Influence of prostaglandins on glucose transport in isolated rat uterus.

Glucose transport by uterine strips from ovariectomized estrogenized rats was explored. Sugar transport was significantly different from saccharose values (non-specific diffusion) only after 60 min of incubation. The addition of cytochalasin B demonstrated that we are measuring a specific mechanism for glucose transport. Insulin-enhanced sugar transport only at 0.5 or 0.25 U/ml prostaglandin E1 (PGE1), PGE2 and PGF2 alpha (10(-7) M) significantly improved glucose transport, but indomethacin (10(-6) M) failed in modifying this parameter in either control nor insulin-treated tissues. We did not observe an additive or synergistic action between PGE2 (10(-7) M) and insulin (used at maximal or submaximal concentration).

Effects of U46619 and of inhibitors of the synthesis of TXA2 on insulin action on the metabolism of labelled glucose in uteri isolated from ovariectomized-diabetic rats.

The production of 14CO2 from labelled glucose by isolated uterine strips from ovariectomized-diabetic rats has been studied. U46619, an analogue of TXA2 did not affect basal glucose metabolism; however, insulin-induced increment in CO2 production was completely blocked, both in ovariectomized (OVD) or ovariectomized-estrogenized (OVED) diabetic uterus. OKY064 as well as UK38485, both inhibitors of TXA2 synthesis, stimulated glucose metabolism (p < 0.05) similar to that of insulin in uterine tissue from OVD and OVED rats. Inhibition in the synthesis and release of TXB2 was detected (p < 0.01) by uterine radioconversion of 14C-arachidonic acid when adding OKY38485 to the incubation medium, and the production of other prostanoids such as 6-keto-PGF1 alpha, PGF2 alpha and PGE2 was enhanced. In summary, TXA2 inhibited insulin-induced glucose metabolism in diabetic animals.

Influences of oxytocin on the synthesis of prostaglandins by uterus from rats in different stages of the estrous cycle.

We explored the oxytocin-prostaglandin interactions during the rat estrous cycle. The experiments were done with uterine preparations isolated from rats in different stages of the sex cycle incubated 'in vitro' with oxytocin (O) (50 mU/ml). We found that the effect of O on prostaglandin (PG) synthesis was associated to the sex hormones, and varied during the estrous cycle. Indeed, during the estrogenic influence (i.e. at proestrus and estrus) O diminished the synthesis of PGE2 and with the highest estradiol concentration (i.e. during estrus) the hormone also augmented the synthesis of PGF2 alpha. During metestrus, no changes in PG synthesis after treatment were found. Likewise, during diestrus, when progesterone levels fall, O enhanced PGF2 alpha uterine synthesis. In this study an inhibitory action of O on the uterine production of 6-keto-PGF1 alpha at proestrus was also seen. The present results indicate that when estrogen concentration increases (during estrus) 6-keto-PGF1 alpha synthesis also increases. In summary, we have observed that sex hormones exert a modulating action on the influences of O on uterine PGs synthesis.

Synthesis and release of prostaglandins D2 and E2 by rat uterine tissue throughout the sex cycle. Effects of 17-beta-estradiol and progesterone.

The synthesis and release of prostaglandins (PGs) D2 and E2 by rat uterine tissue was studied during the whole sex cycle. The PGs released into the bathing solution after 60 min of incubation were measured by specific radioimmunoassays. It was found that PGD2 released at diestrous was significantly higher than at proestrous and estrous. We also observed that PGE2 produced at diestrous was significantly higher than at proestrous and estrous, i.e. both PGs follow the same pattern of production throughout the sex cycle, but in all cases the uterine strips released higher amounts of PGE2 than of PGD2. The influence of the sex hormones on PGD2 and PGE2 synthesis, was also studied. We observed that the treatment of ovariectomized rats with 17-beta-estradiol decreased significantly the synthesis and release of PGD2 and PGE2. On the other hand, progesterone treatment did not modify the production of PGE2 but decreased significantly the synthesis of PGD2. In conclusion, in the present study we have found that PGD2 and PGE2 production varied similarly during the sex cycle and that 17-beta-estradiol negatively regulates their synthesis. In addition, we have found that progesterone depressed only PGD2 synthesis without affecting PGE2 production.

