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PubMed1958

The action of dopamine on the arterial blood pressure of the guinea-pig.

The depressor action of dopamine (beta-3:4-dihydroxyphenylethylamine) upon the arterial blood pressure of the guinea-pig has been studied. This effect begins without a latent period. It is often enhanced after the intravenous injection of iproniazid (Marsilid). The depressor response is sufficiently sensitive to serve as a method of bioassay of dopamine in microgram quantities. Observations on the depressor action of L-dopa have also been made. This effect is also enhanced by iproniazid; it begins after a latent period. Epinine (beta-3:4-dihydroxyphenylethylmethylamine) caused a pressor response, followed by a fall of arterial blood pressure. No evidence was obtained in support of the suggestion that the two amines, which are oxidized at similar rates by amine oxidase, cause a fall of blood pressure after their conversion to an aldehyde by the action of amine oxidase.

Blood Pressure↗
PubMed1985

Effect of some monoamine oxidase inhibitors on the thiamin status of rabbits.

The monamine oxidase (MAO) inhibitors harmaline, tranylcypromine, deprenyl, clorgyline and iproniazid were injected intraperitoneally for five days to rabbits at doses that produced significant MAO inhibition. The first three inhibitors raised the concentrations of pyruvate and lactate in blood, decreased the activity of erythrocyte transketolase (TK) and increased the thiamin pyrophosphate (TPP) effect. The drugs also produced anorexia and loss of body weight. The changes were suggestive of an adverse effect on the thiamin status. Clorgyline and iproniazid, however, raised the blood concentrations of pyruvate and lactate but did not affect significantly erythrocyte TK activity or TPP effect. Treatment of rabbits for 14 days with the thiamin antagonists pyrithiamine (20 micrograms kg-1) or oxythiamine (0.8 mg kg-1) produced a significant drop in TK activity and increase in the lactate and pyruvate concentrations as well as an increase in TPP effect. Pyrithiamine (5, 10 or 20 micrograms kg-1, 14 days) lowered significantly the activity of MAO in the liver and brain of rabbits. Treatment with the other antagonist, oxythiamine, at doses of 0.2 or 0.4 mg kg-1 for 14 days had no significant effect on MAO activity. At a dose of 0.8 mg kg-1 a significant drop in MAO activity occurred. A pair-feeding trial indicated that the biochemical changes produced in animals treated with MAO inhibitors were attributable to the drugs per se, and not to the ensuing anorexia. Thiamin (100 micrograms kg-1, subcutaneously) when given concomitantly with pyrithiamine, oxythiamine, harmaline, deprenyl and tranylcypromine was effective in preventing the development of thiamin deficiency.

Animals↗
PubMed1985

Harmine-, LON-954- and 5-hydroxytryptophan-induced tremors in rats withdrawn from ethanol.

The tremors induced by harmine, LON-954 (N-carbamoyl-2-(2,6-dichlorophenyl)acetamidine hydrochloride) and 5-hydroxytryptophan (5-HTP) were studied in control rats and in rats withdrawn for 16-48 hrs from 6 to 9 days' ethanol administration. The frequencies and the intensities of the tremors were determined electronically. In control rats the frequency spectra of the tremors induced by harmine (20 mg/kg) and LON-954 (10 mg/kg) showed a narrow peak frequency at about 10 Hz. Atropine (1.2 mg/kg) altered neither the frequency nor the intensity of these tremors. 5-HTP (50 mg/kg) when given 3.5 hrs after iproniazid (100 mg/kg) induced tremor with peak frequencies at 6-7 Hz and 12 Hz. In ethanol-withdrawn rats treated with harmine or LON-954 the frequency analysis of tremor revealed a narrow peak frequency at about 12 Hz, which was neither the characteristic frequency of ethanol withdrawal tremor (6 Hz) nor that of harmine or LON-954 (10 Hz). The intensity of both harmine- and LON-954-induced tremor was significantly increased in ethanol-withdrawn rats. The ethanol-withdrawn rats were markedly sensitized to the effect of iproniazid+ 5-HTP, shown by deaths. The peak frequencies of this tremor were the same as those in control rats. The results suggest that harmine-induced tremor involves a dopaminergic-5-HT'ergic imbalance and the tremor induced by LON-954 a dopaminergic-cholinergic imbalance in the brain. The tremor in ethanol-withdrawn rats seems to be mediated by alterations in the activity of the cerebral 5-HT'ergic system.

5-Hydroxytryptophan↗
PubMed2003

Advancing the treatment of mood and anxiety disorders: the first 10 years' experience with paroxetine.

