抄録
The previous experiments of Takasaki (1956), Takasaki et al. (1957, 1959b) have been shown that the mechanism of the reflex apnea caused by nicotine or diphenhydramine may be due to “pulmonary respiratory chemoreflex” as described by Dawes G. S. et al. (1954). Additionaly, the reflex systemic hypotension of veratrum alkaloids (Dawes, 1947, Aviado et al., 1951, Rose et al., 1957) is produced by a reflex from the lungs; it was called “pulmonary depressor chemoreflex” (Dawes et al., 1954). This was confirmed with nicotine by Takasaki (1962) . The localization of receptors responsible for this reflex may be in the lung andthis afferent path ascends in the vagi. On the other hand, it has been shown that the reflex circulatory depressor responses and the impulses from heart receptors were intercepted by intrapericardial administration of procaine or local anesthetics (Kurotubo, 1942, Hukuda, 1951, Kido, 1953). In the former experiment (Takasaki et al., 1959b), it was confirmed that the receptor in the heart is not responsible to the respiratory reflex caused by nicotine . It was also reported that the reflex apnea caused by nicotine was blocked by intravenous injection of tetraethylammonium bromide and hexamethonium bromide but not by atropine (Nakano et al., 1957, Takasaki et al., 1959a). In this report, it was done attempting that the separation of the receptors in the heart and lungs using several blocking agents administered intrapericardially and the absorption of the drugs into the systemic circulation was investigated.