Glucose metabolism, triglyceride and glycogen levels, as well as eicosanoid production in isolated uterine strips and in embryos in a rat model of non-insulin-dependent diabetes mellitus during pregnancy.

Spontaneous contractile activity, glucose (Glu), glycogen (GLY), triglyceride (TG) metabolism and eicosanoid production, was evaluated in isolated uterine strips from control and non-insulin-dependent diabetic rats on day 10 of pregnancy. Metabolism of Glu, levels of GLY and TG and eicosanoid production were also studied in day 10 embryos obtained from both experimental groups. "In vitro" isometric developed tension (IDT), was similar at 0 hr in control and diabetic uterine preparations, but IDT was decreased after a 60 min incubation in the diabetic group. The frequency of contractions (FC) was similar at 0 hr and after 60 min incubation in both experimental groups. On the other hand, the production of 14CO2 from U14C-glucose was lower in isolated uteri and embryos obtained from diabetic rats than in controls. Initial TG levels were similar in uteri isolated from control and diabetic rats, and higher in embryos obtained from diabetic mothers than in controls. Levels of TG in uterine strips suspended in Glu or Glu-free medium did not differ at 0 hr or at 60 min either in controls or in diabetic rats. On the contrary GLY levels in uterine strips from diabetic animals were higher than in controls, whereas in embryos from diabetic mothers GLY levels were similar to controls. Levels of GLY in uterine strips from controls and diabetic animals decreased after 60 min incubation only in the absence of Glu in the incubation medium. Production of PGE2, PGE1, 6-keto-PGF1 alpha, PGF2 alpha, TXB2 and LTB4 was studied in uterine strips and embryos obtained from control and diabetic rats. No differences were found between control and diabetic uterine prostanoid production, but lower production of LTB4 was observed in diabetic uteri. However production of PGE2 and PGF2 alpha was greater in embryos obtained from diabetic mothers than in controls. In this study, we observed lower uterine metabolic alterations than in the pancreatectomized diabetic rat model studied previously, but important anomalies in the embryos obtained from non-insulin-dependent diabetic mother were found.

Glucose, glycogen and triglyceride metabolism, as well as prostaglandin production in uterine strips and in embryos from diabetic pregnant rats. Influences of the presence of substrate in the incubation medium.

"In vitro" isometric developed tension (IDT) and frequency of contractions (FC), glucose (Glu), glycogen (GLY) and triglyceride (TG) metabolism, as well as prostaglandin PGE2 and PGE1 production, were studied in uterine strips and in embryos isolated from controls and diabetic rats at day 10 of pregnancy. The IDT and the FC, at 0 time or after a 60 min incubation, were not different in controls and in preparations from diabetic animals when the uterine strips were incubated in glucose or in glucose-free medium (p > 0.05). The production of 14CO2 and 14C-lactate from 14C-glucose were lower in the diabetic group than in controls (p < or = 0.05). Indomethacin (10(-6) M), an inhibitor of prostaglandin synthesis, failed to modify these results. Labelled Glu metabolism by isolated embryos was similar (p > 0.05) in controls and in embryos obtained from diabetic mothers. On the other hand, the initial TG and GLY levels were higher (p < or = 0.05) in diabetic uterine tissues than in controls. However, the values of TG and GLY in embryos obtained from both experimental groups were similar (p > 0.05). TG levels in uterine strips suspended in Glu or in Glu-free medium did not differ (p > 0.05) at 0 time (postisolation) and at 60 min, either in controls or in diabetic rats. However, Gly levels in uterine strips from diabetic animals, decreased significantly at 60 min in tissues incubated in Glu or in Glu-free medium (p < or = 0.05). In controls, uterine Gly content decreased (p < or = 0.05) only at 60 min time when the strips were incubated in Glu-free medium. Finally, uterine tissue from controls as well as from diabetic pregnant rats release more PGE2 than PGE1 into the incubation medium (p < or = 0.001). Nevertheless, secretion of PGE2 and PGE1 was similar in both experimental groups and was not modified by the presence or absence of glucose. In summary, we found differences in uterine metabolism of glucose, glycogen and triglycerides in controls and in diabetic rats, but metabolic differences have not been detected between embryos obtained from controls and from diabetic mothers.

