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Biomedical subjects

O D Gulati

Publications and source records attributed to O D Gulati.

At least 37 records · Page 2Linked to original sources

Some observations on the development of adrenergic innervation in rabbit intestine.

1 Stimulation of periarterial nerves to the ileum of 1 to 12 day old rabbits with supramaximal voltages and frequencies of 1, 2, 5, 10 and 20 Hz with square wave pulses of 2--5 ms duration for 30--40 s produced responses that were initially contractor. In the course of the first week, the responses changed from motor to inhibitory, the change occurring first at the highest rates of stimulation. By the 7th day of life, almost all responses were inhibitory. 2 The motor responses were potentiated by physostigmine and blocked by hyoscine suggesting that they were mediated by acetylcholine. 3 In preparations from rabbits older than 3 days, motor responses could be converted to inhibitory ones by prior exposure to noradrenaline (NA, 1 microgram/ml) for 20 min. This procedure also significantly increased the responses which were already inhibitory. 4 The ability of the ileum to take up NA increased with age. This uptake was blocked by cocaine. 5 The following explanations are possible: (a) changeover from cholinergic to adrenergic transmission in sympathetic fibres; (b) existence of 'parasympathetic' splanchnic nerves or a permanent cholinergic 'sympathetic' component of splanchnic nerves and (c) temporal delay in the development of adrenergic nerves (compared with cholinergic nerves) in the intestine.

Aging↗

Studies on the sympathomimetic effects of guanoxan on smooth muscles of rat.

In anococcygeus muscle and vas deferens preparations of rat, guanidinomethyl-2-benzo-(1,4)-dioxane (guanoxan) potentiated responses to norepinephrine (NF) in concentrations which exerted a neurone blocking effect. The potentiation was significantly reduced in reserpinized preparations and was abolished in the presence of nialamide. The possible mechanisms of potentiation have been discussed. Higher concentrations of guanoxan produced concentration-related contractions. The contractions were significantly less in reserpinized preparations. Phentolamine both prevented and reversed the contractions while methysergide was ineffective in this respect. Thus the effect of guanoxan appears to be mediated through the activation of alpha-receptors by the released NE.

Animals↗

3H-metaraminol releasing action of mescaline from rat hypothalamus in vitro.

The amine releasing action of mescaline was investigated in rat isolated hypothalamus labeled with 3H-metaraminol. Mescaline had no effect on the uptake of 3H-metaraminol but produced its release in a concentration-related manner. 4 x 10(-4) M mescaline, which produced submaximal effects was used for subsequent experiments. 3 x 10(-5) M cocaine had no effect on the 3H-metaraminol releasing action of mescaline. Mescaline was fully effective in Ca2+-free medium while 6 x 10(-2) M KCl was ineffective. 3 x 10(-7) M tetrodotoxin or 6 x 10(-5) M lidocaine partially blocked mescaline-induced release but substantially or completely blocked 3 x 10(-2) M KCl-induced release. Prior exposure of hypothalamus to 3 x 10(-4) M tyramine reduced the releasing action of mescaline. Thus, mescaline appears to release 3H-metaraminol both by Ca2+-independent (tyramine-like) and Ca2+-dependent (lidocaine-sensitive) mechanisms. 3 x 10(-4) M tyramine and 6 x 10(-2) M KCl released 14C from control hypothalamus labelled with 14C-mescaline, but not from reserpinized hypothalamus. The amounts of 14C recovered in 14C-mescaline labeled control and reserpinized hypothalamus at the end of 50 min of efflux were similar suggesting a poor retention of 14C-mescaline by storage particles.

Animals↗

A comparative study of the beta-adrenoceptors of guinea-pig, rabbit and rat trachea.

The sensitivity to isoprenaline of beta inhibitory adrenoceptors of tracheal chain preparations from guinea-pig, rabbit and rat was compared. For this purpose the tracheal chain preparations were contracted either with KCl or pilocarpine. Isoprenaline (1.0 X 10(-7)M--6.4 X 10(-6)M) caused concentration-related relaxation of guinea-pig trachea, whereas the rabbit and the rat trachea remained insensitive even at very high concentrations of isoprenaline (2.5 X 10(-3)M). Phenoxybenzamine (2.6 X 10(-6)M) potentiated or unmasked the relaxant effects of isoprenaline respectively in the guinea-pig or the rabbit and the rat trachea contracted with KCl. Phentolamine was ineffective in potentiating or unmasking the relaxant effects of isoprenaline. The potentiating or unmasking effects of phenoxybenzamine were absent in reserpinized preparations and lidocaine treated preparations from both guinea-pig and rat. Normetanephrine (5.4 X 10(-7)M) potentiated responses to isoprenaline only in the guinea-pig trachea. Even a 10-fold higher concentration of normetanephrine was ineffective in the rabbit or the rat rachea.

