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To determine whether the peripheral sympathetic neurons of subhuman primates are destroyed by guanacline treatment, we treated Macaca fasicularis with 2 or 20 mg/kg of guanethidine, guanacline, or the saturated analog of guanacline (SAG) 5 times per week for 4 or 12 weeks. All monkeys given 20 mg/kg of guanethidine, guanacline, or SAG showed a marked loss of neurons in the ganglia of the peripheral sympathetic nervous system. Treatment of macaques with 2 mg/kg of the guanidinium compounds resulted in patches of small-cell infiltrate, slight neuronal loss, and degenerative alterations in the sympathetic ganglia.
View Article and Find Full Text PDFGuanacline, a guanidinium adrenergic neuron blocking agent similar to guanethidine, was studied clinically and experimentally during the late 1960s. Like guanethidine, it has been reported to produce sympathetic neuronal destruction in rats. Unlike guanethidine, it has been reported to produce irreversible sympathetic deficits in man and to produce fluorescent lipopigment in rat sympathetic neurons.
View Article and Find Full Text PDFDetails are given of 17 patients who developed parotid pain during treatment with guanacline and which persisted after cessation of guanacline for upto five and a half years. These patients are compared with 17 patients who received similar treatment with guanacline and who did not develop parotid pain. There was no significant difference between patients who experienced parotid pain and those who did not with respect to sex, age, clinical diagnosis, blood urea, previous hypotensive therapy or other drugs given concurrently with guanacline.
View Article and Find Full Text PDF1 In acute experiments guanethidine was considerably more potent than guanacline in reducing contractile responses of the rat vas deferens to electrical stimulation of intramural nerves.2 Chronic treatment of rats for 19 weeks with guanethidine (5mg/kg, daily) reduced responses to electrical stimulation to 25% of control, potentiated responses to exogenous noradrenaline and depleted endogenous noradrenaline.3 After cessation of guanethidine treatment responses to electrical stimulation increased to 60% of control (in one week) but showed no further increase.
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