Effect of chronic ethanol consumption on the spontaneous contractions, prostaglandin production, triglycerides and glucose metabolism of uterine strips isolated from pregnant rats and in embryos.

The constancy of spontaneous isometric developed tension (IDT) and the metabolism of triglycerides (TGs), U-14C-Glucose and 14C-arachidonic acid (14C-AA) in uterine strips isolated from controls and from chronic ethanol (ETOH) fed pregnant rats were explored. The studies were performed on isolated uterine strips suspended in glucose-containing as well as a glucose-free medium. The spontaneous decrement of IDT as time progressed after tissue isolation and mounting was significantly higher in tissue preparations obtained from pregnant rats drinking 20% ETOH, than the controls. This situation was evident in uterine strips isolated from rats at 10 and at 16 days of pregnancy, both in solutions containing glucose or in glucose-free conditions. On the other hand, uterine strips isolated from control rats at 7, 10 and 16 days of pregnancy exhibited almost no decrement of IDT after 60 min of activity in a solution containing glucose or in a glucose-free medium. The absolute values of TGs in uteri obtained from rats drinking ETOH were significantly greater (p < 0.001) than in non-drinking controls. TG levels did not differ at 0 min (initial or postisolation) to those at 60 min in control uterine preparations obtained from pregnant rats at 7, 10 or 16 days of pregnancy and incubated either in a medium with or without glucose. On the contrary, in strips from ETOH-fed animals isolated on the same day of pregnancy, TG levels determined at 60 min following isolation and mounting were significantly lower, when glucose was present or absent from the suspending solution.(ABSTRACT TRUNCATED AT 250 WORDS)

Eicosanoid production by uterine strips and by embryos obtained from diabetic pregnant rats.

Eicosanoid production by uterine strips and by embryos obtained from normal and diabetic rats at day 10 of pregnancy was studied. It was found that the release of 6-keto-PGF1 alpha (representing PGI2 synthesis) and of LTB4 was less in preparations from diabetic animals than in controls. The production of TXB2 (indicating the formation of TXA2) by uterine tissue obtained from diabetic rats was almost double that of controls. The synthesis and release of eicosanoids when tissues were incubated in glucose-containing solution or in glucose-free medium were similar, with the exception of LTB4, which was diminished with uterine strips from diabetic rats. The mean number of embryos in control pregnant rats (12.4 +/- 0.5) and in diabetic mothers (10.1 +/- 1.3) was not significantly different, but in 4 of the 14 diabetic rats studied, all of their embryos were resorbed. Although embryos released large amounts of PGF2 and PGE2, and small amounts of 6-keto-PGF1 alpha, TXB2 and LTB4, the amounts of each eicosanoid in control and diabetic groups were similar. The present results indicate that the diabetic state, which induces alterations in uterine eicosanoid production, do not influence arachidonic metabolism in their corresponding embryos.

Relationship between factors influencing Na(+)-K(+)-ATPase activity and eicosanoid production from 14C-arachidonic acid in spayed rat uterus.

Na(+)-K(+)-ATPase activity has been implicated in the metabolism of arachidonate and the release of prostaglandins (PG). The aim of the present study was to investigate a potential interaction between the activity of this enzyme and the production of bisenoic PG by uteri isolated from spayed rats. Ouabain or the incubation in low K+ medium (conditions which inhibit Na(+)-K(+)-ATPase) diminished the conversion of 14C-arachidonic acid to 6-keto-PGF1 alpha and PGF2 alpha and increased the production of TXB2. The incubation of uterine strips in a high K+ medium (condition which enhances Na(+)-K(+)-ATPase activity) increased the formation and release of 6-keto-PGF1 alpha and PGF2 alpha while the production of TXB2 and PGF2 diminished significantly. These observations suggested that the activity of Na(+)-K(+)-ATPase could modulate the production of PG and that could be involved in the alterations of the metabolism of eicosanoids found in several tissues during diabetes.

Acute effects of a single ethanol injection on in vitro rat uterine spontaneous motility, on uteri prostaglandin production and on tissue metabolism of triglycerides.

