Abstract
Intraventricular administration of cinchophen sodium in a dose of 2.5mg/kg which corresponds to 1/40 of the systemic dose, induced consistently a delayed rise in gastric pepsin output in the unanesthetized Heidenhain pouch dog. The gastric secretory response was more significantly suppressed by electrolytic lesions placed in the median eminence regions than by those in the middle, anterior and posterior areas of the hypothalamus.
A consistent increase in pepsin output was observed following hypothalamic implantation of 1 mg of cinchophen sodium, showing a preponderance of median eminence implants over others.
These results suggest that the median eminence is more deeply involved in the gastric pepsin secretion in response to intraventricular cinchophen than the other areas in the hypothalamus.
