Prostaglandins F in uterine and ovarian compartments and in plasma from the uterine vein, ovarian artery and vein, and abdominal aorta of pseudopregnant rats with and without deciduomata

Prostaglandins F were measured in uterine and ovarian compartments and in uterine venous, ovarian arterial and venous and abdominal aorta plasma and the uptake of 3H-PGF2 alpha by ovarian compartments of 240 pseudopregnant rats with or without bilateral deciduomata in five experiments. Concentrations of PGF in deciduomal tissue, uterine venous plasma, ovarian arterial and venous plasma, corpora lutea, and remainder of the ovary and 3H-PGF2 alpha in the ovary were consistently as high or higher in pseudopregnant rats with deciduomata as in the endometrium, ovarian compartments, or samples of plasma from the same blood vessels of pseudopregnant rats without deciduomata. Levels of PGF were consistently 3 to 7 fold higher in uterine venous than in plasma from the abdominal aorta. It is concluded that extended luteal maintenance by deciduomal tissue is by some mechanism other than an inhibition of PGF synthesis by the uterus, transfer of PGF locally to the ovary, or uptake of PGF by the ovarian compartments.     

Effect of decidual tissue on the uterine production of prostaglandins in pseudopregnant rats.

The concentration of prostaglandin F (PGF) in uterine vein plasma of non-traumatized pseudopregnant rats and pseudopregnant rats with deciduomata were not significantly different from each other at any of the times of pseudopregnancy studied (Days 7, 10 and 12). There was a significant increase in PGF levels on Day 10 in both groups of pseudopregnant animals (P less than 0-05) compared to the Day 4 values, and PGE values were significantly greater on Day 10 in the decidual tissue-bearing rats (P less than 0-01). A slight but not significant elevation in PGE concentration was observed on Days 7 and 12 in rats with deciduomata, but there was no significant difference in the control rats on Days 4, 7, 10 or 12. The results indicate that the prolongation of pseudopregnancy in rats with deciduomata is not due to a decreased production of uterine PGs and lend support to the recent suggestion of a luteotrophic effect of decidual tissue in the rat.     

Prostaglandin F2α back transfer from the mesometrium vasculature into the uterus of the gilt during early pregnancy and estrogen-induced pseudopregnancy

Isolated reproductive tracts from gilts on the days of luteal regression (13–17 day of estrous cycle), pregnant gilts (14–18 days of pregnancy) and estrogen-induced pseudopregnant gilts (15–18 day of estrous cycle) were supplied with autologous, oxygenated blood. ³H-PGF_2α (10⁸ dpm) was infused at a constant rate into three different sites of the most superficial layer of the myometrium along the length of the horn close to the broad ligament. During infusion (60 min) and 60 min after the infusion had been stopped, arterial blood was collected continuously in 5-min samples from a small branch of the uterine artery in the mesometrium area about 10 cm from the uterine horn. A significantly higher concentration of ³H-PGF_2α in the uterine-artery blood plasma was found in pseudopregnant and pregnant gilts than in the control group. The total ³H-PGF_2α back transfer with arterial blood from the broad ligament vasculature into the uterus was 2.4 × 10⁶ dpm, 6.0 × 10⁶ dpm and 19.8 × 10⁶ dpm of infused ³H-PGF_2α in the control, pregnant and pseudopregnant gilts, respectively. We suggest that ability for PGF_2α binding and back transfer from the broad ligament vasculature into the uterus, as observed in pseudopregnant and pregnant gilts, may strongly reduce the peak concentration during the pulsatile release of PGF_2α from the uterus and may protect the corpus luteum against luteolysis.     

Effects of the fetal-placental unit on uterine prostaglandin levels at term in the pregnant rat

Uterine prostaglandins (PGs) increase markedly at term in the pregnant rat. To assess the contribution of the fetal-placental unit (FUP) on uterine tissue and uterine venous blood PG concentrations, each uterine horn of 14 unilaterally pregnant rats at day 21 of pregnancy were compared. In addition, 7 bilaterally pregnant rats were studied. Uterine tissue and uterine venous plasma PGF, PGE, 6-Keto-PGF₁ (6KF) and thromboxane B₂ (TxB₂) and systematic plasma progesterone, estradiol and estrone were determined by radioimmunoassay. Uterine concentrations of PGs (ng/mg DNA) were always greater on the pregnant side of unilaterally pregnant rats (p<.05) although the PGF levels were elevated to a lesser extent than were PGE, TxB₂ or 6KF. However, no differences were detected between uterine tissue from the pregnant side of unilaterally pregnant compared to bilaterally pregnant rats. In addition, no differences were found in uterine venous plasma PGs adjacent or opposite the pregnant uterine horn and in systematic plasma progesterone, estradiol and estrone levels in unilaterally vs bilaterally pregnant rats. These data suggest that the presence of the FPU is associated with an increased capacity of uterine tissue to produce PGE, TxB₂ and 6KF, and to a lesser degree PGF, and thus may contribute to the increase in uterine PGs periparturition.     

