�ber die Wirkung von N-(3?-Phenyl-propyl-(2?))-1,1-diphenyl-propyl-(3)-amin auf den Katecholamin-Stoffwechsel

Schöne, Hans-Hermann; Lindner, E

doi:10.1007/bf01494326

Cited by 43 publications

(14 citation statements)

References 13 publications

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“…PNL is known as a drug which markedly reduces the noradrenalin content of peripheral adrenergic tissues (20), probably by interfering with the amine uptake mechanism in the storage granules in a way similar to that of reserpine (21). However, large doses of PNL do not reduce myocardial noradrenalin by more than 60%, as measured 4 h to 7 days after its injection (22).…”

Section: Discussionmentioning

confidence: 99%

Prenylamine. Autoradiographic and neuropathological studies on myocardial mechanisms of action

Milei

Faccio

1979

Clinical Cardiology

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Summary:Myocardial localization of prenylamine (PNL), a well known antianginal drug, was studied by means of an autoradiographic technique to detect microscopical distribution of tritiated PNL (3H-PLN). Forty Wistar rats received 35 .uCi/kg b. w. 3H-PNL i. p., the animals being killed 30 min after injection.Heart slices, 1 mm thick, were processed for both autoradiographic and conventional histological techniques.3H-PNL was observed, mainly, as striae along sarcolemma; sarcolemmatic/intramyocardial 3H-PNL distribution ratio was 6 : 1. Preferential membrane deposition of 3H-PNL is probably related to the calcium transport inhibiting action of the drug, previously described.

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Section: Discussionmentioning

confidence: 99%

Prenylamine. Autoradiographic and neuropathological studies on myocardial mechanisms of action

Milei

Faccio

1979

Clinical Cardiology

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“…A similar distribution of the nervous catecholamine stores in the heart can be induced by prenylamine (N(3'-phenyl-propyl-(2') -1, 1-diphenyl-propyl-(3) -amine; Segontin; Hoechst) (6), which causes a partial depletion of the catecholamine stores in the sympatho-adrenal system (7)(8)(9)(10)(11)(12). In view of these findings, cats were pretreated with prenylamine and could then be cooled to 17.8 to 17.0°C rectal temperature and subsequently rewarmed without developing ventricular fibrillation (1); in contrast to this, untreated animals always fibrillated at 22 to 19°C.…”

Section: Nielsen Owmanmentioning

confidence: 90%

“…It is notable, however, that the reduction registered after a subcutaneous injection of 20 mg/kg is not further enhanced by larger doses up to 100 mg/kg (7). Also the brain level of dopamine is lowered (10)(11)(12).…”

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confidence: 92%

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Control of Ventricular Fibrillation during Induced Hypothermia in Cats after Differential Depletion of Cardiac Catecholamine Stores with Prenylamine (Segontin)

Nielsen

Owman

1967

Circulation Research

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The role of adrenergic mechanisms for the development of ventricular fibrillation during induced hypothermia was studied in cats. Prenylamine (60 mg/kg) caused a disappearance of the adrenergic transmitter in the muscular nerves; those to the vessels were only slightly affected. Thus pretreated, animals can be cooled to 17.8 to 17°C rectal temperature, and subsequently rewarmed, without developing ventricular fibrillation. Blood pressure was maintained with metaraminol. Without pretreatment the animals constantly develop ventricular fibrillation at 23 to 18.6°C. When prenylamine was given in a dose (20 mg/kg) that does not overtly affect the norepinephrine content of the cardiac adrenergic nerves, ventricular fibrillation was not prevented. In one group of animals receiving 60 mg/kg of prenylamine, norepinephrine instead of metaraminol was infused to maintain the blood pressure during cooling. These animals developed ventricular fibrillation (or cardiac standstill). Fluorescence microscopy showed that the infusion had restored the norepinephrine content in the cardiac nerves previously depleted of their endogenous transmitter by prenylamine. The incidence of ventricular fibrillation seems to be related to the number of intact adrenergic nerves present in relation to the cardiac muscles. Hypothermia caused a distinct release of transmitter from the cardiac adrenergic nerves. ADDITIONAL KEY WORDS metaraminol adrenergic mechanisms norepinephrine• Ventricular fibrillation, usually the terminal event preceding death during induced hypothermia in homeothermic animals, is aFrom the Neurosurgical

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“…(Nielsen & Owman, 1967), or by the application of various chemicals (Lindner, 1963;Szekeres & Papp, 1971), there is no information available on the efficacy of prenylamine (or compounds, like MG 8926, of similar structure) in suppressing the early dysrhythmias that occur in the acute phase of experimental myocardial infarction. This information is of some importance since it is known that 61% of electrical deaths arising from myocardial infarction among patients younger than 65 occur within one hour of onset (Gordon & Kannel, 1971 (Schone & Lindner, 1962). This effectively reduces cardiac sympathetic drive which has been implicated in the genesis of early arrhythmias induced either by coronary ligation (Harris, Estandia & Tillotson, 1951;Harris & Bisteni, 1955;Shanks & Dunlop, 1967) or by infusion of cardiac glycosides (Dohadwalla et al, 1969).…”

Section: Anaesthetized Guinea-pigsmentioning

confidence: 99%

The Haemodynamic and Metabolic Effects of Mg 8926, a Prospective Antidysrhythmic and Antianginal Agent

Marshall

Parratt

1977

British J Pharmacology

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The antidysrhythmic, haemodynamic and metabolic effects of a new prospective antianginal and antidysrhythmic agent, N-(3,3-diphenylpropyl)-a-methyl-/B-cyclohexylethylamine hydrochloride (MG 8926), have been compared with the chemically related substance, prenylamine, in anaesthetized greyhounds and guinea-pigs. 2 When given intravenously 20 min beforehand, both MG 8926 and prenylamine (5 mg/kg) significantly suppressed the early dysrhythmias induced by coronary artery ligation in anaesthetized greyhounds. At a dose of 1 mg/kg, MG 8926 also protected anaesthetized guinea-pigs from dysrhythmias induced by ouabain infusions. 3 In dogs pretreated with MG 8926, metabolic changes indicative of myocardial ischaemia (increased Pco2 and potassium efflux, decreased oxygen content and pH) were less marked than those occurring in control animals. 4 Evidence was obtained that MG 8926, when given either before or after coronary occlusion, was capable of decreasing the severity of myocardial ischaemia as assessed by ST-segment changes in epicardial electrocardiograms.

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�ber die Wirkung von N-(3?-Phenyl-propyl-(2?))-1,1-diphenyl-propyl-(3)-amin auf den Katecholamin-Stoffwechsel

Cited by 43 publications

References 13 publications

Prenylamine. Autoradiographic and neuropathological studies on myocardial mechanisms of action

Prenylamine. Autoradiographic and neuropathological studies on myocardial mechanisms of action

Control of Ventricular Fibrillation during Induced Hypothermia in Cats after Differential Depletion of Cardiac Catecholamine Stores with Prenylamine (Segontin)

The Haemodynamic and Metabolic Effects of Mg 8926, a Prospective Antidysrhythmic and Antianginal Agent

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