The effects of PGF2 alpha, PGE2 and 16, 16 dimethyl PGE2 on gastric emptying and small intestinal transit in rat.

Prostaglandins 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. Thus, studies were undertaken to determine the effect of various prostaglandins on gastric emptying (GE) and small intestinal transit (SIT) in unanesthetized fasted rats. Rats were treated with intravenous, subcutaneous, or oral PGF2 alpha, PGE2, or 16, 16 dimethyl PGE2 at various doses, followed 1 (intravenous), 20 (subcutaneous) or 10 (oral) mins later by intragastric 51Cr oxide in black ink. Forty-five mins 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 prostaglandin 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. The results of these studies show that: (1) intravenous 16, 16 dimethyl PGE2 (5-50 micrograms/kg), but not PGF2 alpha or PGE2, accelerates GE and delays SIT; (2) oral prostaglandin administration increases SIT; (3) oral 16, 16 dimethyl PGE2 delays GE; (4) subcutaneous 16, 16 dimethyl PGE2 accelerates, has no effect upon, or delays GE depending upon dose, but accelerates SIT at all doses tested; and (5) subcutaneous PGE2 accelerates SIT while PGF2 alpha does not. Thus, the effect of prostaglandins on GE and SIT depends upon the dosage and route of administration as well as type of prostaglandin used.