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Biomedical subjects

H Venkatakrishna-Bhatt

Publications and source records attributed to H Venkatakrishna-Bhatt.

At least 37 records · Page 2Linked to original sources
PubMed1987

Blood histamine levels in cotton-dust exposed workers in a textile mill of Ahmedabad.

Blood histamine levels were measured by the bioassay of histamine (on an isolated strip of guinea pig ileum) in workers exposed to cotton dust in a textile mill in Ahmedabad. Byssinotic subjects showed very high levels of blood histamine as compared to nonbyssinotic and control subjects. The blood histamine levels were not well correlated to the dust concentrations or duration of exposure but rather to the day of the week (ie, first, second, third, etc., after weekend break) on which the samples were collected. The blood histamine levels were high on the first day of the work week, when byssinotics complained most of their symptoms.

Byssinosis↗
PubMed1985

Pharmacology of new glutarimide compounds.

New glutarimide compounds were synthesized by incorporating piperidine (compounds 1 to 7), diethylamine (8 and 9), morpholine moities (10 to 13), and alkyl derivatives of 3,5 dicyanoglutarimide (14 to 20) at position -1 of the nitrogen atom. Only compounds 1 to 7 at a dose of 8 mg/kg i.p. caused hypermotility, ataxia, tachypnoea and mild tremors in mice. At higher doses (32 mg/kg i.p.), all compounds induced tonic and clonic convulsions, respiratory paralysis and death. The LD50 values of compounds 1 to 20 in mice range from 152 to 488 mg/kg i.p. and for compounds 21 to 23, the p.o. values are 484, 500 and 525 mg/kg. The relative toxicity of compounds 1 to 7 and 14 to 20 showed inverse ratio in their numbers. Basic compounds 21 to 23 at high dose levels (64 mg/kg i.p.) induced only hypnotic depression. No change was observed in organ-wise histopathological study except patchy necrosis at the site of injection of basic compounds. The CNS pharmacological studies were negative with reference to anti-convulsion, analgesic, antipyretic tests by conventional methods except at higher doses (32 or 64 mg/kg i.p.), which exhibited synergistic effects in mice and rats.

Analgesics↗
PubMed1983

Glucose tolerance in patients with cerebrovascular accidents and their blood relatives.

The present study was undertaken to examine whether there is any hereditary correlation, with reference to the abnormal glucose metabolism, between patients with cerebrovascular accidents and their healthy blood relatives in respect to the occurrence of cerebrovascular disease. The investigation was carried out by intravenous glucose tolerance test (IV-GTT) and prednisolone-primed glucose tolerance test (PP-GTT) in 83 subjects. Of these, 20 were healthy (control) persons (group A), matched in age and sex with 50 patients with cerebrovascular accidents (group B) and 13 family relatives of group B (group C) showing unequivocal GTT or PP-GTT. In controls, the IV-GTT criterion, i.e. k value, was found generally to be 2.82 +/- 0.43 and in persons less than 50 and over 50 years old, it was found to be related with age, i.e. 3.1 +/- 0.73 and 2.53 +/- 0.43, respectively. The 21 patients of group B with normal GTT response had a k value of 2.53 +/- 1.88 and the 29 patients with abnormal GTT response had a k value of 1.2 +/- 0.33. Among the 21 patients of group B, 11 had normal IV-GTT and their PP-GTT was found to be 125 +/- 12.5 mg%. The other 10 patients with abnormal IV-GTT exhibited a PP-GTT of 173.4 +/- 26.43 mg%. In 14 and 15 patients, the time-lapse difference of 7 and 8-21 days after stroke showed an abnormal GTT response and in 6 and 15 patients it showed a normal response. Among 13 healthy relatives of group B (group C), only 1 subject was found to have abnormal IV-GTT (k value of 1.386) and 2 were found to have abnormal PP-GTT (182.8 and 388.0 mg%), thus indicating pre-symptomatic diabetics.

Cerebrovascular Disorders↗
PubMed1981

Syndrome of postoperative depression of vital functions in poor-risk patients: its treatment.