The acute effects of ethanol (ETOH), injected at 3 g.kg-1i.p. on spontaneous contractions, on prostaglandin (PG) production and on the metabolism of triglycerides (TGs), have been studied in uterine strips obtained from rats at diestrus and suspended in glucose-containing or glucose-free solution. The absolute values of isometric developed tension (IDT: expressed in mg) recorded at 0 time (initial or post isolation determinations) and the frequency of contraction (FC), expressed as the number of contraction cycles during 20 min, were similar for uterine strips from controls and from ETOH treated rats. The uterine IDT and the FC expressed as percent changes from internal controls (0 time values) were explored during 180 min in uteri suspended in glucose medium. The magnitude of IDT decreased, as time progressed, both in controls as well as in ETOH-treated rats. Afterwards, uterine strips from controls exhibited a partial recovery of their contractile activity. This pattern of recovery was not observed in uterine strips from ETOH-treated rats. The uterine IDT, in the ETOH-injected animals after 180 min of activity, were significantly smaller than those of controls. On the other hand, the FC decreased progressively up to the end of the experimental period both in controls as well as in ETOH-treated rats. In glucose-free medium, the IDT of uterine strips from ETOH-injected animals diminished significantly more than controls from 100-180 min following isolation and mounting. In addition, the FC of uterine strips from the ETOH group of rats were significantly smaller than in controls suspended in glucose-free solution.(ABSTRACT TRUNCATED AT 250 WORDS)

On the role of 'in vivo' injected progesterone and of the 'in vitro' presence of oxytocin, modulating Ca2+ uptake by the rat uteri from spayed animals and as controllers of the production of arachidonic acid metabolism.

We attempted to explore possible mechanism(s) subserving the influence of oxytocin (O) and of progesterone (P) in the isolated rat uterus studying the action of these hormones on: the synthesis and release of prostaglandins (PGs), the metabolism of labelled arachidonic acid and the uptake of Ca2+ by the tissue from ovariectomized animals. The experiments were done with uterine preparations isolated from spayed rats treated or not with P prior to sacrifice and afterward incubated or not with O 'in vitro'. While uterine strips from untreated spayed rat uterus exhibited a basal release into the incubating medium of approximately the same amounts of PGF2 alpha, and PGE2, the 'in vitro' addition of O (50 mU/ml) increased significantly (p < 0.05) the output of PGF2 alpha without changing the release of PGE2. In tissue from rats injected with P prior to sacrifice the output of PGF2 alpha rose significantly (p < 0.01) as it did after the addition of O to preparations obtained from spayed rats treated with P in comparison to findings in uteri from spayed rats but not in comparison to uteri from spayed rats treated with P alone. Moreover, the 'in vitro' addition of O (50 mU/ml) only increased the formation of PGF2 alpha (p < 0.05) and of 5-HETE (p < 0.05); nevertheless the administration of P to spayed rats diminished significantly (p < 0.05) the formation of 6-keto-PGF1 alpha from uteri, but increased that of PGF2 alpha (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of beta-endorphin on spontaneous uterine contractions. Prostaglandins production and 45Ca2+ uptake in uterine strips from ovariectomized rats.

The effects of beta-endorphin, Met-enkephalin, dynorphin and SKF 10047 on the constancy of the isometric developed tension (IDT) of the spontaneous contractions of uterine strips isolated from ovariectomized rats were explored. beta-endorphin (10(-6) M) was the only opioid that depressed significantly uterine constancy of IDT in a concentration dependent fashion. Naloxone, neither at 10(-8) M nor at 10(-6) M, altered the negative inotropic influence of beta-endorphin. Moreover, the basal synthesis and outputs of some prostaglandins (PGE1, PGE2 and PGF2 alpha) from rat uteri and the effect of beta-endorphin (10(-6) M), were determined. It was found that the basal synthesis and release of PGs in uteri were significantly inhibited by this endogenous opioid. The effects of beta-endorphin (10(-8), 10(-6) and 10(-5) M) on the basal; and oxytocin or A23187, induced 45Ca2+ uptake, as well as the influence of naloxone were also studied. beta-endorphin at three of the concentrations tested decreased basal uterine 45Ca2+ uptake and this action was not prevented by naloxone (10(-8) M). The presence of oxytocin and of A23187 augmented significantly 45Ca2+ uptake, an effect that was antagonized by beta-endorphin (10(-6) M). The possible role of beta-endorphin in uterine functioning via the modulation of uterine PG synthesis and Ca2+ uptake is discussed.

