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Polyphloretin phosphate (PPP) has been reported by previous workers to be a specific antagonist of prostaglandin (PGE(1), PGE(2) & PGF(2 alpha))-induced contractions of isolated jird colon, gerbil colon, guinea pig ileum, and rabbit jejunum. In the present study, we examined the effect of PPP on uterotonic activities of crude papaya latex (a folkloric oxytocic), PGF(2 alpha), oxytocin, acetylcholine, and 5-hydroxytryptamine (standard oxytocics) on non-gravid, oestrogen-primed (50 microg/kg) rats in vitro. The effect of PPP on the oxytocics was evaluated qualitatively by incubating the tissues in PPP (25 - 400 microg/ml) for 20 min prior to the addition of a constant concentration of each oxytocic. PPP concentration dependently inhibited the contractile response of the uterine muscles to all the oxytocics. The inhibition was reversible after washing out the drugs. Results of the present study suggest that PPP is a non-specific and reversible antagonist of the response of non-gravid rat uterine smooth muscle to oxytocics in vitro. The specificity of PPP as a prostaglandin antagonist could therefore be species/tissue dependent.

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Our previous studies indicate that prostaglandin E2 (PGE2) receptors play a role in tumor metastasis. We asked if PGE2 receptor antagonism would affect murine mammary tumor cell attachment to immobilized laminin, a critical step in metastasis. The PGE2 receptor antagonist, LEO101, at a concentration of 20 micrograms/ml, inhibited tumor cell attachment to laminin and the laminin-peptide PA-22 by 41 and 82%, respectively. Immunoprecipitation studies identified the beta 1 integrin subunit as well as the alpha 3 subunit as major membrane components of these cells, whereas little or no alpha 1, alpha 5 or alpha 6 was detected. Antibody blocking studies confirmed that these cells use beta 1, but not the alpha 6 subunit, to attach to laminin. Immunoprecipitation studies of untreated or LEO101-treated cells indicate that the expression of the alpha 3 integrin, but not other integrins, was decreased by LEO101.

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To elucidate the effect of Beraprost, a stable prostaglandin (PG) I2 analogue, on airway smooth muscle functions and its mechanism of action, we studied canine bronchial segments under isometric conditions in vitro. Addition of PGI2 and its analogues dose-dependently relaxed bronchial smooth muscle precontracted with acetylcholine, with the rank order of potency being Beraprost (1) > or = Hoprost (0.65) > PGI2 (0.04), accompanied by the corresponding increase in intracellular cyclic AMP levels. The Beraprost- and PGI2-induced muscle relaxations were significantly inhibited by each of the PG antagonist diphloretin phosphate, the adenylate cyclase inhibitor SQ 22,536, and the Na(+)-K(+)-ATPase inhibitor ouabain. Beraprost and PGI2 at concentrations insufficient to cause muscle relaxation reduced the contractile responses to electrical field stimulation, whereas they were without effect on those to exogenous acetylcholine. These results suggest that Beraprost not only potently relaxes airway smooth muscle through cyclic AMP production and the subsequent stimulation of Na(+)-K(+)-ATPase but also reduces neurally mediated contraction by inhibiting the release of acetylcholine from the cholinergic nerve terminals.

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1. Endothelin-3 (ET-3) elicited relaxations at low concentrations (up to 10(-8) M) and contractions at higher concentrations in dog isolated coronary arteries precontracted with prostaglandin F2 alpha (PGF2 alpha). The relaxation by ET-3 was not affected by endothelium denudation nor treatment with NG-nitro-L-arginine, but was abolished or reversed to a contraction by treatment with indomethacin and markedly suppressed by tranylcypromine, a PGI2 synthetase inhibitor, or diphloretin phosphate, a prostaglandin receptor antagonist. ET-1 produced only concentration-dependent contractions. 2. BQ-123, a new selective ETA receptor antagonist, caused relaxation of the strips contracted with ET-3 in a dose-dependent manner and prevented the ET-3-induced contraction but did not affect the contraction produced by PGF2 alpha. The relaxation caused by ET-3 was enhanced by treatment with BQ-123. 3. It is concluded that the relaxations elicited by ET-3 in dog coronary arteries are mediated via liberation of PGI2 by activation of non-ETA receptors, located in subendothelial tissues, possibly smooth muscle cells, whereas the peptide-induced contractions are mediated via ETA receptors.