Animals↗

Amine releasing action of nicotine from rat hypothalamus in vitro.

Nicotine released 3H-radioactivity from rat hypothalamus labeled with 3H-metaraminol (3H-MA) in a concentration-related manner. The release was not blocked by hexamethonium (1.8 x 10(-5)M - 2.3 x 10(-3)m), tetrodotoxin (3 x 10(-7)M), lidocaine (6 x 10(-5)M or Ca++-free medium. Cocaine (3 x 10(-5)M) blocked the releasing action of nicotine. Nicotine failed to release 3H-MA in tissue exposed to tyramine. It is concluded that the nicotine-induced release of 3H-MA is intracellular.

Animals↗

Effects on rectal temperature in rats of gamma-aminobutyric acid; possible mediation through putative transmitters.

The rectal temperature of male rats was measured in a thermoneutral environment (25 degrees C) and at ambient temperatures of 15 and 35 degrees C. Unless otherwise specified all drugs were administered intracerebroventricularly (i.c.v.) and all results are reported for the thermoneutral environment. Exposure to 15 degrees C did not affect the rectal temperature but exposure to 35 degrees C produced hyperthermia. At 15 and 25 degrees C, 20 mug GABA produced hyperthermia which was longer lasting at the former ambient temperature. GABA (20 mug) prevented the hyperthermic effect of exposure to 35 degrees C and produced hypothermia in animals maintained at this temperature for 1 hr. A low dose (1 mug) of NA produced hyperthermia and a higher dose (mug) hypothermia. In rats pretreated with sodium salicylate (i.p.), 20 mug GABA and 1 mug NA produced hypothermia instead of hyperthermia, suggesting the release of PGE in mediating hyperthermia. The hypothermic effect of 10 mug NA and of GABA observed at 35 degrees C was blocked by phentolamine, an indication of the possibility of alpha-adrenoceptor mediation.

Aminobutyrates↗

Uptake of 3,4-dimethoxyphenylethylamine-1-14C (14C-DMPEA) by rat tissues in vitro.

Rat heart and spleen slices were incubated with 3,4-dimethoxyphenylethylamine-1-14C(14C-DMPEA) in Krebs medium at 37 C. At the end of 5-20 min of incubation, the heart did not take up the radioactivity while the spleen did. The Km and Vmax values of uptake in the spleen were 1 x 10(-4) M and 20 nmole/g per min, respectively, and the uptake was reduced to 16.0-35.1% in the cold (4 C) and to 40.3-64.0% in Na+-free medium. Thus, the uptake was an energy-dependent active process but was only partially Na+-dependent. Spleen slices incubated with 14C-DMPEA-free medium for 15 min following incubation with 14C-DMPEA retained 41.0-74.8% of radioactivity. The uptake was insensitive to norepinephrine (0.313 and 0.939 muM), dopamine (9.98 muM), 5-hydroxytryptamine (5 muM), cocaine (14.8 muM), 1-amphetamine (0.3 and 300 muM), d-amphetamine (300 muM), and normetanephrine (45.7 muM). 6-Hydroxydopamine treatment of rats, which produced 93% reduction in the splenic norepinephrine content, did not significantly reduce uptake. Thus, the uptake of DMPEA into the spleen is not by adrenergic neurones.

Amphetamine↗

Kinetics and some characteristics of uptake of noradrenaline by the human umbilical artery.

The uptake of exogenously added noradrenaline (NA) (0.5-2.5 mug/ml) by the human umbilical artery was linear with time up to 10 minutes. The uptake was saturable and could be described by the Michaelis-Menten equation. The uptake was cocaine-resistant, normetanephrine-sensitive, was considerably inhibited in the cold and was partially inhibited by Na+- deficiency. Of NA accumulated in the artery 31% could be washed out by NA-free medium. It is concluded that the mechanism of uptake of NA by the human umbilical artery is similar to the uptake2 mechanism.

