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Biomedical subjects

N Subramanian

Publications and source records attributed to N Subramanian.

At least 73 records · Page 4Linked to original sources
PubMed1980

Influence of ethanol on histamine metabolism and release in the rat brain. II. Regions of the histaminergic pathway.

Following acute alcohol administration (80-160 mg/100 g body weight) histamine levels of rat brain cortex and thalamus were elevated and histidine decarboxylase activity was decreased. The effect was less pronounced after chronic alcohol treatment (15% v/v in drinking water for 4 weeks). In the striatum there was no change in the metabolic pattern of histamine. Histamine-N-methyltransferase was unaffected in either case. Depolarisation-induced release of histamine was inhibited by alcohol in the hypothalamus, thalamus and cortex. The results indicate that ethanol affects the histamine metabolism and release processes in the histaminergic pathway of the brain.

Animals↗
PubMed1979

Tetrahydronorharmane modulates the depolarisation-induced efflux of 5-hydroxytryptamine and dopamine and is released by high potassium concentration from rat brain slices.

Tetrahydronorharmane (THN), a compound which occurs in man and in rats is supposed to act as a modulator of 5-hydroxytryptaminergic neurones. It is reported here that THN stimulated the potassium-induced release of the neurotransmitter from brain slices. This suggests enhancement of the efflux as a mechanism for the 5-hydroxytryptamine-like action of THN in pharmacological experiments. Furthermore, THN decreased the potassium-evoked efflux of (3H)-dopamine. This is consistent with the inhibition of dopaminergic neurones by THN as seen previously in various in vivo experiments. Finally it is demonstrated that a high concentration of potassium evokes the efflux of (14C)-THN from brain slices. This finding suggests that THN is taken up into neurones and exerts its modulating action on serotonergic neurones either inside or outside the cell.

Animals↗
PubMed1979

Histamine-release in rat gastric mucosa by pentagastrin.

The release of histamine from isolated gastric mucosa of the rat was studied by a superfusion model. Pentagastrin increased the basal efflux of histamine in a dose dependent manner. Secretin failed to influence the release of histamine under similar conditions. The results are compatible with the view that in gastric mucosa pentagastrin releases histamine which then may react with the receptors of the parietal cell thus serving as mediator in the acid secretory process.

Animals↗
PubMed1978

Ethanol-induced alterations in histamine content and release in the rat hypothalamus.

In the rat hypothalamus, histamine content and histidine decarboxylas: activity are enhanced significantly after acute administration (80--160 mg/100g body weight) of ethanol. The effects are less pronounced after chronic treatment (15% v/v in drinking water for 4 weeks). Histamine methyltransferase is unaffected in either case. In hypothalamic slices preloaded with 3H-histamine and superfused with amine free solution the basal and K+-induced efflux of 3H-histamine are inhibited by alcohol. The inhibition of histamine release along with the increased levels of histamine may play an important role in the central effects of alcohol.

Animals↗
PubMed1978

Regional levels of histamine in rat brain after microwave irradiation: evidence for artifacts in the enzymatic--isotopic assay.

Histamine levels in the brain, measured fluorimetrically, were similar for rats killed by decapitation and microwave irradiation. However, enzymatic--isotopic assay yields 5--20 times higher value for microwave irradiation versus decapitation. Thin layer chromatography of the methylated products in the enzymatic--isotopic assay indicated the formation of artifacts following microwave irradiation. The results strongly suggest that a combination of microwave irradiation and enzymatic--isotopic assay is not suitable for histamine analysis in the rat brain.

Animals↗
PubMed1978

Lysine acetylisalicylate inhibits the protein synthesis in the rat gastric mucosa in vivo and in vitro.

Lysine acetylsalicylate (LAS), a water soluble derivative of acetylsalicylic acid and parenterally administrable analgesic, locally inhibits the incorporation of 14C protein hydrolysate into proteins of the rat isolated gastric mucosa. A similar effect on protein synthesis was observed after s.c. administration of the drug, whereas DNA and RNA synthesis were not affected. Obviously, LAS inhibits the translation step during biosynthesis of proteins. It is conceivable that this effect contributes to the potential ulcerogenic action of acetylsalicylate and that parenteral administration is not a criteria to protect the stomach from salicylate-induced side effects.

Animals↗
PubMed1978

A rapid and sensitive enzymatic-isotopic method for routine assay of histamine in blood, plasma and biopsy tissue: re-evaluation.

The enzymatic-isotopic method for determination of histamine has been reevaluated. Modifications, permitting routine analysis of the amine in blood, plasma and biopsy tissues of various origin have been described; this permits convenient application of the technique in various fields of clinical pharmacology, gastroenterology and immunology.

Biological Assay↗
PubMed1977

Modulation by histamine of the efflux of radiolabeled catecholamines from rat brain slices.

