Ingested placenta blocks the effect of morphine on gut transit in Long-Evans rats.

Opioids produce antinociception, and ingested placenta or amniotic fluid modifies that antinociception. More specifically, ingested placenta enhances the antinociception produced by selective activation of central kappa-opioid or delta-opioid receptors but attenuates that produced by activation of central mu-opioid receptors. Opioids also slow gut transit by acting on central or peripheral mu-opioid receptors. Therefore, we hypothesized that ingested placenta would reverse the slowing of gut transit that is produced by morphine, a preferential mu-opioid-receptor agonist. Rats were injected with morphine either centrally or systemically and fed placenta, after which gastrointestinal transit was evaluated. We report here that ingested placenta reversed the slowing of gut transit produced by centrally administered morphine but did not affect the slowing of gut transit produced by systemically administered morphine. These results suggest another likely consequence of placentophagia at parturition in mammals--reversal of opioid-mediated, pregnancy-based disruption of gastrointestinal function--as well as an important consideration in opioid-based treatments for pain in humans--enhancement of desirable effects with attenuation of adverse effects.