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Prostaglandin E2 (PGE2) applied cumulatively (1 nM-1 microM) induced concentration-dependent tonic contractions in the longitudinal muscle of isolated rat rectum. The PGE2 effects were not altered by guanethidine (50 microM), whereas atropine (3 microM), guanethidine plus atropine or tetrodotoxin (0.1 microM) reduced them to an almost equal extent and increased the EC50 values for PGE2. The after-contractions following electrical stimulation were enhanced by PGE2 (10 nM) and inhibited by atropine. Diphloretin phosphate (DPP, 100 microM) shifted the regression lines for PGE2 to the right in both untreated and tetrodotoxin-treated preparations, and thereby increased the EC50 values. Slopes of the concentration-effect lines for PGE2 before and after DPP differed in the presence of tetrodotoxin. The regression line for PGE2 with SC 19220 (100 microM) in tetrodotoxin-treated preparations was shifted to the right in a parallel fashion. It is concluded that PGE2 exerted both a neural (cholinergic) and a smooth muscle effect. There may be a competitive antagonism between SC 19220 and PGE2 but the block by DPP may be nonselective.

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The inhibitory effects of the prostanoid receptor antagonist, di-4-phloretin phosphate (DPP), upon washed human sperm motility were determined in vitro (up to 60 min of incubation). Concentrations tested were: 0.001, 0.01, 0.1, 0.25, 0.5, 2.5, 5.0 and 10.0 mM. All concentrations of DPP investigated caused cessation of sperm movement (percentage motility and average forward velocity) and the antimotility effect was essentially irreversible. The concentrations producing 50% inhibition were: percentage motility--1.31 +/- 0.56 mM (mean +/- SEM) and average forward velocity--1.95 +/- 0.68 mM. The mode of antimotility action appears to be multi-faceted. At high (10 mM) and intermediate (2.5 mM) concentrations, changes in fluidity of sperm plasmalemma (hypoosmotic swelling test) and loss of viability (nigrosin-eosin stain technique) constitute the primary means by which motility was disrupted. In contrast, these two parameters of motility remained unaltered at a lower concentration (0.25 mM) of DPP, and the mechanism precipitating the antimotility effect may involve mobilization of stored calcium ions and modulation of cyclic AMP levels.

PIP: The effect of the prostanoid receptor antagonist, di-4-phloretin PO4, (DPP, Leo Akteibolaget, Helsingborg, Sweden) on percent motility and forward velocity of washed human sperm was investigated. Semen specimens were collected after 305 days of abstinence, allowed to liquefy at room temperature for 15-25 minutes, and washed 3 times in modified Krebs-Ringer bicarbonate buffer. Standardized sperm suspensions were incubated for 60 minutes with DPP, and tested at concentrations form 0.01 to 10.0 mM, all of which halted sperm movement irreversibly. The mean concentration immobilizing 50% of sperm was 1.31 mM, and stopping 50% mean forward velocity, 1.95mM. Experiments aimed at pinpointing the mechanism of action of DPP showed that at medium to high concentrations, 2.5-10 mM, DPP caused hypo-osmotic swelling, an indicator if impaired sperm plasmalemma function, and nigrosin-eosin uptake, a sign of loss of viability. There was no evidence of a physical disruption of the sperm plasma membrane, assessed by leakage of the enzyme glutamic oxaloacetic transaminase (GOT). Experiments were also run in medium with or without caffeine and calcium. DPP 0.25 mM slowed motility significantly (p0.05) in normal and Ca++ free medium after 15 minutes. Caffeine enhanced motility in normal medium, but cont Ca++ free medium. DPP impaired motility somewhat in normal medium containing caffeine, but no in Ca++ free medium with caffeine. These results may indicate that DPP works by mobilizing intracellular Ca++, or by decreasing the level of cyclic AMP.

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We have described a high-affinity receptor for prostaglandin E2 (PGE2) present on metastatic murine mammary tumor cells. Pharmacologic antagonism of this receptor increases metastatic potential. In the present study, we have asked whether the binding activity of PGE on tumor target cells plays a role in natural killer (NK)-target cell interactions. We have used three unrelated PGE-receptor antagonists, SC19220, LEO101, and AH6809, to show inhibition of [3H]PGE2 binding to YAC-1 cells and inhibition of PGE2-mediated elevation of intracellular cyclic AMP (cAMP). Addition of any of these three receptor antagonists to standard 4-h 51Cr-release assays inhibits YAC-1 lysis by NK-enriched populations from murine spleen. This is the first report that antagonism of PGE binding affects NK activity. Our studies demonstrate that these effects are mediated through inhibition of target-effector cell conjugate formation. Studies in which effector and target cells were pretreated separately indicate that the PGE-mediated effects are expressed at the target cell level.