Histamine induced a dose-dependent stimulation of 3H-catecholamine(CA) efflux (superfusion procedure) from hypothalamic, striatal, hippocampal and cortical slices. The extra-hypothalamic regions were the most sensitive to histamine. Efflux of 14C-GABA and 14C-(acetyl)choline was not affected. The effect of histamine on 3H-CA efflux developed slowly, reaching its maximum after 15-20 min. Histamine was inefffective with tissue from reserpinized animals. The major part of the radioactivity released by histamine consisted of CA metabolites. Histamine apparently does not enter catecholaminergic neurons, since tyramine and the CA had no effect on the efflux of 3H-histamine previously taken up by brain slices. After incubation of slices with 3H-CA in the presence of histamine and subsequent superfusion, tyramine or K+ -depolarization induced much less 3H-CA release than from control slices not incubated with histamine. It is suggested that histamine may act as a modulator of presynaptic catecholaminergic processes in the central nervous system by causing a depletion of the transmitter stores in the nerve terminals.

Acetylcholine↗
PubMed1977

Secretin-induced histamine release in duodenal-ulcer patients.

Because a majority of duodenal-ulcer patients responded locally to intradermal secretin, skin samples from 7 patients with duodenal ulceration and 6 patients with goitre or cholelithiasis were incubated with "tris" buffer alone and with tris buffer containing 20 C.U./ml synthetic secretin or 100 microng/ml compound 48/80. Skin from duodenal-ulcer patients released significantly more histamine than did that of controls (p less 0-01). Histological examination of skin samples from these patients showed that the number of histamine-containing mast-cells averaged 5-7 per field and dropped to 1-2 per field after incubation with secretin. It is concluded that in a certain type of duodenal ulceration intradermal secretin releases histamine from mast-cells and thus induces a local anaphylactic reaction. This might prove suitable for preclinical ulcer diagnosis and/or for detection of patients at risk of acquiring that disease.

Adult↗
PubMed1977

Influence of enkephalin on K+-evoked efflux of putative neurotransmitters in rat brain. Selective inhibition of acetylcholine and dopamine release.

In rat brain slices preincubated with various radiolabelled putative neurotransmitters, methionine-enkephalin diminished the potassium-evoked release of dopamine and acetylcholine. The effect was antagonised by naloxone. The potassium-induced effux of three other neurotransmitters, histamine, 5-hydroxy-tryptamine and gamma-aminobutyric acid, were unaffected by methionine-enkephalin. A probable physiological function for the endogenous ligands in specifically affecting the catecholaminergic and cholinergic transmission is suggested.

Acetylcholine↗
PubMed1977

Acid releases motilin from human duodenum in vitro.

The effect of hydrochloric acid and sodium hydroxide on motilin release from human duodenal mucosa was studied in vitro. Tissue was incubated in 2 ml chambers continuously perfused with medium and was exposed repeatedly to the stimuli. Motilin released into the medium was determined by a specific radioimmunoassay. Whereas alkalinisation abolished basal motilin release, acidification resulted in a 14-fold increase of peptide secretion. The results indicate that motilin secretion can be stimulated in vitro and that the perfusion system described may be a useful tool in studying the mechanism of gastrointestinal hormone release.

Duodenum↗
PubMed1977

Gastric mucosal histamine in duodenal-ulcer patients: release by secretin.

In 5 duodenal-ulcer patients with anaphylactic skin reaction to intradermal secretin and in 4 healthy controls, biopsy samples from the fundic region of the stomach were superfused with phosphate buffer alone and with phosphate buffer containing 20 C.U./ml synthetic secretin. In response to secretin, the mucosa from duodenal-ulcer patients released significantly increasing amounts of histamine (P is less than 0.05) whereas control tissue did not respond. Additionally, in duodenal-ulcer patients the histamine content of untreated gastric mucosa was about twice as high as in controls (P is less than 0.02). It is suggested that the elevated mucosal histamine could account for the basal and stimulated gastric hypersecretion of duodenal-ulcer patients. In addition, the results are compatible with the concept that in a certain type of duodenal ulceration, secretin does drive rather than inhibit gastric secretion.

Adult↗
PubMed1977

Enkephalins inhibit intestinal motility: mode of action.

In the guinea pig isolated terminal ileum the opioid pentapeptides, methionine-enkephalin and leucine-enkephalin, dose-dependently inhibit contractile responses induced by electrical field stimulation releasing endogenous acetylcholine, and by specific noncholinergic compounds including histamine, barium chloride, and beta-acetyl-digoxin. Tissue levels of cAMP and cGMP remain unchanged. We conclude that enkephalins exert their effects by a direct action at or within the muscle cell and may play a physiological role in the local control of the gut smooth muscle motility.

Animals↗
PubMed1976

Potassium-induced release of tritiated histamine from rat brain tissue slices.

The release of exogenous histamine was studied by superfusing brain slices following incubation with the radiolabeled amine. Histamine was released in a calcium-dependent way by 40 mM potassium. This release was high in hypothalamus and striatum and low in hippocampus and cortex. Compound 48/80, a mast cell histamine releasing agent, also induced histamine release, but only from hypothalamic tissue slices. It is suggested that the potassium-induced release of accumulated exogenous histamine is mainly from glial cells.

Animals↗