The effects of BY-1949, a novel dibenzoxazepine derivative, injected into the cerebral ventricle on noxious stimulus-induced responses of regional blood flow in the cortex and neuronal activity in the nucleus basalis of Meynert were studied in male rats. These induced responses were markedly enhanced by administration of BY-1949 (16.4 +/- 0.5 ng/100 g, S.E.M.). These data indicate that BY-1949 acts on the central nervous system to modulate the response to a noxious stimulus of regional cerebral blood flow and neuronal activity in the nucleus basalis of Meynert.

01 Apr 1992·European Journal of PharmacologyQ3 · MEDICINE

BY-1949 elicits vasodilatation via preferential elevation of cyclic GMP levels within the cerebral artery: possible involvement of endothelium-mediated mechanisms

Q3 · MEDICINE

Article

Author: Michiaki Takato ; Tohru Koide ; Makoto Sugawa

The pharmacological mechanisms by which BY-1949, a novel dibenzoxazepine derivative, increases in regional cerebral blood flow, were investigated using the canine basilar artery in vitro. BY-1949 inhibited contractions elicited by serotonin (5-HT), prostaglandin (PG) F2 alpha, endothelin and phorbol-12,13-diacetate (PDA), respectively, to the same extent. In addition, pretreatment of the artery with methylene blue significantly suppressed the vasodilating effect of BY-1949. BY-1949 also dose dependently suppressed contractions of the basilar artery induced by CaCl2 (Ca2+) in a non-competitive manner. Biochemical studies disclosed that BY-1949 significantly increased cyclic GMP without causing any apparent change in cyclic AMP. These increases in cyclic GMP were virtually abolished after the endothelial cells were removed. These results strongly suggest that the increased regional cerebral blood flow induced by BY-1949 is explicable, at least partly, in terms of a preferential elevation of cyclic GMP within the cerebral vasculature, where the endothelium plays a pivotal role.

01 Feb 1992·Brain ResearchQ4 · MEDICINE

Neurochemical correlates of selective neuronal loss following cerebral ischemia: role of decreased Na+, K+-ATPase activity

Q4 · MEDICINE

Article

Author: Michiaki Takato ; Tohru Koide ; Toshiaki Nagafuji

In order to investigate the role of Na+,K(+)-ATPase in the development of neuronal necrosis following cerebral ischemia, ischemia was induced in gerbils by occluding the common carotid artery unilaterally for 10 min. A time-course analysis revealed that significant reductions of the Na+,K(+)-ATPase activity in the cerebral cortex and hippocampus were manifested at 15 min, 30 min, and 1 h, and returned to the control level one day following recirculation. No apparent alterations of the Mg(2+)-ATPase activity, on the other hand, were obtained throughout the experimental period. Furthermore, Scatchard analyses of [3H]ouabain binding to the cerebral cortex membranes disclosed that the Bmax values invariably decreased without any change of Kd values following ischemia. It has also been shown that treatment of the animals with an agent known to mitigate ischemic neuronal necrosis, i.e. BY-1949, significantly reversed such derangements. These results suggest that the recovery of decreased Na+,K(+)-ATPase activity shortly after ischemia exerts a protective effect against ischemic brain damage.

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Indication	Highest Phase	Country/Location	Organization	Date
Cognition Disorders	Phase 2	JP	Chugai Pharmaceutical Co., Ltd.	-

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