Extracellular Space↗

Studies on accumulation of (14C)-mescaline in brain homogenates: effects of psychotropic and other agents.

Incubation of rat brain homogenates or 14,500 g pellet isolated from the homogenate with (14C)-mescaline was associated with accumulation of (14C)-mescaline in the pellet. 1.33 mumol/ml of chlorpromazine, trifluoperazine, fluphenazine, imipramine, desmethylimipramine, nortriptyline and amitriptyline inhibited the accumulation of mescaline. Lower concentrations (0.133-0.44 mumol/ml) of the psychotropic drugs were less effective. The tricyclic antidepressants were less potent than the tranquilizers. Although the trimethoxyphenylacetic acid (TMPA) levels of the pellet were also reduced by the psychotropic drugs, the TMPA:mescaline ratios were unchanged indicating that the drugs had no effect on the metabolism of mescaline. The inhibition of accumulation of mescaline by the high concentrations of tranquilizers may divert more of the hallucinogen to the receptor site. Thus, an explanation for the reported worsening of clinical syndrome of hallucinogenic poisoning by tranquilizers is provided.

Animals↗

Accumulation of norepinephrine (NE) by rat organs in vivo.

In anesthetized rats intravenously infused, norepinephrine (NE) was accumulated by the heart, the spleen and the lung in a dose-related manner. With the lower dose of NE (2.5 mg/kg) the organ/blood ratios were more than unity and were generally greater than with higher doses (5 and 10 mg/kg), indicating that accumulation occurred by active uptake. Nialamide and pyrogallol treatment increased accumulation in the three organs. In animals receiving nialamide and pyrogallol treatment, normetanephrine (uptake2 inhibitor) and desmethylimipramine (uptake1 inhibitor) inhibited accumulation in all the organs and the entire accumulation of NE could be ascribed to uptake1 and uptake2 processes. In these animals, phenoxybenzamine and bilateral adrenalectomy inhibited and enhanced, respectively, the accumulation in the heart and the spleen only. NE accumulated in hearts of animals in vivo could be partly washed out by perfusion with NE-free medium in vitro. Washout was prevented by normetanephrine, indicating that this effect was not a passive diffusional leakage.

Adrenal Glands↗

Analysis of the effects on body temperature of intracerebroventricular injection in anaesthetized dogs of gamma-aminobutyric acid.

1 The cerebral ventricles of dogs under intravenous pentobarbitone sodium anaesthesia, were perfused with artificial cerebro-spinal fluid (CSF) at a rate of 0.4-0.5 ml/min from the ventricular to the aqueductal cannulae. The effluent was collected from the aqueductal cannula in 20 min samples. The animals' temperatures were recorded from the rectum.2 gamma-Aminobutyric acid (GABA) 0.1-5 mg when injected into the ventricles produced variable temperature effects. Doses of 0.1 and 0.5 mg always produced hyperthermia and 1 and 5 mg doses sometimes produced hyperthermia and sometimes hypothermia.3 Intraventricular perfusion with 2-bromolysergic acid diethylamide (BOL) and hyoscine did not block hyperthermia. Tests on the rat isolated stomach strip or the guinea-pig isolated superfused ileum for the possible release, respectively, of 5-hydroxytryptamine or acetylcholine by GABA were negative.4 When tested for the presence of prostaglandin E(PGE)-like substances on the isolated rat stomach strip, both the control effluent and the GABA effluent showed activity, the latter being much more potent. There was a temporal correlation between this effect and hyperthermia. Intraventricularly administered sodium salicylate converted the GABA-induced hyperthermia to hypothermia and blocked the release of PGE-like substances.5 Hypothermia induced by GABA alone or in the presence of sodium salicylate was associated with the release of noradrenaline into the effluent.6 Intraventricular administration of GABA in reserpinized dogs produced hyperthermia and not hypothermia. Similar results were obtained with phentolamine perfusion in normal dogs.7 Perfusion with calcium-free solution blocked both the noradrenaline-releasing and hypothermic actions of GABA.8 It is concluded that hyperthermia associated with intraventricular injections of GABA is due to the release of PGE-like substance and hypothermia is due to the release of noradrenaline.

Acetylcholine↗