Detail of "61-75-6"

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Amphetamine inhibits the electrically evoked release of [3H]dopamine from slices of the rabbit caudate

Amphetamine inhibits the electrically evoked release of [3H]dopamine from slices of the rabbit caudate. Kamal, L. A.; Arbilla, S.; Galzin, A. M.; Langer, S. Z. (Dep. Biol., Lab. Etud. Rech. Synthelabo, Paris 75013, Fr.). J. Pharmacol. Exp. Ther., 227(2), 446-58 (English) 1983. CODEN: JPETAB.Several reagents with their cas registry numbers 15180-02-6 and 51-64-9 are used here. ISSN: 0022-3565. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The effects of d-amphetamine [51-64-9] on the spontaneous and elec. evoked release of 3H-labeled dopamine [51-61-6] in slices of the rabbit caudate nucleus were investigated. At a concn. of 0.1 mM, amphetamine did not modify the spontaneous outflow of radioactivity, but significantly inhibited the release of [3H]dopamine elicited elec. stimulation. At a 10-fold higher concn. (1 mM) amphetamine enhanced the spontaneous outflow of radioactivity and also inhibited the stimulation-evoked release of [3H]dopamine. Tyramine [51-67-2] and amfonelic acid [15180-02-6] in low concns. enhanced the spontaneous outflow of radioactivity and, similarly to amphetamine, inhibited the elec. evoked release of [3H]dopamine. Exposure to bretyliumtosylate [61-75-6] (1 and 10 mM) inhibited the release of [3H]dopamine elicited by elec. stimulation. In the presence of bretylium, the inhibition by amphetamine of the stimulation evoked release of [3H]dopamine was still present. In contrast to its inhibitory action on the release of [3H]dopamine, exposure to amphetamine (0.1-1.0 mM) enhanced in a concns.-dependent manner the elec. evoked release of 3H-labeled norepinephrine [51-41-2] from the rabbit hypothalamus. These results indicate that the inhibition by amphetamine of the elec. evoked release of [3H]dopamine does not involve the activation of presynaptic inhibitory dopamine autoreceptors possibly located on dopaminergic nerve terminals. This effect of amphetamine may involve an intracellular site of action that is shared by tyramine and amfonelic acid. Amphetamine may displace releasable dopamine to a nonreleasable site and/or modify the specific activities of releasable pools of dopamine. In contrast to its effects on dopaminergic neurotransmission, amphetamine enhances the elec. evoked release of [3H]norepinephrine, indicating that the drug has a differential action on dopaminergic and noradrenergic nerve terminals. .

A method for quantitating antifibrillatory effects of drugs after coronary reperfusion in dogs: improved outcome with bretylium

A method for quantitating antifibrillatory effects of drugs after coronary reperfusion in dogs: improved outcome with bretylium. Wenger, Thomas L.; Lederman, Samuel; Starmer, C. Frank; Brown, Tim; Strauss, Harold C. (Med. Cent., Duke Univ., Durham, NC 27710, USA). Circulation, 69(1), 142-8 (English) 1984. CODEN: CIRCAZ. ISSN: 0009-7322. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) A quant. approach to assess the antifibrillatory effects of short-term interventions in a canine prepn. of ventricular fibrillation caused by coronary reperfusion was developed. The method was applied in evaluating the antifibrillatory effects of bretylium tosylate [61-75-6]. Twenty-five dogs were given 10 mg/kg infusions of bretylium over 10 min. subjected to a 20 min proximal left anterior descending coronary artery ligation followed by sudden release, and compared with 25 animals given saline placebo. Drug infusion was begun 90 min before reperfusion to avoid evaluation of outcome during the phase of drug-induced catecholamine release and to allow adequate time for bretylium uptake in the myocardium. The relationship between the likelihood of ventricular fibrillation during reperfusion and the amt. of myocardium perfused by the occluded vessel (myocardium at risk) was analyzed with the logistic risk-regression model. This model was developed to control for the effects of amt. of myocardium at risk on outcome. For both the bretylium and the placebo groups the incidence of ventricular fibrillation correlated significantly with amt. of myocardium at risk. However, animals treated with bretylium had an improved outcome for a given amt. of myocardium at risk. The curve relating outcome to myocardium at risk was shifted significantly to the right. The amt. of myocardium at risk required for 50% of the placebo-treated animals to fibrillate was 20.3 g and that required for 50% of the bretylium-treated animals to fibrillate was 27.9 g, or 37% more than that for the placebo group. This logistic risk-regression anal. format permits quantification of treatment effects while accounting for variability in amt. of myocardium at risk.