1. Computer programs for pharmacokinetic analysis have been written in the language BASIC for use on microcomputer. 2. Three programs incorporating respectively the Back-Projection, Wagner-Nelson, and Loo-Riegelman algorithms can estimate the constants for the absorption, distribution and elimination phases of the concentration-time curve, as well as area-under curve. 3. The programs are valid for first-order kinetics. Use of the programs does not require knowledge of programming.

(1) The antipsychotic effects of chlorpromazine have been potentiated by mepyramine and pheniramine, unaffected by diphenhydramine and meclizine, while it is antagonised by promethazine. (2) Regarding extrapyramidal effects, promethazine, diphenhydramine and mepyramine have strong antagonising effect as compared to pheniramine and meclizine. (3) Comparison of risk-benefit ratio, suggest that during neuroleptic therapy, the prophylactic use of promethazine has harmful effect, diphenhydramine and meclizine have no effect, while mepyramine and pheniramine have a beneficial effect.

1. Comparative evaluation of the effect of anti-arrhythmic drugs on ventricular fibrillation threshold (VFT) and on theconcentration of norepinephrine (NE) in the different parts of the myocardium of the cat has been undertaken. 2. In pentobarbitone anaesthetised cats fibrillation induced by electrical stimulation (ES.) of the left ventricle caused reduction of NE in the heart. 3. Quinidine and disopyramide, the membrane stabilizers; lidocaine, a local anaesthetic; adrenergic receptor blockers like phenoxybenzamineand propranoloI, and verapamil, a calcium antagonist, caused bradycardia, hypotension and decrease in NE content. 4. Pretreatment with quinidine, disopyramideand lidocaine inhibited further release of NE from the myocardium following E.S. and significantly raised VFT. 5. Phenoxybenzamine (10 mg/kg), propranolol (5 mg/kg) and verapamil (1 mg/kg) did not inhibit the release of NE. Phenoxybenzamine provided protection against ventricular fibrillation whereas propranolol and verapamil failed. 6. The results suggest the involvement of ( adrenergic receptor as a contributing factor in the onset of ventricular fibrillation induced by E.S.

1. Ergometrine produced a behavioural syndrome in the rat which was characterized by head and body shakes, lateral head weaving, forepaw treading, hindlimb abduction and Straub tail. 2. Pretreatment with 5-HT receptor antagonists, cyproheptadine and methysergide, significantly decreased the intensity of the behavioural syndrome produced by ergometrine. 3. Pretreatment with p-chlorophenylalanine and clomipramine significantly decreased the intensity of the behavioural syndromes induced by fenfluramine and p-chloramphetamine but had no significant effect on the intensity of the behavioural syndrome produced by ergometrine. 4. The results indicate that ergometrine produces the 5-HT mediated behavioural syndrome by directly stimulating the central 5-HT receptors.

1. Twelve different substituted guanidines were prepared by the condensation of different heterocyclic moieties with different aryl cyanamides. 2. Compounds were screened for anti-inflammatory activity and compared with standard drug phenylbutazone. 3. Ten compounds showed significant anti-inflammatory activity and compound IV, N-P-anisyl-N'-5-phenyl-1,3,4-oxadiazol-2-yl guanidine hydrochloride, was the most potent In carrageenin-induced oedema.