Centrally mediated intestinal stimulation by morphine.

A study was designed to examine the effects of intraventricularly (i.vt.) administered morphine, apomorphine and epinephrine on the small intestine. Adult cats of either sex were implanted chronically with extracellular, monopolar electrodes at equal intervals along the entire small intestine. A collison cannula was placed in the left lateral cerebral ventricle in each animal. In animals that did not respond with emesis, morphine sulfate (200 micron g) administered i.vt. increased the incidence of spike potentials over the proximal three-quarters of the small intestine almost immediately. The response to i.vt. morphine was abolished by pretreatment with i.vt. naloxone HC1 (200 micron g) and was not obtained after peripheral (i.p.) injection of morphine at the same dose effective centrall. Now change in the number of spike potentials occure after i.vt. administration of two other potent emetic agents, apomorphine HC1 (200 micron g) and epinephrine HC1 (15O micron g), in animals that did not respond with emesis. The results suggest that the increased incidence of spike potentials after i.vt. morphine is a naloxone-sensitive, centrally mediated event not associated with activation of the central emetic mechanism.