolism , Barbital/metabolism , Barbiturates/metabolism , Hexobarbital/metabolism , Imipramine/metabolism , Pyridines/pharmacology , Pyridoxine/analogs & derivatives , Pyrithioxin/pharmacology , Animals , Brain/metabolism , Drug Synergism , Humans , Liver/metabolism , Pyridoxine/pharmacology , Rats , Sleep/drug effects , Stereotyped Behavior/drug effects , Time FactorsABSTRACT
Intraperitoneal administration of disulphide pyridoxine (pyriditol) to albino mice in a dose of 300 mg/kg brings down the GABA level and the GABA-transaminase activity in the brain, the glutamic acid content and the glutamate-decarboxylase activity remaining unchanged. In the liver and, especially, in the kidneys of test animals the activity of aspartate-and alanine-aminotransferase goes down. The diurnal urinary output of the animals shows a decreased passage of 4-pyridoxic acid. These results are interpreted to be consequent upon the antivitamin action of pyriditol with respect to pyridoxine.
