. Ingestion ofllmnioticfluid enhances opiate analgesia in rats. PHYSIOL BEHAV 38(6) [809][810][811][812][813][814][815] 1986.-Placenta ingestion has recently been shown to enhance opiate-mediated analgesia produced by morphine injection, footshock, or vaginal/cervical stimulation. The enhancement of the effect of endogenous opiates (especially analgesia) may be one of the principal benefits to mammalian mothers of placentophagia at delivery. During labor and delivery, however, mothers also ingest amniotic fluid (AF) which, unlike placenta, becomes available during, or even before expulsion of the infant. The present experiments were undertaken to determine (a) whether AF ingestion, too, enhances analgesia; if so, (b) whether the effect requires ingestion of, or merely exposure to, AF; (c) whether the effect can be produced by AF delivered directly to the stomach by tube; and (d) whether the enhancement, if it exists, can be blocked by administering an opiate antagonist. Nulliparous Long-Evans rats were tested for analgesia using tail-flick latency. We found that (a) rats that ingested AF after receiving a morphine injection showed significantly more analgesia than did rats that ingested a control substance;' (b) AF ingestion, alone, did not produce analgesia; (c) ingestion of AF, rather than just smelling and seeing it, was necessary to produce analgesia enhancement; (d) AF produced enhance ment when oropharyngeal factors were eliminated by delivering it through an orogastric tube; and (e) treatment of the rats with naltrexone blocked the enhancement of morphine-induced analgesia that results from AF ingestion. . Furthermore, placenta does not seem to contain a substance that, by itself, is analgesic, since in gestion of placenta in the absence of an analgesia-producing treatment does not elevate pain threshold [15,16]. We have also demonstrated that the analgesia-enhancing effect of placenta ingestion seems to be specific to opiate-mediated analgesia, since treatment with naltrexone, an opiate antagonist, not only attenuates the analgesia produced by footshock, as expected, but also blocks the enhancing effect of placenta ingestion [15]. Endogenous opiate levels rise during pregnancy and de livery in both humans and rats [4,6,9,12,13,[19][20][21][22][23]. Pain threshold has been observed to rise over the course of preg nancy in rats, and this "analgesia of pregnancy" has been demonstrated to be opiate mediated [1,7,8]. Enhancement of such analgesia, therefore, may be one of the principal benefits of parturitional placentophagia, and, in contrast to other hypotheses about advantages (e.g., nest hygiene, mother-infant attachment, reduction of predator-attracting stimuli [14,17]), this hypothesis suggests a benefit that would apply to virtually all species of mammals.However, if placenta, alone, contains the substance that enhances opiate-mediated analgesia during the perinatal period, the fact that placenta is delivered after the neonate (anywhere from 5 to 75 min after) would render it effective only during th...
. Dose-dependent enhancement oJmorphine-induced analgesia by ingestion oj amniotic fluid and placenta. PHARMACOL BIOCHEM BEHAV 31(2) [351][352][353][354][355][356] 1988.-Ingestion of amniotic fluid and placenta by rats has been shown to enhance opioid-mediated analgesia. The present studies were designed to examine the effect of several doses and volumes of placenta and amniotic fluid on tail-flick latency in rats treated with 3 mg/kg morphine. The optimal dose of amniotic fluid was found to be 0.25 ml, although 0.50 and 1.0 ml also produced significant enhancement. Doses of 0.125 and 2 ml of amniotic fluid were ineffective, as was a dose of 0.25 ml diluted to 2 ml with saline. The optimal dose of placenta was found to be 1 placenta, although the resulting enhancement was not significantly greater than that produced by 0.25, 0.50, 2.0 or 4.0 placentas. Doses smaller than 0.25 placenta or larger than 4.0 placentas were ineffective. The most effective doses of amniotic fluid and placenta correspond to the amounts delivered with each pup during parturition.
A substance in amniotic fluid and placenta (POEF for Placental Opioid-Enhancing Factor) has been shown to enhance opiate- or opioid-mediated analgesia in rats. Recent studies have only touched on the generalizability of the phenomenon. The present studies further tested the generalizability of the POEF effect: they examined sex specificity of the mechanism; whether POEF activity exists in afterbirth material of species other than the rat; whether POEF activity exists in tissue other than afterbirth material; whether POEF activity could be demonstrated after injection rather than ingestion of afterbirth material; and whether POEF enhances all opioid-mediated phenomena. We found that (a) POEF is effective in male rats as well as in female rats; (b) POEF activity exists in human and dolphin afterbirth material; (c) ingestion of pregnant-rat liver does not produce enhancement of opioid-mediated analgesia; (d) POEF does not seem to be effective when amniotic fluid is injected either IP or SC; and (e) POEF does not modify morphine-induced hyperthermia.
Amniotic fluid and placenta contain a substance (POEF, for Placental Opioid-Enhancing Factor) that, when ingested, enhances opioid-mediated analgesia in nonpregnant rats; ingestion of the substance by rats not experiencing opioid-mediated analgesia, however, does not produce analgesia. It is highly likely that periparturitional analgesia-enhancement is a significant benefit of ingestion of the afterbirth (placentophagia) during delivery. Here we report that prepartum ingestion of amniotic fluid (via orogastric infusion) does indeed enhance the endogenous-opioid-mediated analgesia evident at the end of pregnancy and during delivery; that the degree of enhancement is greater with 0.75 ml than with 0.25 ml; and that the prepartum enhancement of analgesia can be blocked with the opioid antagonist naloxone.
A substance in amniotic fluid (AF) and placenta has been shown to enhance analgesia produced by morphine, late pregnancy, footshock, and vaginal/cervical stimulation (VS). When morphine-induced analgesia was assessed previously, the degree of enhancement by ingestion of AF or placenta was found to be a function of the amount of analgesia being generated. We have extended these results to include the analgesia produced by VS. Analgesia induced by 75, 125, 175, or 225 g of vaginal/cervical pressure was measured in rats pretreated with 0.25 ml (by orogastric infusion) of either AF or saline. AF infusion enhanced the analgesia produced by 125 g VS, but did not affect the analgesia produced by 75, 175, or 225 g VS. Unexpectedly, we also found that infusion of AF shortly before the application of VS prevents VS-induced pseudopregnancy (PsP). Whereas the incidence of PsP following 75, 125, or 175 g VS was less than 19% and not statistically different for AF and saline pretreatments, the incidence of PsP after 225 g VS was 44% in saline-pretreated rats, but only 10% in AF-pretreated rats. Protection from the induction of pseudopregnancy, which could be caused by mechanical stimulation of the cervical area during delivery, may be an additional benefit of parturitional ingestion of placenta and amniotic fluid (placentophagia).
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