Unlabelled: An intravenous infusion of orphenadrine or imipramine to artificially ventilated, urethane anaesthetized rats, completely blocked the physostigmine induced increase in blood pressure and the blood pressure increase induced by electrical stimulation of the posterior hypothalamus; effects mediated via the sympathetic nerve. The noradrenaline induced blood pressure increase was not changed during an infusion with orphenadrine but was markedly depressed during an infusion with imipramine. During an infusion with both orphenadrine or imipramine the pressor response induced by stimulation of the spinal cord were completely blocked in pithed rats. The pattern of the blockade was comparable with the blockade of the pressor response after hypothalamic stimulation. These results show that at least in rats both orphenadrine and imipramine prevents the central stimulatory sympathetic effects on the cardiovascular system by interfering with the sympathetic nervous system. The site of action is discussed.
In Conclusion: the present results show that although physostigmine may be helpful in the treatment of central anticholinergic effects caused by overdoses of orphenadrine and imipramine it is of no use for combating the direct toxic effects of both drugs on the cardiovascular system.
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http://dx.doi.org/10.1111/j.1600-0773.1983.tb01082.x | DOI Listing |
Int J Mol Sci
March 2024
Experimental Nephrology, Department of Internal Medicine D, University Hospital Münster, 48149 Münster, Germany.
Cisplatin (CDDP) stands out as an effective chemotherapeutic agent; however, its application is linked to the development of significant adverse effects, notably nephro- and ototoxicity. The human organic cation transporter 2 (hOCT2), found in abundance in the basolateral membrane domain of renal proximal tubules and the Corti organ, plays a crucial role in the initiation of nephro- and ototoxicity associated with CDDP by facilitating its uptake in kidney and ear cells. Given its limited presence in cancer cells, hOCT2 emerges as a potential druggable target for mitigating unwanted toxicities associated with CDDP.
View Article and Find Full Text PDFDrugs Exp Clin Res
February 1992
Institute of the Psychiatric Clinic, University of Pisa, Italy.
In an attempt to clarify the possible mode of action of nefopam, a new analgesic compound, the authors tested its effects on imipramine (IMI) binding to platelet membranes. The results showed that nefopam exerted a concentration-dependent inhibition of IMI binding, with a potency comparable to that of tricyclic antidepressants. This finding suggests a possible intervention of serotonergic mechanisms in nefopam-related analgesia.
View Article and Find Full Text PDFPhoton correlation spectroscopy (PCS) has been used to examine the aggregation in aqueous NaCl solution of a series of antidepressant and antihistamine drugs (hydrochlorides of imipramine, clomipramine, amitriptyline, butriptyline, protriptyline, doxepin, dothiepin, iprindole, diphenhydramine, bromodiphenhydramine, orphenadrine) propranolol hydrochloride and propantheline bromide. Critical micelle concentrations were measured by surface tension and PCS. Micellar sizes were investigated as functions of drug structure and drug and NaCl concentration.
View Article and Find Full Text PDFActa Pharmacol Toxicol (Copenh)
March 1983
Unlabelled: An intravenous infusion of orphenadrine or imipramine to artificially ventilated, urethane anaesthetized rats, completely blocked the physostigmine induced increase in blood pressure and the blood pressure increase induced by electrical stimulation of the posterior hypothalamus; effects mediated via the sympathetic nerve. The noradrenaline induced blood pressure increase was not changed during an infusion with orphenadrine but was markedly depressed during an infusion with imipramine. During an infusion with both orphenadrine or imipramine the pressor response induced by stimulation of the spinal cord were completely blocked in pithed rats.
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