1. Effects of three doses of diazepam (5,10 and 20 mg) and promethazine (10,25 and 50) mg) given orally were studied on psychomotor performance and mental function tests in unrestricted conditions. 2. Both diazepam and promethazine caused dose related increase in the choice reaction time (R.T.) and decreased critical flicker fusion frequency (C.F.F.) in a dose dependent manner, the effects of the former being more pronounced than that of the latter drug on R.T., short term memory (S.T.M.) was depressed by diazepam only. Arithmetic ability (A.A.) and Digital symbol substitution test (D.S.S.T.) proved to be insensitive to the effects of both drugs. 3. Subjectively, volunteers rated 5 mg of diazepam and 10 mg promethazine and 10 mg diazepam and 25 mg promethazine to be equisedative. 4. Subjective rating along the Visual Analogue mood scales (V.A.S.) indicates that volunteers do discriminate between the drugs and their doses along certain scales, (drowsy-alert. tired-active, and depressed-euphoric) but not along other scales (tense-relaxed, anxious-confident).

1. Clonidine (50 mg/kg ip) induced a peculiar aggressive behavior in mice, associated with drastically reduced ACh level (p < 0.0001) in the whole brain. Footshock also caused significant reduction in ACh level (p < 0.001). 2. Perhaps central cholinoceptive mechanisms are involved in both clonidine and shock- induced aggression (CIA and SIA). Nitrazepam (NTZ), haloperidol (HAL) and propranolol (PROP) reduced the ACh level(s) significantly (p< 0.001). 3. All the drugs decreased the biting/fighting episodes. However, correlation between the anti-aggressive action and the changes in ACh - lowering effect of CIA and SIA caused by these drugs was absent. 4. Nitrazepam, HAL, AND PROP significantly raised the diminished CIA-induced Ach level (p <0.001), but they potentiated the Ach-lowering effect of SIA. When HAL or PROP administration preceded CIA or SIA, they antagonized the Ach-lowering effect of drug(s) alone. 5. Interestingly NTZ, administered prior to CIA or SIA was fount to be further potentiate (p <0.001) the Ach reduction caused by NTZ alone.

1. The relative effects of blood volume contraction and hypertonicity on the vasopressin content and ultrastructure of the neural lobe have been examined after daily consecutive administration of polyethelene glycol (PEG) and hypertonic NaCl solution to mastromys natalensis. 2. Treatment with PEG and hypertonic saline caused a significant decrease in the total vasopressin content of the neural lobe (187(41 and 255(45 mU. neural lobe respectively) as compared to that of the control value (542(56 mU/neural lobe). 3. The decrease is correlated with the depletion of neurosecretory granules as observed under the electron microscope. 4. An interesting finding relates to the fact that hypovolemia not only stimulates the release of vasopressin but also effects the lipid content of the pituicytes. 5. The present studies are in agreement with the findings of the other workers in mammalian species. However, in this species of animals the activation of volume receptors is more predominent than that of Osmoreceptors.

1. Ibuprofen in doses of 100 and 200 mg/kg, p.o. for six consecutive days produced gastric ulceration in albino rats. 2. An increase in acid output seems to be responsible for this ulcerogenic response. 3. Pretreatment with adrenergic, cholinergic, tryptaminergic and histaminergic (H1) receptor antagonists provided partial protection, while metiamide pretreatment afforded almost complete protection and reduced the acidity. 4. It appears that histamine H2 receptors are predominently involved in the ulcerogenicity of ibuprofen.

1. The dose-response curves of adrenaline for its cutaneous vasoconstrictor action, were analysed in 21 normal and 24 asthmatic subjects. 2. The vasoconstrictor responses to adrenaline were studied by determining the to 5 of disappearance of interacutaneously injected radioactive iodine (Na131) in absence and presence of doses of adrenaline (8-256 pg) and were expressed in terms of percent reduction in basal blood flow. 3. The skin blood flow in normal subjects was 15.82 ( 0.60 ml/min/100g of tissue. It was noted that there were two distinctly heterogenous groups in asthmatic subjects, with respect to skin blood flow, one with values similar to normal and the other with significantly higher blood flow (23.94 ( 1.39). The subjects in the latter group showed marked tendency of wealing at the injection sites. 4. The vasoconstrictor responses to the threshold doses of adrenaline (8+ 16 pg) were not significantly different in asthmatics having higher skin blood flow, as compared with that in the normal subjects. However, in asthmatics whose skin blood flow was similar to that of normal subjects this threshold response was significantly enhanced. 5. The dose-response curve in asthmatic subjects, exhibited a marked shift to the left, indicating an increased responsiveness of the alpha-adrenoceptors. The slope of the curve in asthmatic subjects was steeper and the maximal response attainable was higher. 6. It is possible that the basal hyperemia, observed in a group of asthmatics, presumably due to hyper-responsiveness to injection trauma (histamine hypersensitivity), counteracted the weak vasoconstrictor action of threshold dose of adrenaline. 7. The present observations confirm that the enhanced vasoconstrictor responses, seen in asthmatics indicate a true hyper responsiveness of the alpha- adrenoceptors and are not evident due to higher basal blood flow values.

(1) The results showed that only 5-(6'-methoxyindan-1'-y) methyltetrazole was more potent antiinflammatory agent than phenylbutazone in chronic tests though both the tetrazole derivatives were less potent than phenylbutaione in acute test models. (2) The tetrazole derivatives were about 1.5 times more potent antipyretics than phenylbutazone whereas their analgesic potency was about 4 times less than that of the latter. (3) These derivatives were much safer than phenylbutazone both in respect of their gastric ulcerogenicity and acute lethal toxicity.

1. Experimental atherosclerosis in rabbits generally required at least eight week's of feeding atherosclerotic diet. . 2. In the present study on rabbits by supplementing the atherogenic diet with calcium and weekly injections of cholecalciferol (Vit.D), atherosclerosis could be induced in three weeks time. 3. Since the atherosclerosis in rabbits can be induced now in a short time of three weeks, the present rabbit model may be preferred for anti-atherosclerotic studies.

(1) Cardiac arrhythmias were induced in guinea pigs anaesthetised with urethane and pentobarbitone sodium by slow intravenous infusion of ouabain. (2) The doses of ouabain required for the development of early arrhythmias, ventricular fibrillation and cardiac arrest in guinea pigs anaesthetised with urethane were significantly less compared to guinea pigs anaesthetised with pentobarbitone sodium. This may possibly be due to the inhibition of cardiovascular responses mediated via the inhibition of alpha, adrenoceptors by urethane.