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Results for “Dibenzylchlorethamine”

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At least 19 recordsLinked to original sources
PubMed1980

Protection against adrenochrome-induced myocardial damage by various pharmacological interventions.

Perfusion of the isolated rat heart with Krebs-Henseleit solution containing adrenochrome (25 or 50 mg/l), and oxidation product of catechalmines, resulted in contractile failure and myocardial necrosis. Various pharmacological agents known to protect the myocardium against catecholamine-induced necrosis were also found to be effective against adrenochrome-induced changes in the ultrastructure of the isolated perfused rat heart. The alpha-receptor-blocking drugs tolazoline and Dibenamine (dibenzylchlorethamine), and the adrenergic neurone-blocking agents guanethidine and bretylium did not alter the development of contractile failure and necrosis due to adrenochrome. The beta-receptor-blocking compounds propranolol and practolol effectively protected the heart from adrenochrome-induced necrotic damage, and partially prevented contractile failure. The hydrazine-type monoamine oxidase inhibitor iproniazid completely prevented ultrastructural damage and partially maintained contractile-force development in adrenochrome perfused hearts. The non-hydrazine-type monoamine oxidase inhibitor tranylcypromine partially protected the isolated rat heart against adrenochrome necrosis, but disruption of mitochondrial structure was still seen. Tranylcypromine did not significantly improve contractile force development during adrenochrome perfusion. The calcium antagonist D-600 reduced the severity of adrenochrome-induced ultrastructural damage. These results provide strong support for the view that catecholamine-induced cardiotoxicity is mediated through the formation of adrenochrome.

Adrenochrome↗
PubMed1998

Mineralocorticoid receptor-mediated enhancement of neuronal excitability and synaptic plasticity in the dentate gyrus in vivo is dependent on the beta-adrenergic activity.

The dentate gyrus neurons in the hippocampus contain a high density of both mineralocorticoid and adrenergic receptors. By in vivo extracellular recording from adrenalectomized rats we investigated the possible relationships between the two systems with regard to neuronal excitability and activity-dependent synaptic plasticity. Pretreatment with aldosterone significantly enhanced both basal neuronal excitability and tetanically evoked synaptic plasticity in adrenalectomized, but not sham-operated rats. The enhancement was blocked by spironolactone, indicating a mineralocorticoid receptor-dependent effect. The adrenomedullary hormone epinephrine also significantly enhanced synaptic plasticity via activation of beta-adrenergic receptors. Beta-adrenergic antagonist propranolol, infused directly into the dentate gyrus granule cell layer, significantly reduced the effect of aldosterone on neuronal excitability and partly canceled the aldosterone-enhanced synaptic plasticity. No effect of propranolol was found after its amygdaloid infusion. The mineralocorticoid receptor antagonist spironolactone did not affect the epinephrine-induced effects. These results indicate that the pretreated adrenal steroids interact with the catecholaminergic system in the dentate gyrus of adrenalectomized rats and that the functional beta-adrenergic pathway is involved in the mechanism of mineralocorticoid-induced cellular effects in vivo.

Adrenalectomy↗
PubMed1979

13C-NMR spectra of alpha-adrenergic blocking agents.

The natural abundance 13C-NMR spectra of five alpha-adrenergic blocking agents, tolazoline, dibenamine, azapetine, phenoxybenzamine, and phentolamine, are reported. The chemical shifts of various carbon resonances were assigned on the basis of chemical shift theory, multiplicities observed in single-frequency off-resonance-decoupled spectra, relaxation times, and comparisons with the chemical shifts of model compounds.

Adrenergic alpha-Antagonists↗
PubMed1976

Autonomic and pharmacological control of oxygen autoregulation mechanisms in brain tissue.

The effect of several agents active on autonomic nervous system functions was tested on brain oxygen autoregulation parameters. It was found that atropine, propranolol and isproterenol had no influence on the measured parameters. Phenoxybenzamine, tolazoline and dibenamine all suppress autoregulation. In an additional experimental series, a phenoxybenzamine infusion was given during O2 breathing. The infusion induced a marked rise in TpO2. It is concluded that an alpha-adrenergic mechanism is part of the autoregulation process, and its pharmacological blockade could be used to raise TpO2 levels in brain with O2 breathing at normal atmospheric pressure. Also, the increase in brain TpO2 induced by 95% O2 - 5% CO2 breathing seems to be blocked by alpha-adrenolytic drugs.

Animals↗
PubMed1988

Involvement of the sympathetic nervous system in the cardiovascular effects of ACTH-(1-24) during hemorrhagic shock in rats.

In urethane-anesthetized rats, removal of about 50% of the total blood volume over a period of 25-30 min caused hypovolemic shock, with extreme hypotension (MAP = 18-25 mm Hg and death of all animals within 22 +/- 5 min. The i.v. injection of ACTH-(1-24) in the dose range of 40-160 micrograms/kg induced a sustained, dose-dependent, and, at the highest dose used, an almost complete recovery of blood pressure, and 100% survival, at least for 2 h after treatment. The effect of ACTH-(1-24) was completely prevented by reserpine (5 mg/kg) and clonidine (0.1 mg/kg), significantly reduced by prazosin (0.1 mg/kg), dibenamine (15 mg/kg) and i.v. yohimbine (1 mg/kg) and unaffected by i.c.v. yohimbine (0.2 mg/kg) and i.v. practolol (15 mg/kg). These data suggest that the effect of ACTH-(1-24) in hypovolemic shock depends on the functional integrity of the sympathetic nervous system and is mediated through an activation of peripheral alpha-adrenoceptors.

Animals↗