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We have shown previously that murine mammary adenocarcinoma cells both synthesize prostaglandin E2 (PGE2) and have a high affinity receptor for this ligand. Modulation of either PGE synthesis or PGE receptor function changes the metastatic potential of these cells. Because of the importance of laminin and laminin receptors to the metastatic process, we asked whether or not the PGE receptor participates in tumor cell-laminin interactions. As has been reported for many other tumor cells, laminin and the laminin-derived peptide PA22-2, containing the sequence IKVAV, mediate attachment of line 410.4 mammary tumor cells in vitro. We now demonstrate that the attachment of 410.4 cells to laminin or peptide PA22-2 was significantly inhibited by three PGE receptor antagonists, LE0101, SC19220, and sodium meclofenamate. LE0101 was most active, inhibiting tumor cell adhesion in a dose-dependent manner in the absence of nonspecific toxicity. These receptor antagonists had no effect on the PA22-2-mediated attachment of a PGE receptor negative tumor cell line, except at the highest concentration of LE0101 tested. No inhibition of adhesion to Type I collagen was seen. These results indicate that the PGE2 receptor modulates tumor cell adhesion to laminin which may subsequently affect the in vivo process of metastasis.

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Bradykinin (BK) and related kinins are potent stimulants of the rabbit jugular vein, the hamster urinary bladder, and the guinea pig trachea. The characterization of kinin receptors in these tissues was made with agonists and antagonists. Results obtained with agonists indicate that bradykinin and kallidin are much more active than des-Arg9-BK and suggest the presence of B2 receptors in the three organs. Some new agonists were also tested and the BK analogue, [Hyp3,Tyr(Me)8]BK, was found to be a potent and selective stimulant of the three preparations, with pD2 values of 8.56, 8.00, and 8.39, respectively, but inactive on the rabbit aorta (a B1-receptor system). Contractile effects of kinins in the rabbit jugular vein and hamster urinary bladder were reduced or eliminated by B2-receptor antagonists but at different concentration levels; e.g., acetyl-D-Arg[Hyp3,D-Phe7]BK showed pA2 values of 7.78 on the rabbit jugular vein but only 5.72 on hamster urinary bladder. This compound contracted the guinea-pig trachea and was found to be inactive as an antagonist on this preparation. Contractions of the hamster urinary bladder and the guinea-pig trachea in response to bradykinin were markedly reduced or eliminated by indomethacin and by BW 755C, while those of the rabbit jugular vein were not modified. The present findings indicate that the myotropic effect of kinins on the rabbit jugular vein depends on the activation of B2 receptors and suggest that B2 receptors are largely responsible also for the response of the hamster urinary bladder. B2 receptors and (or) a nonreceptor mechanism appear to be involved in the stimulant effects of the kinin agonists and some antagonists in the guinea-pig trachea.

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Carrageenin paw oedema and croton oil ear oedema induced simultaneously in rats are inhibited in a dose-dependent manner and to statistically significant degrees by lipoxygenase- and cyclooxygenase-blocker flavonoids (diosmin, fisetin, quercetin, myricetin, galangin, sophoricoside, hesperidin-methylchalcone, oligomeric procyanidin, anthocyanidins (delphinidin, pelargonidin], and the prostaglandin antagonist polyphloretin phosphate and di-4-phloretin phosphate. Outstanding anti-inflammatory effects are displayed by myricetin and delphinidin, which contain vicinal hydroxy groups in ring B. The results confirm the importance of hydroxy group substitution in ring B. The most effective of the examined substances proved to be the prostaglandin antagonist di-4-phloretin phosphate.

