Migrating action potential complex of cholera: a possible prostaglandin-induced response.

Abstract

Distal ileal loops of New Zealand white rabbits exposed to cholera toxin demonstrated the presence of a highly organized myoelectric pattern defined as the migrating action potential complex (MAPC). We investigated the mechanism by which cholera enterotoxin stimulates MAPC activity. Certain anti-inflammatory drugs have altered the secretory component of cholera diarrhea. We investigated effects of these anti-inflammatory drugs on the MAPC. Indomethacin, 5.0 mg/kg iv, abolished all MAPC activity. Indomethacin, 1.5 mg/kg iv, or acetylsalicylic acid, 150 mg/kg given intragastrically, altered propagation velocity and at times its direction of propagation, but did not abolish the MAPC. An infusion of prostaglandin F2alpha, 2 microng/kg per min intraluminally, induced MAPC activity similar to that of the cholera complex. Indomethacin, 5.0 mg/kg iv, produced no significant changes in number of complexes or propagation velocity. These observations suggested that inhibition of the cholera complex by indomethacin may result from the alteration of prostaglandin synthesis and that prostaglandins may initiate the motility component of cholera diarrhea.