The last half of the 20th century witnessed remarkable advances in the field of psychiatry that began with serendipity and were realized through the combined efforts of astute clinical observation, scientific investigation, and patient advocacy. The modern era of psychopharmacology of mood disorders began in the late 1940s with John Cade's discovery of the mood-stabilizing properties of lithium.1 Less than 5 years later came the unexpected observation of elevated mood and activation among patients on a tuberculosis ward who were treated with the antitubercular agent, iproniazid. Subsequent clinical trials led to the widespread, but short-lived, use of iproniazid for treatment of depression in 1957 and demonstration of its monoamine oxidase inhibitor properties.

Antidepressive Agents, Second-Generation↗
PubMed1965

[Effect of the activity of an indirect anticoagulant by a monoamine oxidase inhibitor].

The combinations of some anticoagulants (phenindione, chlorphenadione, diphenadione, phenprocoumon, 3-[1-(p-chlorophenyl)propyl]-4-hydroxycoumarin, cumachlor and acenocoumarol) with MAO-inhibitors (phenylcyclopropylamino hydrochloride, isocarboxazid, iproniazid, nialamide and p-chloro-N'-[2-(isopropylcarbamoyl)-1-methylethyl]benzohydrazide) were investigated with regard to modification of the anticoagulant activity in the rat. The activity of some anticoagulants like phenindione may be enhanced by the addition of MAO-inhibitors, whereas others (chlorphenadione, phenprocoumon) are only slightly or not at all influenced. The MAO-inhibitors phenylcyclopropylamino hydrochloride and nialamide show enhancement of activity in most combinations whereas iproniazid never does. The other MAO-inhibitors lie between these two extremes.

Animals↗
PubMedDate not supplied

[Novel comparative profile of the clinical activity of antidepressive agents].

In order to develop practical criteria to guide in the selection of antidepressant medication according to depressive symptomatology, we propose a graphical representation of the clinical activity of 24 antidepressants according to a "star" model. Six parameters have been evaluated from 0 to 5 in comparison to reference drugs (rated 5) by 11 independent "blind" psychiatrists expert in pharmacotherapy. Three parameters were used as measures of therapeutic activity: antidepressant, psychostimulant, and anxiolytic, with iproniazide 75 mg/d, metamphetamine 15 mg/d, and diazepam 20 mg/d as reference drugs respectively. Three additional parameters assessed the level of side-effects: anticholinergic, sedative, and hypotensive, with atropine 0.75 mg/d, phenobarbital 200 mg/d, and iproniazide 75 mg/d as reference drugs respectively. The defined dose represented the standard maintenance daily dose for depressive outpatients. Mean values for each parameter, rounded off to the closest number, were used for the graphical representation. Results showed an excellent agreement among evaluators for the clinical profile of classical tricyclic and MAOI antidepressants, but serious divergences for the more recent drugs (e.g., viloxazine and mianserine), possibly reflecting more atypical or more variable clinical profile of these compounds.

Antidepressive Agents↗
PubMed1977

Influence of MAO inhibitors on uptake and release of norepinephrine in rat brain in vitro.

MAO inhibitors of diverse chemical structures were found to inhibit the uptake of 3H-NE into chopped rat cerebral cortex in vitro. The following molar (M) IC50 values to inhibit 3H-NE uptake were obtained: iproniazid, 7.9 X 10(-4)M; pargyline, 3.1 X 10(-4)M; pheniprazine, 6.3 X 10(-6)M; phenelzine, 3.9 X 10(-6)M; tranylcypromine, 2.5 X 10(-6)M; amphetamine, 2.5 X10(-7)M. In addition to decreasing deaminative catabolism, 5 X 10(-5)M amphetamine, tranylcypromine and pheniprazine plus 10(-3)M phenelzine produced a release of 3H-NE from tissue stores into incubation media. Similar concentrations of pargyline and iproniazid were ineffective to release 3H-NE from brain tissue.

Animals↗
PubMed1965

THE CONVERSION OF PYRIDOXINE PHOSPHATE INTO PYRIDOXAL PHOSPHATE IN ESCHERICHIA COLI.

1. Evidence is presented for the presence of pyridoxine phosphate oxidase in aqueous extracts of Escherichia coli. Some comparison is made with pyridoxamine phosphate oxidase. 2. Isoniazid and iproniazid were found to combine with pyridoxal phosphate, but isoniazid did not combine with either pyridoxamine phosphate or pyridoxine phosphate. Both oxidase activities were somewhat inhibited by benzylamine and putrescine, but not by phenethylamine or cadaverine. 3. The significance of pyridoxine phosphate oxidase in cell metabolism is discussed.

Amines↗
PubMed1962

Noradrenaline content in the heart and spleen of the mouse under normal conditions and after administration of some drugs.