Probable influence of ova and embryo prostaglandins in the differential ovum transport in pregnant and cycling rats.

In this study we explored the possible underlying mechanism(s) of the differential transport of unfertilized and fertilized ova in cycling and pregnant rats. The number of ova recovered from rat oviducts and uterus was not significantly different in estrus, metestrus and diestrus but dropped sharply at proestrus. When estrus rats were injected with indomethacin (10(-6)), a well known inhibitor of cyclooxygenase, delivered into both ovarian bursae, and sacrificed next day at metestrus, the number of ova in the oviduct was significantly smaller (p less than 0.025) than in controls at metestrus. On the other hand, when diestrus rats were injected with PGE1 (10(-6)) delivered into both ovarian bursae, and sacrificed next day at proestrus, no ova were found in the oviducts, and only a few of them were in the uterus. When fertilized ova were recovered from oviducts and uteri at day 4 of pregnancy (corresponding to proestrus of cycling rats) an average of 4 embryos were still found in the oviducts, proving a differential ovum transport between cycling and pregnant rats. In order to establish if there exists any ova or embryo releasing factor responsible for this difference, the prostaglandins released to the incubation medium by ovum or 3-day embryo were measured. Unfertilized ova produced significantly more PGE1 (p less than 0.05) than PGE2 or PGF2 alpha. The same pattern of PG production was observed with incubated embryos, but in this case the amount of PGE1 released was significantly higher (p less than 0.01) that the PGE1 released by unfertilized ova.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of prostaglandins and of leukotriene C4 on the metabolism of labelled glucose in uteri isolated from ovariectomized-diabetic rats. Influences of 17-beta-estradiol and of insulin.

The influences of exogenous PGE1, PGE2, PGF2 alpha, LTC4 and insulin (INS) on glucose oxidation in uterine strips isolated from ovariectomized-diabetic (OVD) and ovariectomized-estrogenized-diabetic (OVED) rats, were studied. The spayed animals were made diabetic by a single injection of streptozotocin (65 mg.kg-1 body weight). The effects of prostaglandins were studied in the presence of indomethacin (INDO) in the incubation medium and the effects of LTC4 in the presence of INDO and nordihydroguaretic acid (NDGA). These procedures were followed in order to avoid the possible influences of endogenous derivatives of arachidonic acid formed by the activity of cyclooxygenase and of lipoxygenases. INDO and NDGA did not modify significantly the formation of 14CO2 from U-14C-glucose in uteri from OVD and from OVED rats. INS (0.5 U.ml-1) augmented significantly labelled glucose metabolism, both in OVD as well as in OVED rats. On the other hand, added PGE1, PGE2, PGF2 alpha or LTC4 failed to alter glucose metabolism in uteri from OVD rats. Only PGE1 was able to increase significantly (p less than 0.05) 14CO2 production from labelled glucose in uterine strips from OVED rats. In OVD rats the stimulatory action of INS on uterine glucose metabolism was significantly enhanced by exogenous PGE1, but not modified by PGE2, by PGF2 alpha or by LTC4. PGE1, PGE2 and LTC4 sensitized uterine strips obtained from OVED rats to the effects of INS. The possible importance of PGE1 in improving uterine glucose metabolism in diabetic animals is discussed.

Effect of exogenous phospholipase A2 and triacylglycerol lipase on the synthesis and release of monoenoic and bisenoic prostaglandins from isolated rat uterus.

The possible existence of a selective and independent mechanism subserving the formation of prostaglandin E1 (PGE1) and of prostaglandin E2 (PGE2) has been reported in previous studies from our group. In the present experiments we have demonstrated that neutral lipid lipases play an important role yielding dihomo-gamma-linolenic acid for the formation of PGE1. Indeed, exogenous triglyceride lipase added to the incubation bathing solution at a concentration of 150 U/ml increased several fold the production of PGE1 by isolated uterine strips obtained from spayed rats. Nevertheless the presence of the enzyme did not modify significantly the synthesis and release of bisenoic PGs (PGE2 and PGF2 alpha). When triarachidonin was added, as an artificial substrate into the incubating medium in order to detect the presence of endogenous triacylglycerol lipase, we observed a significant increment in the generation of PGE2 (p less than 0.005) and of PGF2 alpha (p less than 0.001) without evident changes in the basal release of PGE1. On the other hand, the addition of phospholipase A2 (PLA2) at 0.2 U/ml, increased significantly the production of PGE2 (p less than 0.001) but failed to alter the concentration of PGE1 in the incubating solution. Surprisingly, PLA2 did not enhance the synthesis of PGF2 alpha in the present experiments, a situation for which we do not have a clear explanation. Exogenous bradykinin (10(-6) M), a well known stimulant of PLA2 activity in several tissues, also increased significantly (p less than 0.001) the production of PGE2 without altering that of PGE1.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of chronic alcohol consumption on rat uterine spontaneous motility, prostaglandin production and triglyceride metabolism.