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U46619, a stable thromboxane A2 (TXA2) mimetic, and prostaglandin F2 alpha (PGF2 alpha) contracted helical strips of cat coronary, renal and mesenteric arteries in a concentration-dependent manner. The EC50 values for U46619 did not differ significantly in these arteries, but those for PGF2 alpha were in the order of coronary less than renal less than mesenteric arteries. Contractions induced by U46619 were antagonized by S-145, a selective TXA2 receptor antagonist, with similar activity in these arteries. On the other hand, contractions induced by low concentrations of PGF2 alpha (10(-9) to 10(-7) M) were not influenced by treatment with S-145 in coronary arteries, although those induced by high concentrations (5 x 10(-7) to 10(-5) M) were partially attenuated. These contractions resistant to the TXA2 antagonist were antagonized by diphloretin phosphate (DPP), a non-selective PG antagonist. Contractions induced by PGF2 alpha (5 x 10(-7) to 5 x 10(-5) M) in mesenteric arteries were inhibited by S-145 in a concentration-dependent manner. Contractions induced by PGF2 alpha in renal arteries were partially inhibited by S-145. The inhibitory activity of S-145 to PGF2 alpha-induced contractions at EC50 was in the order of coronary less than renal less than mesenteric arteries. Treatment with indomethacin slightly potentiated the contractions induced by PGF2 alpha in mesenteric arteries. Removal of the endothelium did not affect the contractile responses induced by PGF2 alpha and the inhibitory activity of S-145 in the arteries. These results suggest that the contractile responses induced by low concentrations of PGF2 alpha (up to 10(-7) M) are associated with their action via PG receptor(s), which is different from TXA2 receptor, and those induced by high concentrations of PGF2 alpha (5 x 10(-7) M or higher) interact with TXA2 receptors in cat vascular smooth muscles. It appears that the functional expression of this PG receptor(s) is greater in coronary arteries than in renal arteries, and that it is not found in mesenteric arteries.

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Several polyphloretin phosphate (PPP) fractions (low mol. wt LC1259; high mol. wt LC1261; crude mixture, LC101) were confirmed in their established property as antagonists of the pharmacological actions of prostaglandins in a preparation of guinea-pig isolated ileum stimulated by prostaglandin (PG)E2. Further samples of the same material were then compared in-vitro with indomethacin in their ability to inhibit prostaglandin biosynthesis from arachidonic acid by a microsomal enzyme preparation. All three PPP fractions potently inhibited prostaglandin generation, with the rank order of potency LC1259 = LC101 = indomethacin greater than LC1261. The oral LD50 in mice was 25 mg kg-1 for indomethacin and greater than 1 g kg-1 for LC101. PPP fractions (especially LC101) may therefore have therapeutic potential as anti-inflammatory agents.

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The effects of angiotensin II (A II) on adenylate cyclase activities in membranes of the zona glomerulosa (the capsular fraction) and the zona fasciculata (the decapsulated fraction) from rat adrenocortical glands were investigated. A time- and GTP-dependent stimulation by A II of adenylate cyclase activity was observed in the capsular fraction but not in the decapsulated fraction. The activation of adenylate cyclase by ACTH and A II was additive. Stimulation by A II was inhibited by an angiotensin antagonist, DD-3487 (DD). Moreover, the addition of a prostaglandin antagonist, a mixture of polyesters of polyphloretin phosphate (PPP) and an inhibitor of prostaglandin synthesis, indomethacin, was effective in inhibiting A II-induced stimulation of the capsular adenylate cyclase activity, suggesting that the activation of A II receptors located on the capsular membrane leads to the release of prostaglandins, which in turn stimulates the adenylate cyclase.

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In helical strips of dog cerebral, coronary, mesenteric, and renal arteries treated with ONO3708, an inhibitor of vasoconstricting prostaglandin (PG) receptors, and previously contracted with serotonin, PGF2 alpha, PGD2 and epithio-methano thromboxane A2 (sTxA2), a TxA2 analog, caused a relaxation. The cerebral arterial relaxation was suppressed by treatment with indomethacin and abolished by diphloretin phosphate (DPP), a PG antagonist. On the other hand, the relaxation of mesenteric arteries was not influenced by indomethacin but was markedly attenuated by DPP. Removal of endothelium did not alter the relaxation. Relaxations of coronary and renal arteries by PGF2 alpha were suppressed by indomethacin and DPP, whereas the PGD2-induced relaxation was not affected by indomethacin but was abolished by DPP. Concentration--relaxation curves for PGI2 were shifted to the right by treatment with DPP. It is concluded that after ablation of the constrictor response, dog cerebral arteries relax in response to PGs and TxA2, probably due mainly to the release of PGI2-like substance from the arterial wall and to the action of PGI2 receptive sites, whereas the mesenteric arterial relaxation appears to be associated with their action on PGI2 receptors in smooth muscle cells. PGF2 alpha-induced relaxations in coronary and renal arteries may result from the release of PGI2, and relaxations by PGD2 from the action on PGI2 receptors.