The noradrenaline content of the heart and spleen was investigated in normal mice and in mice treated with drugs. A modification of the methods of Bertler, Carlsson & Rosengren (1958) was used for extraction, and of v. Euler & Floding (1955) for fluorimetric estimation of the amine. In normal mice the mean noradrenaline content of the heart was 0.55 mug/g and that of the spleen 0.26 mug/g fresh tissue. Iproniazid (100 mg/kg), nicotine (0.1 mg/kg) and histamine (0.5 mg/kg), given 1 and 3 hr before killing the mice, did not significantly change the concentration of noradrenaline in the heart. Neither did nicotine and histamine, administered 1 hr before death, significantly alter the noradrenaline content of the spleen. The rapid changes in the catechol amine content of mouse tissues reported with these drugs by De Schaepdryver & Preziosi (1959) were not observed. In contrast, reserpine (2.5 mg/kg), methyl reserpate methyl ether (1 mg/kg), and methyl 18-epireserpate methyl ether (2 mg/kg) caused severe depletion of noradrenaline from the heart and spleen of the mice.

Anesthetics, General↗
PubMed1964

INHIBITORS OF HISTAMINE CATABOLISM AND THE ACTION OF GASTRIN IN THE RAT.

A method is described for the partial purification of hog's antral gastrin by gel filtration and ion-exchange chromatography. Gastrin was assayed by its effect on the pH of the effluent fluid from the perfused lumen of the stomach of the anaesthetized rat. The latency of the response to gastrin given intravenously was shorter than the latency to a similar dose of histamine. The response to gastrin injected into the arterial circulation of the stomach appeared sooner than the response to gastrin injected intravenously. Iproniazid and aminoguanidine potentiated responses to gastrin. Incubation in vitro with monamine oxidase or diamine oxidase did not inactivate gastrin. Chlorpromazine and bromolysergic acid diethylamide, in doses which enhance the effects of histamine on acid gastric secretion, did not affect responses to gastrin.

Administration, Intravenous↗
PubMed1977

Production of 5-hydroxyindoleacetic acid from serotonin by cultured endothelial cells.

Endothelial cells cells from bovine aorta and human umbilical vein and fibroblasts from human foreskin were cultured and subsequently evaluated for ability to metabolize serotonin (5-HT) to 5-hydroxyindoleacetic acid (5-HIAA). Cells were incubated for three hours with 4 X 10(-6) M [14C] 5-HT creatinine sulfate. [14C] 5-HIAA was separated from labeled 5-HT by column chromatography and measured for scintillation counting. Production of 5-HIAA by bovine aorta cells was 39.0+/-7.5 (S.E.M., n=6) nmoles per 10(9) cells per hour. Production of 5-HIAA was markedly inhibited by the presence of 10(-4) M iproniazid (an inhibitor of monoamine oxidase) or 10(-4) M imipramine (an inhibitor of amine transport). 5-HIAA was the only product of 5-HT metabolism detected by thin layer chromatography. Production of 5-HIAA by human umbilical vein endothelial cells was 5.4+/-2.0 nmoles per 10(9) cells per hour (n=5) and by human foreskin fibroblasts was 3.9+/-1.4 nmoles per 10(9) cells per hour (n=5). The results obtained during incubation in the presence and absence of inhibitors indicate that bovine aorta endothelial cells maintained in tissue culture are able to transport serotonin with subsequent production of 5-HIAA. By contrast, human umbilical vein endothelial cells and fibroblasts exhibited relatively low rates of 5-HT uptake and metabolism.

Animals↗
PubMed2006

Metabolism of dopamine by the nasal mucosa.

The nasal route of administration offers several advantages over oral and intravenous administration, including the ability to avoid hepatic first pass metabolism. Dopamine deficiency has been associated with several neurological disorders; it has been shown to have good systemic bioavailability and significant uptake into the CNS following intranasal administration. The purpose of these studies was to investigate the limiting role of mucosal metabolism of dopamine during nasal absorption. In vitro transport and initial rate studies were carried out using nasal mucosal explants to study dopamine permeability and metabolism. Dihydroxyphenylacetic acid (DOPAC) was the only metabolite detected. Monoamine oxidase (MAO), the enzyme responsible for DOPAC formation, was localized to the submucosal region of the nasal explants. The amount of DOPAC formed during the transport studies was less than 0.5% of the initial amount of dopamine placed into the system. Iproniazid, an MAO inhibitor, blocked DOPAC formation but had no effect on dopamine transport. The limited extent of dopamine metabolism compared to its mucosal transport demonstrates that nasal dopamine transport is not significantly reduced by mucosal metabolism and suggests that the nasal route may be promising for the efficient delivery of dopamine to the CNS.

2,4-Dinitrophenol↗
PubMed1993

Effects of two substituted hydrazine monoamine oxidase (MAO) inhibitors on neurotransmitter amines, gamma-aminobutyric acid, and alanine in rat brain.

