Effects of L-arginine on picrotoxin-induced increase in brain ammonia concentrations and convulsions in rats.

The effect of L-arginine (840 mg/kg) pre- (30 min before challenge) and post-treatment (5 min after challenge) period was tested on picrotoxin-induced increase in ammonia concentrations in brain regions (cerebral cortex, brain stem and cerebellum) and the accompanying convulsive responses in adult male rats. The combined effect of L-arginine and diazepam was also tested against picrotoxin-induced convulsions. Picrotoxin-induced increase in ammonia was reverted partially by L-arginine pretreatment. However, L-arginine pretreatment did not show anticonvulsant effect independently or concurrently with diazepam. On the other hand, L-arginine post-treatment reverted ammonia to control level in all brain regions. A partial but significant inhibition of convulsion responses was found in these animals. The combined effect of diazepam and L-arginine post-treatment was much greater than that produced by these agents independently. These findings suggest that ammonia has a partial but significant participation in the convulsant action of picrotoxin. L-arginine has a potential to revert brain ammonia to control level in picrotoxin-treated animals and thereby it has produced a partial protection. The data further indicate that the duration of action of L-arginine is considerably short and has an additive anticonvulsant action with diazepam.

Independent and combined effects of L-arginine and diazepam on ammonium chloride-induced convulsions in rats.

The independent and combined effects of L-arginine (840 mg/kg) and diazepam (0.75 mg/kg) pretreatment (30 min) were tested on ammonium chloride (400 mg/kg)-induced convulsions in rats. Ammonia concentrations were determined in blood and brain regions (cerebral cortex, brain stem and cerebellum) 30 min after L-arginine or diazepam treatment. Ammonia concentrations were measured at the time of induction of convulsions by ammonium chloride in L-arginine, diazepam or saline pretreated animals. L-arginine and not diazepam decreased ammonia concentrations in control as well as in ammonium chloride-treated animals. However, both the compounds suppressed convulsions elicited by ammonium chloride. Protection produced concurrently by these agents was much greater than that produced by them independently. It is concluded that convulsions caused by hyperammonemic condition can be suppressed either by preventing a rise in brain ammonia to toxic level or by anticonvulsant agents having a GABA potentiating action. A much greater protection can be achieved if agents having these properties are administered concurrently.

Peripheral immune response in albino rats following cerebroventricular and intraperitoneal antigen challenge.

Success in neural tissue transplants at central nervous system suggest that the site may be immunologically privileged. However, this experimental study in which an antigen (Sheep Red Blood Cells) was administered into the third ventricle does not support the above concept. The antibody titre and soluble immune complex levels seen in these animals are similar to the levels seen in animals immunized with the same amount of antigen through the intraperitoneal route. Intraventricular immunization is rather a more potent modulator in decreasing the total WBC count (P < 0.05) and neutrophils (P < 0.001). Further a marked increase in lymphocytes (P < 0.01) in peripheral blood was observed in these animals. Intraventricular immunization also increased the killing power (NBT reduction) of the neutrophils (P < 0.05).