Loss of proprioception due to depressed neuromuscular transmitter following continued action of skeletomuscular relaxant drugs may not be the main cause of stupor, respiratory depression, and suppression of motor and sensory reflex activity in the immediate or delayed post-operative period in surgical patients. Those with a chronic history of suffering (termed poor-risk types because of other associated derangements in electrolytes, body water, etc.), hyper-react to surgical stress as well as postoperative pain and apprehension. This leads to the release of large quantities of stress products (noradrenaline and its cognates) into the central nervous system (CNS), thus inducing a phase of depression of the cerebral cortex and other vulnerable parts of the CNS in such a way that the stupor analgesic stage is induced in the affected persons (called the "syndrome of post-operative depression of vital functions"). Treatment of such a syndrome thus involved removal of the stress products from the CNS as well as from peripheral circulation by extraction therapy (20% mannitol administration), coupled with judicious use of atropine and neostigmine to stimulate the CNS itself, i.e., the production of acetylcholine in the mesencephalic reticulo-activating system.

Catheterization↗
PubMed1980

Reduction of barbiturate anaesthesia by new glutarimide compounds in mice.

Newly synthesized glutarimide compounds (Table 1) at doses of 4, 8 and 16 mg/kg (IP) reduced the duration of sleep induced by pentobarbitone in mice. Compounds 1 to 7 and 21 were more potent than the other compounds and their activity was comparable to the reference drug, bemegride. The structure activity relationship for the decrease in duration of barbiturate anaesthesia caused by the various groups of these compounds was mainly found to be inversely related to the length of the alkyl side chain at position 4 of the beta carbon atom. It was also shown that the presence of piperidine, diethylamine and morpholine moieties attached to 3,5-dicyanoglutarimide was partly responsible for the reduction in barbiturate anaesthesia by these compounds.

Animals↗
PubMed1978

Electrophysiological changes induced by paradoxical sleep deprivation and lithium chloride poisoning in rats.

In an attempt to analyze the disruption of conditioned taste aversion (CTA) caused by pre-acquisition paradoxical sleep deprivation (PSD), the effect of poisoning (0.15 M LiCl, 4% body weight) on the sleep--wakefulness pattern was studied in 12 rats with chronically implanted electrodes. The polygraphic recording showed that poisoning reduced the total sleep time in the subsequent 3 h from 57 to 42% and REM sleep from 6 to 2%. The lithium chloride effect was still more pronounced after 24-h REM sleep deprivation: the total sleep time decreased from 67 to 46% and REM sleep from 13 to 2%. The change of sleep--wakefulness pattern, most pronounced during the first hour of poisoning, gradually returned to normal but REM sleep was significantly reduced even 3 h after poisoning. It is concluded that 24-h PSD does not alleviate the subsequent poisoning. On the other hand, the lithium chloride induced reduction of post-acquisition REM sleep many enhance the learning impairment caused by pre-acquisition PSD.

Activity Cycles↗
PubMed1977

Sleep induced by drugs injected into the inferior horn of the lateral cerebral ventricle in dogs.

1 In unanaesthetized dogs, cholinomimetic drugs and their antagonists were injected into the inferior horn of the left lateral cerebral ventricle. Injection volumes of 5 mul were used to limit spread of the drugs beyond the inferior horn. The effects on EEG and behaviour were recorded and compared with the effects of the same doses given into the body of the right lateral ventricle a little behind the foramen on Monro. 2 injections of cholinomimetic drugs into the inferior horn (acetylcholine 1-2 mug, physostigmine 1.0 mug, pilocarpine 100 mug and nicotine 10 mug) induced sleep during the following hour. The same doses injected into the body of the lateral ventricle did not produce sleep. 3 Cholinolytic drugs (atropine 10-20 mug, hyoscine 0.4-1.6 mug (+/-)-tubocuraine 10-20 ng and hexamethonium 40 mug) injected into the inferior horn also produced sleep, but the same doses injected into the body of the lateral ventricle were without effect. The EEG recorded after tubocurarine showed high voltage slow waves during sleep and desynchronized activation during rapid eye movement sleep. 4 Noradrenaline (10 mug) injected into the inferior horn produced sleep whereas the same dose given into the body of lateral ventricle did not produce sleep. The results with 5-hydroxytryptamine were equivocal. 5 It is suggested that the site for induction of sleep lies in structures lining the inferior horn of the lateral cerebral ventricle and that the cholinomimetic drugs probably act by a depolarizing block and the acetlycholine antagonists by a competitive block.

Acetylcholine↗