Search PubMed⌕ Search

Biomedical subjects

L Cherian

Publications and source records attributed to L Cherian.

43 records · Page 3Linked to original sources

Gangliosides, or sialic acid, antagonize ethanol intoxication.

Because ethanol elicits a dose-dependent hydrolysis of brain sialogangliosides, we tested the possibility that injected gangliosides might antagonize intoxicating doses of ethanol. Clear anti-intoxication effects were seen at 24 hr post-injection of mixed mouse-brain gangliosides at 125-130 mg/kg, but not at lower or higher doses. Sleep time was reduced on the order of 50%, and roto-rod agility was significantly enhanced. Sialic acid (SA) similarly antagonized ethanol; however, the precursor of SA, N-acetyl-D-mannosamine, as well as ceramide and asialoganglioside did not.

Alcohol Deterrents↗

Alpha noradrenergic agonists promote catalepsy in the mouse.

Alpha adrenergic receptors are important in motor control. Adrenergic drugs reportedly modulate the catalepsy caused by other agents, such as opiates and neuroleptics. We tested a variety of adrenergic agonists and blockers in a nondrug, mouse model of catalepsy. A major cataleptic effect was produced by both alpha agonists, phenylephrine (0.5 to 3 mg/kg, IP) and clonidine (0.5 to 2 mg/kg), and this catalepsy was antagonized by pretreatment with both of the respective antagonists, phenoxybenzamine (alpha-1) and yohimbine (alpha-2) (p less than 0.0001). The mixed beta agonist, isoproterenol (2 mg/kg), appeared to have a minor cataleptic effect, and this was abolished by beta antagonist. Open-field locomotor scores during the same treatments revealed that catalepsy and hypokinesia are dissociable.

Adrenergic alpha-Agonists↗

In vitro stimulation of pancreatic enzyme discharge by calcium.

The mechanism for acute hypercalcaemia increasing pancreatic enzyme secretion is unknown. To determine if raised extracellular calcium concentrations can directly stimulate pancreatic enzyme output, we measured discharges of pulse labelled protein and chymotrypsin from isolated cat pancreatic lobules in the presence of normal and raised calcium concentrations. Incubation in 5.0 mmol/l calcium increased discharges of pulse labelled protein (four fold), chymotrypsin (2.5 fold) and amylase (2.2 fold), compared with control experiments with 2.5 mmol/l calcium (p less than 0.001). This effect was similar to the maximal effect of carbachol or caerulein. Compared with 5.0 mmol/l calcium, incubation at the higher calcium concentration of 10.0 mmol/l induced similar discharges of chymotrypsin and amylase, whereas the increase in discharge of pulse labelled protein was smaller (p less than 0.01). The effects of raised calcium were not altered by atropine. Incubation in a high calcium medium did not impair pancreatic acinar response to subsequent stimulation with carbachol, but incubation in hypothermia abolished the effects of high calcium concentrations, suggesting that increased enzyme discharge is caused by stimulation of secretion not to cell damage. These data are consistent with a direct stimulatory effect of raised extracellular calcium concentrations on pancreatic acinar cell function.

Animals↗

Ethanol effects on total sialic acid of various brain regions and visceral organs.

These experiments were designed to extend our earlier observations on acute ethanol effects on brain sialic acid (SA), an acidic sugar component of membrane gangliosides and many glycoproteins. Here, we tested for differential effects of ethanol on total sialic acid in various brain regions and for effects on other organs, such as liver, kidney, heart, and skeletal muscle. Subjects were young adult, male rats. The first experiment compared two commonly accepted analytical methods for brain SA on peripheral tissues. Consistently higher levels were evident with the resorcinol method in all tissues, especially in liver, compared with the thiobarbiturate method. Resorcinol-measured levels in the liver and kidney were on the order of 350 micrograms/g, wet weight. In the brain of controls, the resorcinol method revealed total SA levels to be on the order of 550-650 micrograms/g in the basal ganglia, cerebral cortex, cerebellum, and hippocampus. Brainstem levels were significantly lower. Ethanol, given IP at 2 g/kg, seemed to decrease total SA in all brain regions at four hours after injection, with statistically significant decreases in the hippocampus and brainstem. With 3 g/kg, only the cerebellum showed a significant decrease at four hours, compared to saline-injected controls, but the decrease was large (25%). Analysis of the other organs showed that, compared to saline-injected controls, ethanol decreased SA in the liver. There was a small, but significant, decrease in heart SA at four hours after 3 g/kg. In skeletal muscle, ethanol significantly increased total SA at 2 g/kg, but not at 3 g/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