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Biomedical subjects

R Vijayaraghavan

Publications and source records attributed to R Vijayaraghavan.

114 records · Page 7Linked to original sources
PubMedDate not supplied

Acute toxicity studies of alpha-ketoglutarate: a promising antidote for cyanide poisoning.

Recently we have shown that cyanide poisoning by the oral (p.o.) route could be antagonized significantly by pretreatment or simultaneous treatment of alpha-ketoglutarate (alpha-KG), administered p.o. in rodents. The protective effect of alpha-KG was dose dependent (0.125-2.0 g kg(-1)) and the effect was significant at a dose above 1.0 g kg(-1). In order to establish the safety of alpha-KG, various haematological, biochemical and histological parameters were studied following p.o. administration of 2.0 g kg(-1)alpha-KG in female rats, and various physiological parameters were studied following p.o. administration of 2.0 or 4.0 g kg(-1)alpha-KG in anaesthetized male rats. The p.o. LD(50) of alpha-KG in male and female rats was >5.0 g kg(-1) and no toxic signs were observed in the surviving animals. Except for an increase in plasma alkaline phosphatase and urea levels after 1 h and a decrease in inorganic phosphorus levels after 7 days of treatment, no significant change in haematology, biochemistry or histology of the vital organs were observed. Mean arterial pressure and neuromuscular transmission were decreased at 4.0 g kg(-1)alpha-KG but other physiological variables such as heart rate, respiratory rate, rectal temperature, left ventricular pressure (systolic), arterial pressure (systolic) and arterial pressure (diastolic) were not altered. The changes observed at 4.0 g kg(-1)alpha-KG are unlikely to be of toxicological concern. The results indicate that alpha-KG at 2.0 g kg(-1) (p.o.)-a dose offering maximum antidotal efficacy-is non-toxic and therefore can be considered suitable for cyanide poisoning.

Administration, Oral↗
PubMedDate not supplied

Acute toxicity of methyl isocyanate in mammals. II. Induction of hyperglycemia, lactic acidosis, uraemia, and hypothermia in rats.

When rats were administered methyl isocyanate (MIC) by inhalation or subcutaneous route it produced severe hyperglycemia, clinical lactic acidosis, highly elevated plasma urea, and reduced plasma cholinesterase activity with unaltered erythrocyte acetyl cholinesterase activity. Irrespective of the route of administration, MIC also caused severe hypothermia, which was not ameliorated by prior administration of atropine sulphate. Acute toxic effects of MIC are essentially similar by either route except for the intensity of the effects.

Acidosis, Lactic↗
PubMedDate not supplied

True giant intra-abdominal esophageal cyst.

Isolated intra-abdominal duplication cysts of foregut origin are extremely rare and are discovered incidentally. We report a 70-year-old lady with a giant, truly intra-abdominal esophageal duplication cyst. She was symptom-free one year after excision of the cyst.

Abdomen↗
PubMedDate not supplied

Inflammatory fibroid polyp of jejunum causing jejuno-jejunal intussusception.

Intussusceptions originating in the jejunum are rare. We report a 20-year-old woman who had a chronic jejuno-jejunal intussusception due to an inflammatory fibroid polyp manifesting in the post-partum period as peritonitis. Resection-anastomosis of the intussuscepted segment was done. She is well one year later.

Abdominal Pain↗
PubMedDate not supplied

DFP induced changes in acetylcholinesterase activity and glycogen level in certain brain regions of mice.

DFP in acute dose (2 mg/kg i. p.) in mice significantly inhibited acetylcholinesterase AChE) activity in five regions of brain i.e. cerebral cortex, corpus striatum, medulla, cerebellum and hypothalamus. The inhibition was accompanied by depletion of glycogen from these regions 1 hr after DFP administration. The inhibition of enzyme activity was more in corpus striatum and medulla and glycogen depletion was more in cerebral cortex in comparison to other regions of the brain. These changes may be due to stimulatory effect of DFP on these regions of brain in mice.

Acetylcholinesterase↗