Indian journal of experimental biology
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Indian J. Exp. Biol. · Apr 1995
Possible involvement of superoxide radical in biochemical lesions induced by nitrous oxide.
Inactivation of methionine synthase (MS) by nitrous oxide (N2O) administration to animals and man has been postulated to be mediated by hydroxyl radical (OH). An alternate mechanism has been proposed which involves superoxide radical (O2.-) originating from N2O in the inactivation of MS by OH that may arise from O2.- through Fenton/Haber-Weiss reaction. ⋯ Pretreatment of rats with superoxide dismutase (SOD) at two doses, 0.1 mg and 3.5 mg/100 g body weight, retarded the in vivo inactivation of MS by N2O, to 76% and 47% respectively. In vitro inactivation of MS with N2O could not be retarded by DMSO or Na-benzoate, or either exogenous SOD or catalase.
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Indian J. Exp. Biol. · May 1994
Effect of nifedipine, a calcium channel inhibitor, on sedation produced by reserpine, clonidine and propranolol in mice.
Spontaneous motor activity, rotarod test and observational rating of sedation were employed to study effect of nifedipine on sedation produced by reserpine, clonidine and propranolol. Reserpine (2 mg kg-1), clonidine (4 mg kg-1), and propranolol (40 mg kg-1) significantly reduced spontaneous motor activity and staying capacity of animals on accelerating rotarod (P < 0.01). Observational sedation was also caused significantly as indicated by a higher score in test. ⋯ Nifedipine did not oppose the sedation produced by propranolol which actually became significantly greater in the animals pretreated with nifedipine in all three tests. It is concluded that nifedipine antagonizes the sedation produced by reserpine and clonidine, probably by blocking central alpha 2-adrenoceptors. The sedative effect of propranolol can be potentiated by nifedipine possibly because of a pharmacokinetic interaction.
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Indian J. Exp. Biol. · Feb 1989
Changes in noradrenaline and histamine in monkey spinal cords traumatised by weight drop, compression and subsequent decompression.
Levels of noradrenaline (NA) and histamine (H) in the spinal cord of monkeys at 8, 24 and 48 hr following 200 g/cm contusion injury, 50 g of compression injury at 8 hr and decompression for 16 and 40 hr following 8 hr of compression were studied in the traumatised and in an adjacent non-traumatised segment. The NA level doubled in the traumatised and non-traumatised segments at 8 hr contusion injury followed by a slow decline to control values at 24 and 48 hr of contusion injury. There was no change in NA content of the spinal cord segments at 8 hr of compression injury. ⋯ H levels decreased in the traumatised and non-traumatised segments at 24 and 48 hr of contusion injury. Compression for 8 hr elevated H in the traumatised and non-traumatised segments. On decompression H level was further increased in the traumatised segment.