Different extracts and oils from 13 plant materials were tested in vitro for antifungal activity against Trichophyton verrucosum, Trichophyton mentagrophytes and Trichophyton simii by cup plate method. Eight extracts/oils from 6 plants showing zone of inhibition more than 10 mm in radius against T. mentagrophytes and T. simil in the preliminary screening were further tested to determine the MIC against T. mentagrophytes. Ether and chloroform extracts of seeds of Mucuna pruriens and stem of Curcume longa were found to be fungistatic. Ether extract of the resin of Shores robusta, chloroform extract of Moringa pterlgosperma and oils of Azadirachts Indica and Pongamia gbbrs were found to be fungicidal.

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Fresh leaes of Ricinus communis, known as "Erandi or Endi" offered protection against experimentally induced liver injury by Ccl4 in albino rats, while cold aqueous extract and the glycoside only provided partial protection.

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Administration of digitalis in healthy controls. miscellaneous diseased and ischaemie heart patients produces ECG changes simulating ischaemic heart disease. Exercise further aggravates these changes, in digitalised patients, posing greater difficulty in ECG evaluation of ischaemic heart patients. The QT ratio and DX/QT fraction, in such situations can be of great help in differentiating the changes induced by ischaemia from those induced by digitals.

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A series of 10-N-acylamino phenothaizines posse-sing N-(-hydroxyethyl piperazine moiety in their side chain showed antihistaminic, antispasmodic and antiserotoninergic activity. On comparison with promethazine HCI, diphenhydramine HCI and cyproheptadine HCI, the compounds of this series were found feeble in potency but less toxic. All the test compounds were devoid of central nervous system depressant activity.

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Eight isoxazoles (1 to 8) were synthesised in our laboratory. Five compounds (1 to 5) were selected for pharmacological screening. All the compounds showed local anaesthetic, spasmolytic and anti-epileptic activity. Dibenzylamino derivative was found to be most potent. less irritant and less toxic compound comparable to lignocaine.

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Cardiovascular effects of ketamine (KT) were studied in dogs in varying doses upto 20 mg/kg body weight. KT when administered intravenously in small doses produced a transient rise in blood pressure and subsequently a fall in blood pressure was observed with a dose of 10 mg/kg and above, The transient rise in blood pressure might be due to the release of catecholamines. KT is a relaxant to the plain muscle, mainly intestines and peripheral vasculature. It is a mild analgesic agent when compared to pethidine and morphine. KT raises the body temperature in rabbits by about 1ø C.

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The antidiuretic effect of chlorpropamide was investigated in the present study. Bioassay of ADH was done in the dog's serum after administering hypotonic saline, 2% alcohol and chlorpropamide. The nature of the chlorpropamide induced antidiuretic response w a s investigated and for this purpose sodium thioglycollate inactivation of ADH activity was done. In normal serum, 64.12% activity of ADH was lost by incubation with sodium thioglycollate. In case of serum after treating with chlorpropamide the loss of ADH like activity was only in the order of 46.35%. The antidiuretic response produced by serum after chlorpropamide to dogs is largely due to the drug itself and not due to ADH. This study shows that chlorpropamide produces an antidiuretic effect of its own and not through the facilitated release of ADH.

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Mongrel dogs of either sex were treated orally with methyldopa (100 mg/kg) twice daily for three days. The frequency dependent tachycardia observed at the cessation of stimulation of the peripheral end of vagus was inhibited only at the lower frequency of stimulation in the methyldopa treated dogs, while there were no differences in the tachycardia observed at higher frequencies of stimulation between control and treated dogs. Atropine pm-treatment followed with desipramine enhanced the magnitude as well as duration of postvagal tachycardia in control and treated dogs. Propranolol administration almost completely abolished the postvagal tachycardia in both the groups of dogs. These results indicate that, as observed with other adrenergic neuron blocking agents. methyl-dopa treatment causes slight inhibition of postvagal tachycardia by impairing neuronal function of efferent sympathetic fibers present in the vagosympathetic trunk and does not alter the release of catecholamines from cardiac chromaffin cells.

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The pattern of spontaneous end tyramine-induced outflow of 3H-norepinephrine (3HNE) end its metabolites in rat isolated vas deferens was evaluated. The tritium content of spontaneous outflow. obtained prior to the addition of tyramine, was found to be consistent. This outflow consisted of unchanged 3H-NE (27.9%) and its metabolites mainly, DOPEG (32.3%) and MOPEG (18.5%). Tyramine (2 x10-5 g/ml) caused a 10 fold increase over the spontaneous outflow of tritium. This increased outflow contained higher proportion of unchanged 3H-NE (68%) with DOPEG (12.1 %) and MOPEG (8.5%) as the major metabolites. The tissues prior to the addition of tyramine contained almost all the tritium in the form of unchanged 3H-NE. These findings suggest that only after 3H-NE has been released from its storage sites. It is metabolised. Also these results revealed that in rat vas deferens, 3H-NE is preferentially metabolised into two glycol derivatives i.e. DOPEG and MOPEG.

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Both clonidine and apomorphine lowered the open field performance of albino rats. Both when given individually along with antiparkinsonian agents like I-DOPA. benztropine and d -amphetamine lowered the open field scores of these antiparkinsonian agents. The parallel effects of apomorphine and clonidine suggest a common mechanism for their action i.e. stimulation of prarynaptic dopamine and/or norepinephrine receptors in CNS which regulate synthesis and release of DA and/or NE.

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An attempt has been made to assess under double blind trial, the hypnotic potency of five commonly used hypnotics, in the face of a rapidly filling bladder. All drugs significantly prolonged sleep interval and increased depth of sleep when compared to placebo. When drugs were compared in pairs. there was no significant difference between them except that methaqualone diphenhydramine combination significantly prolonged sleep interval when compared to seconol sodium. The incidence of drowsiness was significant with diphenhydramine (P <0.02) and the occurrence of dreams was very significant with nitrazepum (P <0.001). Head-ache, heaviness of head and dizziness was complained of with methaqualone-diphenhydramine combination (P <0.02). There was no correlation between volume of urine on awakening and sleep interval.

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Intracerebroventricular administration of angiotensin (10 (g) caused a rise in blood glucose level in rabbits. The hyperglycaemia was not affected by bilateral vagotomy and was less marked in adrenalectomized rabbits. The hyperglycaemic effect was not observed in reserpinized and spinal vagotomized rabbits. It is suggested that intracerebroventricular administration of angiotensin stimulates the hypothalamic or medullary accelerator neurons (central sympathetic structures) to cause a marked release of catecholamines from peripheral stores specially adrenal medulla. This excessive release of catecholamines is responsible for hyperglyoaemia induced by angiotensin-II in rabbits.

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