Thyroid hormones and [14C] glucose metabolism in bacteria.

The effects of triiodothyronine and thyroxine on metabolism and growth of bacteria were studied. It was observed that over a certain range of concentration thyroxine and triiodothyronine produced increase in 14CO2 release from [14C]-labeled glucose and also stimulated bacteria growth.

Radiorespirometric testing of antibiotic sensitivity in urinary tract infections: concise communication.

A radiometric method, based on inhibition of 14CO2 release from bacterial metabolism of C-14-labeled glucose, was applied to test the susceptibility of urinary organisms to antibiotics. The testing was also carried out by the routine disc diffusion method after isolation of the organisms. Results of susceptibility to antibiotics could be obtained within 2 to 4 hr by the radiometric technique, compared with the 48 hr required for the disc method.

Role of catecholamines in the central mechanism of emetic response induced by peruvoside and ouabain in cats.

1 Peruvoside, (a glycoside obtained from the plant, Thevetia neriifolia Juss) and ouabain produce emesis in cats. Vomiting is not produced by these drugs in animals pretreated with catecholamine depleting drugs like reserpine, tetrabenazine or syrosingopine. Chloropromazine hydrochloride, mepyramine maleate, or BOL-148 administered intravenously or intracerebro-ventricularly do not afford protection.2 Phenoxybenzamine produces partial protection against peruvoside-induced emesis.3 Haloperidol (1 mg/kg i.v.) prevents vomiting induced by peruvoside or ouabain. Intracerebroventricularly administered haloperidol is ineffective.4 Cats pretreated with SKF-525-A, are not protected by haloperidol. Animals pretreated with phenobarbitone in a dose of 25 mg/kg for a week were protected by haloperidol, 250 mug/kg i.e. one quarter of the effective antiemetic dose in normal cats.5 It is postulated that catecholamines are involved in the mechanism of vomiting induced by cardiac gycosides. Further, a metabolite of haloperidol seems to be responsible for its effective antiemetic action.

Interaction of bretylium and guanethidine on the relaxations of the rat isolated fundal strip preparation, evoked by indirect stimulation.

1. Isolated rat stomach fundal strip bathed in Krebs solution containing atropine (1 mug/ml), responded to indirect stimulation by a relaxation which was frequency dependent. These responses were blocked by phenoxybenzamine (6 mug/ml) or phentolamine (8 mug/ml).2. Strips obtained from rats previously treated with reserpine did not show relaxation to indirect stimulation. These responses were therefore adrenergic in nature.3. Bretylium (0.1-100 mug/ml) failed to block the relaxations produced by indirect stimulation, in fact relaxations were potentiated by the drug.4. Guanethidine (10 mug/ml) blocked the relaxations induced by indirect stimulation.5. Guanethidine may be taken up by adrenergic nerves actively since its action is not seen at 12 degrees C.6. Bretylium (10 mug/ml) prevented the actions of guanethidine at 37 degrees C.

Mechanism of neurotoxicity of cardiotonic glycosides.

1 In cats intracerebroventricular administration of 5, 10, 20 mug of peruvoside, a cardiac glycoside obtained from the plant, Thevetia neriifolia, and 10 and 20 mug of ouabain, produced marked neurotoxicity. This was dose-related. 2 Prior administration reserpine (2 mg/kg i.m., 500 mug i.c.v.) or tetrabenazine (25 mg/kg i.v., 50 mg/kg i.v. and 2 mg/,g i.c.v.) suppressed the neurotoxicity, but lithium carbonate (100 mg/,g i.p., 2 mg 2.c.v.) and haloperidol (200 mug i.c.v.) were ineffective. 3 Prior administration of 2-bromolysergic acid diethylamide (BOL-148, 200 mug i.c.v.) or p-chlorophenylalanine (PCPA) (400 mg/kg i.p.) suppressed the neurotoxicity induced by peruvoside and ouabain. 4 Perfusion of the lateral ventricles of cats with 10, 20 and 30 mug of peruvoside or ouqbain produced a massive release of 5-hydroxytryptamine (5-HT). This was dose-related. Prior administration PCPA suppressed the release of 5-HT. 5 The results of the findings indicate the involvement of 5-HT in the genesis of neurotoxicity induced by peruvoside or ouabain.

Interactions between acetylcholine, 5-hydroxytryptamine, nicotine and morphine on isolated rabbit atria.

1. The effects of 5-hydroxytryptamine (5-HT) and morphine on the responses to acetylcholine and nicotine of isolated rabbit atria were studied.2. 5-Hydroxytryptamine (10 mug/ml.) and morphine (20 mug/ml.) blocked the negative chronotropic and inotropic actions of acetylcholine.3. Nicotine (20 mug/ml.) produced stimulation of the atria, which was blocked by dichlorisoprenaline, morphine, 5-HT, bretylium and hemicholinium. Hemicholinium block was reversed by choline.4. In reserpinized preparations, nicotine produced inhibition of atria and this action was also blocked by atropine, 5-HT and morphine. Inhibition induced by nicotine was potentiated by physostigmine.5. 5-Hydroxytryptamine (20 mug/ml.) produced stimulation of atria. This was blocked by bretylium and reduced by hemicholinium. Hemicholinium block was reversed by choline.6. It is concluded that 5-HT in low concentrations acts as a weak agonist at the cholinoceptive receptors and therefore blocks the action of acetylcholine. Furthermore, nicotine and larger doses of 5-HT have actions on ganglionic structures and liberate acetylcholine, which in turn releases catecholamines.

Isolation and characterisation of toxic components from the venom of the common Indian sea snake (Enhydrina schistosa).

Three neurotoxic components, enhydrotoxins a, b and c, were isolated by a three step procedure from the venom of the sea snake Enhydrina schistosa, caught in the Arabian sea. The i.v. LD50 values in mice were 0.042, 0.045 and 0.052 mg/kg, respectively. All three toxins irreversibly blocked neuromuscular transmission. Abolition of responses to acetylcholine indicated a post-synaptic site of action of these toxins. The molecular weight and amino acid composition of enhydrotoxin a are similar to values earlier reported for Enhydrina toxins.

Effects of early thiamin deficiency and subsequent rehabilitation on the cholinergic system in developing rat brain.

The effects of thiamin deficiency during pregnancy and/or lactation on brain cholinergic system in rat pups were studied. Dietary rehabilitation for a period of 5 weeks from the 28th day was instituted to study possible 'catch-up' in the brain acetylcholine levels. Brain acetylcholine level was found to be significantly decreased on the 21st and 28th days in pups of the dams fed thiamin deficient diet during gestation and lactation, whereas it was decreased on the 28th day in pups of the dams fed thiamin deficient diet during lactation. Activities of cholinergic enzymes remained unaltered in both the deficient groups. Subsequent dietary rehabilitation was found to reverse the deficits in brain acetylcholine levels.

Further studies on the mechanism of rise in blood pressure and tachycardia after intraventricular administration of aconitine.

Intraventricular administration of aconitine nitrate (10 mug) consistently produced hypertension and tachycardia. Peripheral vaso-constriction due to increase in central vasomomotor tone mainly responsible for hypertension whereas stimulation of central beta-receptors with sympathoadr renal discharge responsible for tachycardia.