The effect of mephentermine on isolated dog hearts, normal and pretreated with reserpine. (1/5)

The inotropic activity of the non-catechol sympathomimetic amine, mephentermine sulphate, on the failing dog heart-lung preparation, was 1/10 to 1/20 that of adrenaline. Mephentermine showed no inotropic effect on preparations from animals pretreated with reserpine. The chronotropic and "calorigenic" actions of mephentermine were tested on modified heart-lung preparations to permit a more accurate measurement of coronary flow, and were found to be greater than its inotropic effect relative to adrenaline. Furthermore, the action of mephentermine was longerlasting than that of adrenaline. If adrenaline was infused 15 min after the termination of mephentermine administration and when the action of the latter was still at a maximum, a further increase in heart rate and especially oxygen consumption was observed. In preparations from dogs treated with enough reserpine to deplete the heart of noradrenaline, mephentermine had only slight chronotropic and calorigenic actions. However, further addition of adrenaline after a 15 min pause caused a rise in heart rate, oxygen consumption, and coronary flow which almost duplicated the additive effects of both amines on the preparations not treated with reserpine. It would appear that adrenaline acted on its own and in addition "restored" the action of mephentermine on the reserpinized preparations. The action of adrenaline alone on reserpinized preparations was not increased compared with that on normal preparations. These observations are relevant to a consideration of the mechanism of action of non-catechol sympathomimetic amines on the heart, and are in harmony with the concept that mephentermine, a non-catechol amine, requires the presence of added or stored catechol amines for its action. Reserpine treatment did not alter the mechanical efficiency of the heart despite its depletion of noradrenaline.  (+info)

Confirming urinary excretion of mephentermine and phentermine following the ingestion of oxethazaine by gas chromatography-mass spectrometry analysis. (2/5)

Mephentermine and phentermine, substances prohibited in sports by the World Anti-Doping Agency, were found for the first time in urine specimens following the administration of a therapeutic medication, oxethazaine. In a recent sporting event, a urine specimen donor who tested positive for mephentermine and phentermine claimed consumption of Mucaine((R)) for treating stomach pain was the reason for testing positive. Five volunteers were administrated oxethazaine (a topical anesthetic found in the multi-ingredient medication Mucaine and its generic equivalent, Stoin, both of which are available in Taiwan), mephentermine, and phentermine. Excretion profiles of mephentermine and phentermine following the administration of these drugs were found to be similar. However, the mephentermine/phentermine ratios found in urine specimens collected at different time points following the administration of oxethazine and mephentermine were found to be characteristically different.  (+info)

The effect of vasopressor agents upon uterine artery blood flow velocity in the gravid guinea pig subjected to ritodrine infusion. (3/5)

The purpose of the present study was to assess the effects of intravenously administered vasopressors upon uterine artery blood flow velocity (UBFV) in the gravid guinea pig subjected to ritodrine infusion. Fourteen experiments were performed in 14 chronically instrumented pregnant guinea pigs near term. Immediately following a 1-h intravenous infusion of ritodrine (0.05-0.20, each animal received an intravenous bolus of vasopressor solution: 1) epinephrine, 0.001 mg/kg; 2) phenylephrine, 0.01 mg/kg; 3) mephentermine, 1.0 mg/kg; 4) ephedrine, 1.0 mg/kg; or 5) placebo. The experimental sequence was performed five times, so that each animal received all five solutions. The vasopressor sequence was randomly altered between animals. Infusion of ritodrine increased maternal heart rate 18 +/- 1% (P less than .0001), decreased maternal mean arterial pressure (MMAP) 4 +/- 1% (P less than .01), and decreased UBFV 5 +/- 1% (P less than .001). The four active vasopressor solutions resulted in similar, though not equivalent, increases in MMAP. Further, the MMAP response to each active vasopressor differed from the response to placebo (P less than .0001). Epinephrine and phenylephrine each significantly decreased UBFV (P less than .002). Ephedrine clearly preserved UBFV, whereas mephentermine appeared to result in an intermediate response.  (+info)

Effect of sympathomimetic drugs in eliciting hypertensive responses to reserpine in the rat, after pretreatment with monoamineoxidase inhibitors. (4/5)

1. The effects of some rapidly metabolized sympathomimetic amines, such as beta-phenylethylamine and p-tyramine, in eliciting hypertensive responses to reserpine in the anaesthetized rat, have been studied.2. Retardation of metabolism, by pretreatment with the monoamineoxidase inhibitors iproniazid or phenelzine, causes beta-phenylethylamine (which in untreated rats has no effect) to induce hypertensive responses to reserpine. Tyramine and other hydroxy substituted phenylethylamines are much less active in this respect, probably because of relatively poor lipid solubility.3. Hypertensive responses to reserpine are due to catecholamine release, which is believed to be from stores made accessible to indirectly acting sympathomimetic amines with high lipid solubility by an action of reserpine on cell membranes.  (+info)

Effects of amphetamine derivatives on brain dopamine and noradrenaline. (5/5)

1. Intracisternally administered metaraminol, alpha-methyl-octopamine, alpha-methyl-m-tyramine, and alpha-methyl tyramine were found to lower brain noradrenaline without having an effect on brain dopamine.2. Amphetamine, mephentermine, and norephedrine had no effect on brain catecholamines after intracisternal injection.3. There was no reduction in brain dopamine content after intracisternal injection of alpha-methyl-m-tyramine, yet the resulting brain concentration of alpha-methyl-m-tyramine was several times higher than after intraperitoneal injection of alpha-methyl-m-tyrosine, which decreased brain dopamine.4. The decreased synthesis of labelled catecholamines from (14)C-tyrosine after alpha-methyl-m-tyrosine suggested that this compound inhibits tyrosine hydroxylase in addition to its action of displacing brain amines.  (+info)