The spontaneous isometric developed tension (IDT), the synthesis and release of prostaglandins (PGs) into the incubating medium and the metabolism of triglycerides (TGs) in uterine strips isolated from controls and chronic ethanol fed rats, were studied. In order to observe how the uterus of rats fed alcohol reacts during a situation of metabolic emergency, the above mentioned studies were done in the presence or in the absence of glucose in the incubating medium. The decrement of IDT as time progressed was significantly greater in strips obtained from rats which had been drinking 20% ETOH than in controls. Nevertheless, the absolute magnitude of the initial IDT was similar in both groups. On the other hand, the decline of the frequency of contractions (FC) of uterine strips isolated from controls and from ETOH-exposed rats, after 60 min of spontaneous activity was similar. When the uterine strips isolated from ETOH-exposed and from control rats were suspended in glucose-free solution they exhibited the same decrement of IDT and FC after 60 min of activity. The basal release of PGE1 and PGE2 was similar in control tissues incubated in medium containing glucose, but the output of PGE2 was significantly smaller than that of PGE1 in uterine strips isolated from ETOH-exposed rats. The production of PGE1 and PGE2 by uteri suspended in glucose-free medium was similar in control preparations. On the contrary the release of both PGs differs in uterine strips from ETOH-exposed rats, i.e. the output of PGE2 was significantly smaller than in controls and the release of PGE1 increased around 4-fold in comparison with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of morphine on arachidonic acid metabolism, on Ca2(+)-uptake and on cAMP synthesis in uterine strips from spayed rats.

The effects of morphine on arachidonic acid metabolism, on cAMP levels and on basal and induced 45Ca2(+)-uptake, in uterine strips isolated from ovariectomized rats as well as the influence of naloxone, were explored. The presence of morphine (10(-6) M) did not change significantly 14C-arachidonic acid metabolism, basal cAMP levels, or cAMP increment induced by PGE2 or by PGE1. On the other hand morphine (10(-6) M) decreased basal uterine 45Ca2(+)-uptake as much as verapamil (10(-6) M) did, and this action was not prevented by naloxone (10(-8) M). The presence of oxytocin (50 mU.ml-1) augmented 45Ca2(+)-uptake, an effect which was antagonized by morphine (10(-6) M). This inhibitory action of morphine on oxytocin-induced 45Ca2(+)-uptake was not prevented by naloxone (10(-8) M). Furthermore, PGE1 (10(-8) M and (10(-6) M) but not PGE2 (10(-8) and 10(-6) M), stimulated the incorporation of 45Ca2+ into uterine strips, and this action was not altered by morphine. The inhibitory influence of morphine on uterine spontaneous motility and on prostaglandin synthesis and release, previously described by us, is now explained in terms of an inhibition of tissue Ca2(+)-uptake.

Uptake and incorporation of arachidonic acid and of dihomogamma-linolenic acid into tissue lipids in uterine strips isolated from ovariectomized and from ovariectomized-diabetic rats. Effects of 17-beta-estradiol.

