THE EFFECTS OF PGF2-ALPHA, PGE2 AND 16, 16 DIMETHYL PGE2 ON GASTRIC-EMPTYING AND SMALL INTESTINAL TRANSIT IN RAT

Prostaglandins [PG] are well known for their ability to stimulate contraction in gastrointestinal smooth muscle, yet very little information is available on how their activity affects propulsion in vivo. The effect of various PG on gastric emptying (GE) and small intestinal transit (SIT) was investigated in unanesthetized fasted rats. Rats were treated with i.v., s.c., or oral PGF2.alpha., PGE2, or 16,16-dimethyl PGE2 at various doses, followed 1 (i.v.), 20 (s.c.) or 10 (oral) min later by intragastric 51Cr oxide in black ink. Forty-five min later, rats were sacrificed by CO2 asphyxiation, the pylorus clamped, and the gut excised. SIT was expressed as the percent of intestinal length traveled by the most distal portion of ink. GE was expressed as the percent of the 51Cr emptied into the intestines. If GE was affected by PG treatment, the experiments were repeated with rats pre-implanted with duodenal cannula. This preparation allowed the visual transit marker to be deposited directly into the duodenum, thus avoiding acceleration or delay of SIT caused by fluctuations in GE. I.v. 16,16-dimethyl PGE2 (5-50 .mu.g/kg), but not PGF2.alpha. or PGE2, accelerated GE and delays SIT. Oral PG administration increases SIT. Oral 16,16-dimethyl PGE2 delays GE. S.c. 16,16-dimethyl PGE2 accelerates, has no effect upon, or delays GE depending upon dose, buy accelerates SIT at all doses tested. S.c. PGE2 accelerates SIT while PGF2.alpha. does not. The effect of PG on GE and SIT depends upon the dosage and route of administration as well as type of PG used.