Abstract

Experiments were carried out on 17 adult cats, each fitted with a gastric fistula and two monopolar electrodes bilaterally implanted in the midlateral or anterolateral hypothalamus (nine cats) or in the ventromedial hypothalamus (eight cats). In each cat basal gastric secretion was collected two to three times a week during a 105-min session. During the nonsession days, 24-h food intake was measured throughout the experimental period. After five control sessions, electrolytic lesions were made with DC 2 mA for 90 s bilaterally in the hypothalamus through the implanted electrodes. Two days later experimental sessions were resumed. In the majority of cats which became aphagic or hypophagic because of the lesions, gastric acid secretion was increased in the 1st week and then decreased in the 3rd and 4th week after the lesions. In half of the cats which became hyperphagic because of the lesions, gastric acid secretion was increased during the 2nd and 3rd week after the lesions; in other hyperphagic cats acid output remained unchanged or was decreased. These results support the idea that gastric acid secretion may be related to a hypothalamic system different than that controlling food intake.

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