Detail of "1937-89-9"

Reference

Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts

Effects of antiarrhythmic drugs on the extraneuronal accumulation of isoprenaline in perfused rat hearts. Sono, Kazumi; Akimoto, Yoshinobu; Kurahashi, Kazuyoshi; Fujiwara, Motohatsu (Fac. Med., Kyoto Univ., Kyoto 606, Japan). Naunyn-Schmiedeberg's Arch. Pharmacol., 334(2), 145-8 (English) 1986. CODEN: NSAPCC. ISSN: 0028-1298. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The effects of class I, II, III, and IV antiarrhythmic drugs (as classified by Vaughan Williams 1974), tetrodotoxin [4368-28-9] and b2-adrenoceptor antagonists on the extraneuronal accumulation of (±)-isoprenaline [149-53-1] were examd. in isolated rat hearts perfused with [3H]isoprenaline (1 mM) and tropolone (100 mM) for 30 min at a const. flow rate (6.5 mL/min) at 40°. Quinidine [56-54-2] (class I), (±)-verapamil [56949-77-0] (IV), (+)-diltiazem [42399-41-7] (IV), dilazep [35898-87-4] (IV), nifedipine [21829-25-4] (IV), tetrodotoxin and (±)-butoxamine [1937-89-9], at a concn. of 10 mM significantly decreased the extraneuronal accumulation of isoprenaline. The present study demonstrated that quinidine (class I) and all of the Ca2+-channel blockers (class IV) had potent inhibitory effects on the extraneuronal accumulation of isoprenaline. The concns. of these drugs needed for this decrease were nearly comparable to those needed to suppress isoprenaline-tropolone-induced ventricular fibrillation. The antiarrhythmic effects of quinidine and Ca2+-channel blockers in this exptl. model may be partly due to a decrease in the extraneuronal accumulation of isoprenaline.Except for chemicals metioned above, 23846-70-0 and 61-75-6 are also used. .

In vivo protection of normal mouse hematopoiesis by a b2 blocking agent during S-phase chemotherapy

In vivo protection of normal mouse hematopoiesis by a b2 blocking agent during S-phase chemotherapy. Dresch, C.; Minc, J.; Mary, J. Y. (Hop. St.-Louis, Paris 75475, Fr.). Cancer Res., 44(2), 493-7 (English) 1984. CODEN: CNREA8. ISSN: 0008-5472. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Butoxamine [1937-89-9] depressed the granulocyte-labeling index and granulocyte-monocyte colony-forming Cell (GM-CFC) suicide rate in mice at a dose of 3 mg/g. A max. effect was obsd. 6-12 h after injection. Butoxamine administered 8 h before an injection of ara-C [147-94-4] modified the proportion of GM-CFC in S-phase as compared with the no. found after ara-C alone. After a series of 5 ara-C injections, administered at intervals of 16 h, 70% of the treated mice died within 2 wk, whereas only 42% of mice pretreated with butoxamine 7-9 h before each ara-C injection died. This difference was due to the more rapid return to normal of GM-CFC nos. and an increase in the proportion of GM-CFC and granulocyte precursors in S-phase in the butoxamine-pretreated animals. Thus, butoxamine may have a potential use in protecting hematopoiesis during intensive cancer chemotherapy.