Some cardiovascular effects of crude scorpion venom.
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Biomedical subjects
Publications and source records attributed to D K Ganguly.
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In intercollicular decerebrate cats, some of which were made spinal in addition, the effect of oxotremorine (intravenous injection, 10-30 mug/kg) was tested on antidromically activated Renshaw cells. Methylatropine premedication prevented the otherwise often fatal drop in blood pressure; ipsilateral dorsal roots L6-S1 and contralateral hindlimb nerves were cut to exclude segmental receptor interference. During supramaximal stimulation of ventral root L7 or the gastrocnemius nerves, an increase of activity ranging from 10-110% was observed. The drug occasionally evoked spontaneous discharges in Renshaw cells, or enhanced activity already present. Alpha motoneuron activity decreased in most cases. The interaction of oxotremorine with atropine and eserine was also investigated on Renshaw cells. Our results suggest that one of the effects of oxotremorine may be a disbalance between motor output and recurrent inhibition.
1. The influence of propranolol on the neuromuscular, tremor-producing and muscarinic effects of oxotremorine was examined. 2. In the isolated rat phrenic nerve-diaphragm preparation the neuromuscular blocking effect of oxotremorine was inhibited by propranolol in a dose-dependent manner. 3. Propranolol intensified the paralytic effect of tubocurarine in the rat diaphragm and prevented antagonism of tubocurarine paralysis by tetraethylammonium. 4. Propranolol was devoid of any curare-like effect in the isolated rectus abdominis muscle of the frog. 5. Vasodepressor responses to oxotremorine in rats and spasmogenic responses to oxotremorine in guinea-pig ileum were not antagonized by propranolol. 6. A dose-dependent antagonism of oxotremorine-induced tremor in mice was observed after pretreatment with propranolol and it is suggested that this effect is due to an antagonism of a presynaptic effect of oxotremorine at skeletal neuromuscular junctions.
Cycrimine hydrochloride, an anti-Parkinson drug having central cholinolytic properties, was found to cause neuromuscular blockade in the isolated rat diaphragm preparation. The neuromuscular blockade by cycrimine remained unaffected in presence of neostigmine and tetraethylammonium. Lower concentrations of cycrimine potentiated the paralytic effect of d-tubocurarine. A similar paralytic effect of cycrimine was observed in the pharmacologically denervated rat diaphragm. Responses to acetylcholine administered by retrograde i.v. injection were found to be inhibited in presence of cycrimine. These results suggest that the neuromuscular blockade by cycrimine is produced by a postsynaptic direct effect on the muscle.
In presence of dibenzyline, isoproterenol and adrenaline produced impairment of the responses of the guniea-pig urinary bladder to hypogastric nerve stimulation. Submaximal responses of isolated rat and guinea-pig urinary bladders to exogenous acytylcholine were similarly inhibited by these drugs. The inhibitory effects were reversed in presence of propranolol. The extent of maximal inhibition ranged between 60 and 80 per cent. The results provide evidence for the presence of inhibitory beta adrenoceptors in the urinary bladder of rats and guinea-pigs.
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