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Biomedical subjects

S Sood

Publications and source records attributed to S Sood.

At least 163 records · Page 9Linked to original sources

Role of medial preoptic area beta adrenoceptors in the regulation of sleep-wakefulness.

The role of the medial preoptic area (mPOA) beta adrenergic receptors in the regulation of sleep-wakefulness (S-W) was investigated in this study. S-W was assessed on the basis of polygraphic recording of EEG, EMG and EOG in free moving rats. Intracerebral microinjection of beta agonist, isoproterenol, into the mPOA produced arousal. The study was also conducted on another set of rats in which noradrenergic (NE) innervation to the mPOA was destroyed by injecting 6-hydroxydopamine into the ventral noradrenergic bundle, in the brain stem. Local application of isoproterenol, into the mPOA, in these animals, did not produce any significant change in S-W. Thus, the increase in awake period obtained on isoproterenol administration was the result of its action on the presynaptic NE terminals. Possible involvement of other responses in the isoproterenol induced increase in wakefulness, is discussed.

Adrenergic beta-Agonists↗

Mechanism of antinociceptive effect of nimodipine in experimental diabetic neuropathic pain.

This study used streptozotocin-(STZ; 50 mg/kg, i.v.) diabetic rats and monitored the weekly thermal nociceptive thresholds for 8-week diabetes. Nimodipine (10 mg/kg i.p.) treatment initiated after 8 weeks of diabetes antagonized the hyperalgesic response in diabetic rats. However, insulin treatment showed a partial response in these animals. Thermal hyperalgesia showed reduced sensitivity to the antinociceptive effect of morphine (5 mg/kg, i.p.). Furthermore, a reduced sensitivity to the antinociceptive effect of baclofen (GABAB agonist; 4 mg/kg i.p.) was observed. Five days of treatment with MK-801 (N-methyl-D-aspartate [NMDA] receptor antagonist 0.5 mg/kg i.p.) completely reversed 8-week diabetes-induced thermal hyperalgesia. These data suggest that diabetes-induced hyperalgesia may be the consequence of increased excitatory tone within the spinal cord. An increased release of glutamate and activation of the NMDA receptor would maintain the hyperalgesic state. Reduced activity of both opioidergic and GABAB ergic inhibitory systems might accelerate the increased excitation, thus contributing to the ongoing pain in diabetic rats.

Analgesics↗

Effect of estrogen on hypoglycemia-induced neurological impairment in ovariectomized rats.

The risk of hypoglycemia and the resulting functional derangement of the brain are one of the major complications with stringently controlled diabetes mellitus. Ovarian steroid hormones, particularly estradiol, play a modulatory role in the ability of the female brain to utilize glucose. In the present study, the effects of estrogen on hypoglycemia-induced neurological impairment were done in ovariectomized rats. Animals received either vehicle or estradiol benzoate treatment. Hypoglycemia (Blood glucose levels <50 mg/dl) was induced in all the rats by insulin (2 U/kg, IP). Neurological functions were assessed using an 18 point scale at different time intervals of hypoglycemia. Estradiol benzoate (100 microg/kg IP) significantly (p<0.05) deteriorated the neurological functions in ovariectomized rats during hypoglycemia. The present study thus reveals that estradiol benzoate is responsible for further aggravation of neurological impairment induced by insulin hypoglycemia in female rats.

Animals↗

Effect of adenotonsillitis on peak exploratory flow rate in children.

Peak Exploratory Flow Rate (PEFR) is a simple, economical, reproducible, non-invasive test, which can be quickly performed with ease. PEFR was assessed in 36 children with adenotonsillar enlargement with mean age 10.75 years and equal number of age and sex matched normal children who acted as controls. PEFR was found to be 250. 61 +/- 66.92 lt/min in controls and 216.85 +/- 59.76 lt/min in children with adenotonsillar enlargement signifying impairment of PEFR in children in the second group.

Case-Control Studies↗

Effect of acute environmental heat stress on urinary water and electrolyte excretion in the rat.

Plasma cortisol and urinary excretion of water, sodium, potassium, calcium and magnesium have been studied in the rat after application of heat stress. There was a significant increase in plasma cortisol level after exposure to heat. During heat stress complete cessation of urine formation was observed. In the next 30 min there was statistically significant increase in the urinary excretion of water, sodium and calcium but not of potassium and magnesium. Urinary calcium/magnesium ratio was also significantly elevated. The increase in urinary water and electrolyte excretion seemed to be mediated through prostaglandins since it could be abolished by administration of indomethacin prior to the application of heat stress. On the basis of these results, the possible role of heat stress in the genesis of urolithiasis has been discussed.

Animals↗

Acute effects of neurogenic stress on urinary electrolyte excretion.

Plasma Cortisol and urinary excretion of water, sodium, potassium, calcium and magnesium have been studied in the rat after application of 2 types of neurogenic stress:--(a) tight rubber band tourniquet and (b) electric shock. Plasma cortisol levels increased significantly after application of either type of stress. During both type of stress, there was statistically significant increase in the urinary excretion of water, sodium and calcium but not of potassium and magnesium. Urinary calcium/magnesium ratio was also significantly elevated. The results suggest that stress may be one of the factors involved in the genesis of urolithiasis.

Animals↗