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1. Thromboxane (TX) B2 and epithiomethano (sTXA2), in concentrations that were insufficient to alter the basal tone, potentiated contractile responses of helical strips of dog mesenteric arteries to transmural electrical stimulation. The potentiating effect of TXB2 (up to 10(-6) M) was not abolished by diphloretin phosphate (DPP), a prostaglandin antagonist, whereas the potentiation by sTXA2 was abolished by the antagonist. 2. sTXA2 and TXB2 (3 x 10(-6) M or higher) potentiated the responses to noradrenaline, the potentiation being antagonized by DPP. 3. 3H-overflow evoked by transmural stimulation in superfused arterial strips previously soaked in medium containing [3H]-noradrenaline was increased by TXB2, but not altered by sTXA2. 4. TXB2 in low concentrations potentiated the contractile response to adrenergic nerve stimulation, possibly by increasing the release of noradrenaline, while the potentiation by the TXA2 analogue appears to be due to increased sensitivity of the arteries to noradrenaline. Prejunctional effects of TXB2 may be mediated by receptor sites functionally different from those located postjunctionally.

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Intracaecal administration of rhein anthrone, the intraluminally active metabolite of sennosides A and B, to mice quickly induced severe diarrhoea. Pretreatment with the prostaglandin (PG) biosynthesis inhibitor, indomethacin, and PGE2 antagonist, SC-19220, prevented the onset of diarrhoea induced by rhein anthrone, but the PGE2 antagonist polyphoretin phosphate (PPP) showed only a weak inhibitory effect. Rhein anthrone stimulated the production of PGE-like material only in the colon and its large intestinal propulsive activity was depressed by indomethacin and SC-19220, but not by PPP which suggests that the release of PGE-like material has some role in its purgative action.

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TRK-100, a stable analogue of prostaglandin I2 (PGI2), relaxed isolated arteries of the dog precontracted with PGF2 alpha or K+; the relaxation was in the order of mesenteric and renal greater than coronary and femoral greater than basilar and middle cerebral arteries. The relaxation by TRK-100 was not affected by treatment with atropine, propranolol, cimetidine, aminophylline, and indomethacin, but was suppressed by diphloretin phosphate, a prostaglandin antagonist. Treatment with TRK-100 attenuated the contraction induced by PGF2 alpha and Ca2+ in mesenteric and basilar arteries previously exposed to Ca2+-free medium, but did not significantly alter the contractile response to Ca2+ in the arteries exposed to Ca2+-free medium and depolarized by excess K+. TRK-100 and nitroglycerin relaxed isolated mesenteric arteries to a similar extent; however, when continuously infused into mesenteric arteries in anaesthetized dogs, TRK-100 produced greater vasodilatation than nitroglycerin. It is concluded that TRK-100 relaxes dog mesenteric and renal arteries more than cerebral arteries; the relaxation appears to derive from interference with the release of Ca2+ from intracellular stores and with the transmembrane Ca2+ influx through a receptor-operated channel. TRK-100 may vasodilate large and small mesenteric arteries and resistance vessels to a similar extent, whereas nitroglycerin preferentially dilates the large artery.