Time- and dose-response analyses were undertaken to investigate the effects of the substituted hydrazine monoamine oxidase (MAO) inhibitors iproniazid and nialamide on the following: MAO-A and -B activity; levels of gamma-aminobutyric acid (GABA), alanine (ALA), and the neurotransmitter amines dopamine, noradrenaline, and 5-hydroxytryptamine (serotonin) and their acid metabolites; and the activity of GABA-transaminase and ALA-transaminase. The results showed that these drugs are relatively potent MAO inhibitors but, unlike the unsubstituted hydrazine MAO inhibitor phenelzine, they do not produce increased GABA and ALA levels in brain. These experiments suggest that a free hydrazine group is necessary for MAO inhibitors to also have marked effects on GABA and ALA.

Alanine↗
PubMed1986

The effect of mixed-function oxidase and amine oxidase inhibitors on the activation of dialkylnitrosamines and 1,2-dimethylhydrazine to bacterial mutagens in mice.

The effect of the mixed-function oxidase inhibitor phenylimidazole (PI) and the amine oxidase inhibitors iproniazid (IPRO) and aminoacetonitrile (AAN) on the mutagenic activity of various carcinogens was determined in intrasanguineous host-mediated assays, using mice as hosts and E. coli 343/113 as an indicator of mutagenic activity. The carcinogenic compounds dimethyl-, diethyl-, methylethyl-, and diethanolnitrosamine (DMNA, DENA, MENA, and DELNA respectively) and 1,2-dimethylhydrazine (SDMH) were administered i.p. to mice pretreated or not with one of the inhibitors. After 4 h exposure to each of the carcinogens, E. coli cells recovered from the liver of non-pretreated mice showed considerable induction of VALr mutations; after pretreatment of the hosts with the three inhibitors, significant reduction of the amounts of induced mutants in vivo was observed. Particularly, PI proved a very efficient inhibitor of DENA, MENA, DELNA, and SDMH mutagenicity (93%-97% reduction), suggesting that these carcinogens are mainly activated by cytochrome P-450-dependent enzymes. However, since PI might also inhibit the NAD-mediated activation of DELNA by alcohol dehydrogenase (ADH), the present experiments do not rule out an additional role of ADH in the in vivo mutagenic activation of DELNA. AAN and IPRO were less and much less effective, respectively, in reducing the mutagenic activity of all compounds. Surprisingly, PI showed less inhibition of the mutagenic activity of DMNA (60% reduction), as compared to the other carcinogens; this indicates that metabolic routes other than the cytochrome P-450-dependent enzyme system may be important for the activation of DMNA.

1,2-Dimethylhydrazine↗
PubMed1979

MAO inhibition and the effects of centrally administered LSD, serotonin, and 5-methoxytryptamine on the conditioned avoidance response in rats.

Pretreatment with the MAO-inhibitors iproniazid, clorgyline, or deprenyl abolishes the effects of LSD on the conditioned avoidance response (CAR) in rats. The effects of serotonin (5-HT) and 5-methoxytryptamine (5-MT) are greatly potentiated by these substances. Brain levels of LSD are not affected by MAO inhibition whereas levels of 5-HT and 5-MT are significantly elevated. It is postulated that the decreased behavioral response to LSD is the result of 'MAO inhibitor-induced' changes whereas the increased response of 5-HT and 5-MT results from increased brain levels of these compounds.

5-Methoxytryptamine↗
PubMed1982

Effects of monoamine oxidase inhibitors on performance during differential reinforcement of low response rate.

The effects of three monoamine oxidase inhibitors (MAOI) on performance under a differential-reinforcement-of-low-rate 72-s schedule (DRL 72-s) for water reinforcement were determined. All three drugs (isocarboxazid, iproniazid, phenelzine) reduced response rate and increased reinforcement rate in rats performing under the DRL schedule. Drugs from other classes (alcohol, chlordiazepoxide, morphine, pentobarbital) did not produce similar effects. The ability of MAOI to increase reinforcement rate under a DRL 72-s schedule is similar to that recently reported for tricyclic antidepressants and the two atypical antidepressants mianserin and iprindole. These findings support the contention that the DRL schedule may be useful as a test for identifying new antidepressants and for elucidating the neurochemical effects of antidepressants that are responsible for their therapeutic actions.

Animals↗
PubMed1975

Histochemical study of monoamine oxidase latency in the liver of the rat.

In a histochemical test system with adrenaline as substrate and nitroblue tetrazolium (NBT) as electron acceptor, an increase of NBT reduction in rat liver sections was found microspectrophotometrically following short hypotonic treatment. Investigations with iproniazide, a monoamine oxidase inhibitor, and non-enzymatic NBT reduction showed that the increased formazan formation was related to the presence of monoamine oxidase. It is suggested that the reason for the observed increase of formazan formation is due to increased permeability of the inner mitochondrial membrane to NBT. Consequently, the increase of monoamine oxidase observed in the histochemical test system does not represent mobilization of a latent activity, but rather complete assessment of activity that is normally present.

Animals↗