The uptake of 14C-arachidonic acid (14C-AA) and 14C-dihomogamma-linolenic acid (14C-DGLA) into phospholipids (PLs) and neutral lipids (NLs) in uterine tissue obtained from ovariectomized controls (C) and from ovariectomized-diabetic rats (D) was studied. Uterine strips from D rats incorporate significantly less (P less than 0.05) 14C-AA into PLs than C rats. On the other hand the uptake of 14C-AA into NLs is significantly smaller (P less than 0.05) in uterine tissue from C than from D animals. The estrogenization of the C animals did not modify the incorporation of 14C-AA into PLs or NLs. On the contrary, uterine tissue obtained from D rats treated with 17-beta-estradiol incorporated significantly more labelled AA (P less than 0.05) into PLs and significantly less 14C-AA (P less than 0.05) into NLs than untreated D animals. The incorporation of 14C-DGLA into PLs shows similar pattern in uterine tissue obtained from C and D animals. Estrogenization increased significantly (P less than 0.01) in both cases, the incorporation into PLs. Regarding the incorporation of 14C-DGLA, it was clearly shown that DGLA is taken up significantly more (P less than 0.01) by NLs than by PLs, both in C and D rats. The estrogenization of C and D rats induces a significant decrease in the incorporation of 14C-DGLA into NLs in both experimental groups. The distribution of 14C-AA into the different subfractions of PLs is not uniform.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of ova within rat oviducts on spontaneous motility and on prostaglandin production.

The present study was performed in order to explore the influence of ova present within rat oviducts on: a) tubal spontaneous motility and b) oviduct prostaglandin production. It was found that the isometric developed tension (IDT) of tubes isolated from proestrous rats (preovulatory oviducts) was significantly higher (P less than 0.01) than the IDT of tubes from rats at estrus and at metestrus (postovulatory oviducts). After flushing the oviducts with KRB solution (i.e., after removing existing ova) the IDT of the oviducts obtained from estrous rats increased significantly (P less than 0.01), whereas the IDT of tubes isolated from proestrous rats (i.e., preparations without ova) was not modified. On the other hand, isolated tubes containing their corresponding ova released into the suspending solution significantly more PGE1 than PGE2 or PGF2 alpha (P less than 0.005). It was particularly interesting to find that after flushing the oviducts, tissue production of PGE1, PGE2 and PGF2 alpha was similar. Finally, when dose response curves for PGE1 and for PGE2 on the spontaneous contractions of oviducts isolated from rats at proestrus, estrus and metestrus were constructed, both PGs evoked an inhibitory inotropic action. The ED50 for PGE1 in tubes from estrous rats was significantly smaller (P less than 0.01) than that for metestrous animals but significantly greater (P less than 0.01) than that observed in oviducts from proestrous rats. The ED50 for PGE2 did not change in the different tested periods of the sex cycle. Results reported herein suggest the possibility that the ova present within rat oviducts, may influence their own transport along the tubes by modifying the amount of prostaglandins produced by the oviducts or via their own prostaglandin synthesis.

Oxytocin enhances the basal release of uterine prostaglandin F2 alpha, but not that of PGE1, or of PGE2, and changes the metabolism of exogenous arachidonate, favouring the formation of prostaglandin F2 alpha and 5-HETE. Relationships with its uterotonic action and modulation by estradiol.

We attempted to explore possible mechanism(s) subserving the influence of oxytocin on uterine motility by studying the action of the hormone on: 1) the contractile activity of isolated rat uteri in the presence or absence of indomethacin; 2) the synthesis and release of prostaglandins (PGs) into the solution incubating the uterine tissue as well as the metabolism of labelled arachidonic acid; 3) the uptake of 45Ca2+ by uterine strips. The experiments were bone with uterine preparations isolated from spayed rats treated or not with 17-beta-estradiol. The values of isometric developed tension (IDT) and of frequency of contractions (FC) induced by oxytocin in uterine strips isolated from spayed and spayed-estrogenized rats, were not modified by indomethacin at 10(-6) M. On the other hand, uterine strips from untreated spayed rats, release into the incubating medium approximately equal amounts of PGE1, PGE2 and PGF2 alpha. The in vitro presence of oxytocin (50 mU/ml) increased significantly (p 0.05) the output of PGF 2 alpha without changing the release of PGE1 or PGE2. Uteri from spayed rats injected prior to sacrifice with 17-beta-estradiol released significantly less PGE1 and PGE2 (p less than 0.005) than preparations from non-injected animals, whereas the output of PGF2 alpha in the suspending solution remained unchanged. Following estrogenization the addition of oxytocin to preparations obtained from spayed-estrogenized rats also increased the output of uterine PGF2 alpha (p less than 0.001) without changing that of PGs E1 or E2.(ABSTRACT TRUNCATED AT 250 WORDS)