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Alveolar transfer of prostaglandin E2 (PGE2) was characterized in isolated perfused guinea pig lungs (n = 19) by measuring radioactivity appearing in the venous effluent during 30 min after intratracheal instillation of [3H]PGE2, [14C]-mannitol, and [125I]iodoantipyrine. Recovery of lipid-soluble [125I]iodoantipyrine [91 +/- 3% (SE)] after 30 min was used to estimate total 3H and 14C delivered to the exchanging region of lung at time 0. In seven control lungs, 58 +/- 4% of [14C]mannitol and 16 +/- 4% of [3H]PGE2 was retained 10 min after instillation. Neither perfusion with diphloretin phosphate (10 micrograms/ml; n = 4) nor hypothermia (5 degrees C; n = 5) significantly affected the amount of [14C]mannitol retained; however, [3H]PGE2 remaining in these lungs increased significantly to 36 +/- 4 and 53 +/- 2%, respectively. Addition of unlabeled PGE2 (200 micrograms) to the instilled solution (n = 3) increased retention of both [14C]mannitol (80 +/- 3%) and [3H]PGE2 (65 +/- 4%). Alveolar transfer of [3H]PGE2 was calculated as the difference in percent retention of [14C]mannitol and [3H]PGE2 and normalized to that of [14C]mannitol. After 10 min, alveolar transfer of [3H]PGE2 was 71 +/- 8% in control lungs but was decreased to 26 +/- 7, 10 +/- 5, and 19 +/- 6% by diphloretin phosphate, hypothermia, or unlabeled PGE2, respectively. These data suggest that alveolar clearance of PGE2 involves a saturable drug- and temperature-sensitive process.

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The responsiveness of the guinea-pig esophageal muscularis mucosae to arachidonic acid (AA) and its cyclooxygenase and lipoxygenase metabolites was examined in vitro. AA (0.1-30 microM) produced a concentration-dependent contraction of the muscularis mucosae (mean EC50 +/- S.E.M. = 5.1 +/- 1.0 microM). The contractions in response to low concentrations of AA (0.1-3 microM) were prevented by pretreatment of the tissue with indomethacin (1-10 microM), while those in response to high concentrations (10-100 micron) were prevented by BW755C (10-100 microM). The contractile response to AA was antagonized by polyphloretin phosphate (PPP, 1-10 micrograms/ml) and by FPL 55712 (1-10 microM). All cyclooxygenase and lipoxygenase metabolites of AA tested also produced a sustained contraction of the muscularis mucosae with the following order of sensitivity; leukotriene (LT) D4 greater than LTC4 greater than prostaglandin (PG) E2 greater than PGF2 alpha greater than PGI2 greater than thromboxane B2. The responses to LTC4 and LTD4 were antagonized by FPL 55712 (0.1-1 microM), while those to PGE2 and PGF2 alpha were antagonized by PPP (3-100 micrograms/ml). The present results indicate that exogenously applied AA contracts the isolated muscularis mucosae of the guinea-pig esophagus by an indirect action via its metabolism to both PGs and LTs. The putative PG and LT receptors located in this tissue are probably similar to those in the ileal longitudinal muscle, but differ from those in the airway smooth muscle.

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The present study provides information regarding the effects of the sow follicular fluid (FF) on the motility of isolated segments of swine and rabbit oviducts. In addition, the concentration of prostaglandins (PGs) F2 alpha, E2 and E1 in the follicular fluid of sow ovaries isolated at different stages of the sex cycle as well as the generation of the same PGs by walls of ovarian follicles in early and late proestrus, in estrus, in metestrus and in diestrus, were explored. The stimulatory contractile effect of proestrous FF in isolated segments of sow fimbria was antagonized by polyphloretin phosphate (PPP), a PG receptor blocker and by indomethacin, an inhibitor of PG synthesis. The positive inotropism evoked by the FF was mimiked by bradykinin and the influences of both interventions were similarly antagonized by PPP. It appears plausible that the inotropic effect of the preovulatory FF on the sow fimbria could be not only by PGs already present in the fluid, but also by the stimulation of the synthesis of tubal PGs by follicular fluid bradykinin. The FF also stimulated the ampullary tubal segments isolated from proestrous sows whereas the same volume of FF depressed significantly the isometric developed tension of rabbit ampulla. The total concentration of the three PGs in the FF from late proestrous follicles was significantly greater than that of the same PGs in the other two stages of the sex cycle (early proestrus and diestrus), whereas the concentration of each PG (PGE2, PGF2 alpha or PGE1), did not differ within any of the stages of the cycle. Furthermore, the total amount of the three PGs produced by the walls of follicles from late proestrous ovaries was also significantly greater than that generated by ovarian follicles from early proestrus, estrus, metestrus and diestrus. In summary the results document that the concentration of each one of the PGs measured (E2, E1 or F2 alpha) attained maximal values at the time of ovulation. The results regarding the effects of FF on the inotropic activity of fimbrial and ampullary segments of sow oviducts also suggest that the fluid might play a physiological role, favouring the capture and transfer of ova into the oviducts at the moment of ovulation.

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