Detail of "23887-46-9"

Reference

The purinergic nerve ending: experimental contributions

The purinergic nerve ending: experimental contributions. Lampa, E.; Caputi, A. P.; Rossi, F.; Vacca, C.; Brita, G.; Giordano, L.; Rosatti, F.; Marmo, E. (I Fac. Med. Chir., Univ. Napoli, Naples, Italy). Rend. Atti Accad. Sci. Med. Chir., 130, 175-223 (Italian) 1976. CODEN: RSMCA7. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) After a review of the purinergic system, data are given on the effects of .apprx.35 drugs on this system, as detd. by their action on adenosinase [9075-41-6] in dog serum and on various pharmacol. responses to adenosine (I) [58-61-7] in vivo and in vitro (hypotension in rats and dogs, effects on the isolated frog heart, cardiac effects in rats, and effects on the isolated duodenal and uterine musculature of rats and mice). The methylxanthines, quinidine [56-54-2], phenotolamine [50-60-2], and chlorpromazine [50-53-3] were considered as competitive antagonists of I at the purinergic receptors, whereas .beta.-adrenolytic drugs and drugs typically used to treat coronary insufficiency, (hexobendine [54-03-5], cinepazide [23887-46-9], and dipyridamole [58-32-2]), were adenosinase inhibitors and hence purinergic agonists. The efficacy of these drugs in treating coronary insufficiency may be related to their ability to increase coronary purinergic reactivity.

Protective action of vinpocetine against cerebral ischemia and anoxia

Protective action of vinpocetine against cerebral ischemia and anoxia. Nagaoka, Akinobu; Miyamoto, Masaomi; Hamajo, Kazuhiro; Kiyota, Yoshihiro (Cent. Res. Div., Takeda Chemical Ind., Ltd., Japan). Yakuri to Chiryo, 12(7), 2867-71 (Japanese) 1984. CODEN: YACHDS. ISSN: 0386-3603. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The protective action of vinpocetine (I) [42971-09-5] against cerebral ischemia and anoxia was investigated in stroke-prone spontaneously hypertensive rats (SHRSP) and in mice. The cerebral ischemia was produced by bilateral occlusion of the common carotid arteries in SHRSP, and cerebral anoxia was induced by CO2 inhalation in mice. At 1 mg/kg, i.p., vinpocetine delayed the onset of ischemic seizure in the SHRSP, and at 1-5 mg/kg, i.p., it also prolonged the survival time of the mice in a dose-dependent manner. Other drugs that cause cerebral vasodilation and improve cerebral metab. were similarly investigated, using dosages detd. by considering clin. dosages and the effective dosage of vinpocetine. However, these drugs: dihydroergotoxine [11032-41-0], cinepazide [23887-46-9], nicardipine [55985-32-5], cinnarizine [298-57-7], brovincamine [57475-17-9] and ifenprodil [23210-56-2] were not effective in either situation.