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PubMed1984

[Dextrofer-100 with B12 and dextrofer-100--comparative pharmacological and clinico-pharmacological studies].

Comparative studies were carried out with dextrofer-100 with B12 and dextrofer-100 in terms of acute toxicity (albino mice), absorption (rabbits, pigs, and lambs), deposition of iron in the liver and spleen (rabbits, pigs, and lambs) and antianemic action (pigs and lambs). It was found that LD50 of dextrofer-100 with B12 at i/v introduction into 18-20-gram albino mice was 1750 mg Fe3+/kg body mass; with regard to toxicity it was shown to correspond to the British Veterinary Code. The toxicity of dextrofer-100, studied by the same test, was practically undeterminable. By the level of sideremia dextrofer-100 with B12 did not differ essentially from dextrofer-100 and was said to belong to preparations with rapid absorption. It was most rapidly absorbed in pigs, rabbits and lambs following next. It supplied enough iron to the reticuloendothelial organs--in pigs it was (on a percent basis) highest in the liver, and in lambs--in the spleen. In pigs on the 10th day following treatment with dextrofer-100 with B12 the liver was shown to have vitamin B12 5 times as much. By its antianemic effect at i/m application to newborn pigs and lambs dextrofer-100 with B12 did not differ essentially from dextrofer-100 (its action was negligibly broader), however, it was beneficial to the growth of pigs.

Absorption↗
PubMed1984

[Pharmacological and clinico-pharmacological studies of diazepam powder in suspensions].

Studied was the preparation diazepam-pulvis for suspension (DPS) with regard to its tranquillizing and myorelaxing doses, inhibiting the aggression, and preventing the stress conditions in domestic animals and birds. It was established that at oral application to pigs at rates of 1 to 2 mg/kg body mass DPS produced a pronounced tranquillizing effect, while at 3 mg/kg it led to myorelaxation as well. In sheep tranquillizing effect was seen when amounts of 3 to 5 mg/kg body mass were used, and myorelaxation was achieved with 6.6 to 13.2 mg/kg. In male calves tranquillization was manifested after doses of 3 mg/kg body mass were applied. In hens the tranquillizing dose was found to be 3 mg/kg body mass, and the myorelaxing one--4 mg/kg; in cocks the respective doses were 5 and 7 mg/kg body mass. At the rate of 3 mg/kg body mass DPS was found to enhance the thiopental-sodium narcosis. When offered to pigs at 2 mg/kg body mass in admixture with the feed DPS led to tranquillization and suppression of the active and passive defense response. No full prevention of cannibalism could be achieved. The daily administration in the course of 30 days with the ration of bull-calves at the rate of 3 mg/kg body mass was shown to calm the animals under loose housing in boxes and affect favourably their weight gain. Admixed with the feed of cocks at 5 mg/kg DPS suppressed aggressiveness.

Adaptation, Physiological↗
PubMed1981

The clinical pharmacology of naltrexone: pharmacology and pharmacodynamics.

The time-action of opiate antagonist activity of naltrexone was evaluated in detoxified ex-opiate addicts, using 25 mg intravenous heroin challenges. A 100 mg naltrexone dose provided 96% blockade at 24 hr, 86.5% blockade at 48 hr and 46.6% blockade at 72 hr. Following oral administration, naltrexone was rapidly and completely absorbed. Peak levels of naltrexone and its major metabolite 6 beta-naltrexol were reached 1 hr after the dose. The high 6 beta-naltrexol plasma concentrations only 1 hr after drug administration indicate a rapid biotransformation process, converting a large fraction of the dose to less active metabolites. Over 70% of the dose was excreted in the 24 hr urine and less than 0.5% in the feces. No change was observed in the rate of naltrexone disposition during chronic dosing vs. the acute study, indicating no metabolic induction. The rapid achievement of steady state naltrexone plasma levels eliminates the need of stepwise induction at the beginning of naltrexone treatment.

Animals↗
PubMed1981

The pharmacology and clinical pharmacology of indapamide.

At low doses indapamide is a potent and long acting antihypertensive agent in various hypertensive animals and in man, but is without activity in normotensive subjects. A daily dose of 2.5 mg produces a minimal diuresis but at higher doses this increases without any significant augmentation of hypotensive activity. It appears to have no effect on most blood biochemical parameters, including glucose, high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides, noradrenaline, adrenaline, but potassium levels may decrease and uric acid and renin increase. Indapamide had no effect on renal function nor does it alter left ventricular function, electrocardiograph (ECG) or heart rate, although cardiac output may marginally increase. Total peripheral resistance is significantly decreased and it may exert its antihypertensive effect by reducing vascular reactivity to various pressor stimuli by inhibiting the net inward flow of calcium and resultant phasic contractions in vascular smooth muscle. Indapamide differs from the diuretics in that it has a comparatively high lipid solubility; it is also bound to blood proteins and elastin in vascular smooth muscle and little is eliminated in the urine. It may be for these reasons that the drug has less diuretic activity but more pronounced effect on vascular smooth muscle than compounds of similar structure.

Animals↗
PubMed1995

Relating pharmacology to clinical practice: the pharmacologic basis of rational polypharmacy.

Many patients with epilepsy can be successfully treated with a single antiepileptic drug (monotherapy). However, in a substantial number of patients, monotherapy does not provide satisfactory seizure control, and the use of two or more drugs, or polypharmacy, is required. Selection of rational combination therapy requires consideration of the clinical antiepileptic or anticonvulsant effects, adverse effects, drug interactions, and relationship between effective and toxic drug levels. Mechanisms of action of each agent must also be studied. Optimal combination therapy often is achieved with drugs that have different mechanisms of action, relatively few adverse effects, high therapeutic indexes, and limited or no drug interactions. The goal of rational polypharmacy is to produce improved seizure control with minimal or no adverse effects.

Anticonvulsants↗