Progesterone, 20α-dihydroprogesterone and PGF; Interrelated hormonal changes during pseudo-pregnancy in the rat

Ovarian and uterine tissue concentrations of progesterone, 20α-dihydroprogesterone (20_αOHP) and prostaglandin F (PGF) were measured during hormonally-induced pseudopregnancy, as were plasma levels of progesterone and 20αOHP, in hysterectomised and sham-operated rats. Elevated levels of PGF in uterine and ovarian tissues were coincident with declining concentrations of progesterone and increasing concentrations of 20αOHP in the sham-operated rats. Maximum PGF concentrations were apparent in uterine tissue 14 days after hCG injection, coincident with the plasma, ovarian and uterine nadir concentrations of progesterone. A small but statistically significant increase in ovarian PGF was apparent at this time in sham-operated rats. This elevation of ovarian PGF was abolished by hysterectomy.     

Prostaglandins F in uterine and ovarian venous plasma from nonpregnant and pregnant ewes collected by cannulation.

Periodic collections of uterine venous blood were obtained from three nonmated, three pregnant and two mated but nonpregnant ewes in which uterine veins were cannulated with polyvinyl tubing on day 11 postestrus. Frequent sampling was achieved in three of these ewes with additional cannulae in the ovarian veins. Blood samples were collected at 3-hr intervals from 0600 on day 12 to 1800 on day 13 and then 6-hr intervals through day 15. On day 13, three additional samples at 30-min intervals were collected between 1400 and 1530. Prostaglandins F (PGF) in plasma were quantified by radioimmunoassay. On day 12, one ewe in each group had at least one measurement which suggested an increased rate of release of PGF into the uterine vein. Seven of eight ewes on day 13 appeared to have increased rates of release of PGF from the uterus between 0900 and 1500. The highest level measured in each ewe during this period ranged from 2.7 to 11 ng per milliliter. Concentrations of PGF in ovarian venous plasma in two of three ewes were positively correlated (P less than .05) with concentrations of PGF in uterine venous plasma (r equals .64 in each ewe). No evidence was obtained that pregnant and nonpregnant ewes differ in rate or pattern of release of PGF from the uterus into the uterine vein on days 12 and 13. Comparisons could not be made with confidence concerning PGF either in uterine veins on days 14 and 15 or in ovarian veins on all days due to limited number of observations.     

Temporal response of uterine prostaglandins to estradiol treatment in the ovariectomized-prenant rat

Previous studies in our laboratory have shown that 24 hours of estradiol treatment significantly enhanced uterine prostaglandin (PG)F, PGE and thromboxane B₂ (TxB₂) leels but had no effect on 6-Keto-PGF_1α (6KF) concentrations in ovariectomized-pregnant rats. One explanatior for the lack of an augmentation in 6KF was a temporal differences in response (i.e. 6KF increased and decreased within the 24 hour period). To test this possibility rats were ovariectomized on day 19 of pregnancy and sacrificed 0, 4, 8, 12, 16, 20 and 24 hours after estradiol treatment. Uterine tissue and venous plasma were analyzed for PGs by radioimmunoassay. No significant (p > .05) alterations were detected for any of the uterine PGs at 0, 4, 8 and 12 hours. However, at 16 hours PGF, TxB₂ and PGE all showed significant (p > .05) increases (2.4, 3.4 and 2.1 fold, respectively) compared to 12 hours. In contrast, no significant augmentation in 6KF levels (p > .05, 1.3 fold) was detected at 16 compared to 12 hours although it was enhanced relative to 0 and 4 hours. In addition, PGF, TxB₂ and PGE, but not 6KF, showed further increases 24 hours after estradiol administration. No alterations were found (p > .05) for any of the PGs in uterine venous plasma at the time points studied. In summary, uterine PGF, PGE and TxB₂ net production appears to be more enhanced by estradiol treatment than 6KF at the time points studied. In addition, there is a slight, but significant, difference in the temporal response characteristics of 6KF compared to the other PGs. The data suggest that the dramatic increase in uterine PGF, PGE and TxB₂ levels at parturition in the rat are probably significantly related to enhanced levels of estradiol. However, the majority of the increase in uterine 6KF levels at labor is more likely caused by factors other than augmented plasma estradiol.     

Role of prostaglandin F2alpha in ovulation.

Using radioimmunoassay procedures, the levels of plasma, uterine and ovarian prostaglandin (PG) F2alpha, and those of plasma estradiol and progesterone were measured in intact, hysterectomized or ovariectomized immature female rats pretreated with PMS and subsequent HCG. Occurrence of ovulation was confirmed at 8 hours after the HCG administration not only in the intact rats but also in the hysterectomzied rats. The levels of plasma estradiol and progesterone, and of uterine and ovarian PGF2alpha rose with the PMS injection alone, but they did not reach the peaks before the HCG administration. Both plasma estradiol and uterine PGF2alpha showed a peak at 2 hours after the HCG injection. These peaks were antecedent 2 or 6 hours before the peaks of ovarian and plasma PGF2alpha, respectively. However, such increase of uterine PGF2alpha does not seem to be indispensable for ovulation, because ovulation could occur in the hysterectomized rats. The levels of ovarian PGF2alpha showed a high plateau from 4 to 8 hours after the HCG injection, and then rapidly decreased after ovulation. The levels of plasma PGF2alpha peaked not only in the intact rats but also in the hysterectomized rats at 8 hours after the HCG treatment. But in the ovariectomized rats, this plasma PGF2alpha peak at 8 hours disappeared and there was no statistical change of plasma PGF2alpha throughout the PMS-HCG treatment. Plasma progesterone gradually increased and reached the maximum at 10 hours after the HCG injection. These results conclude that the main source of increased plasma PGF2alpha during the ovulatory process induced with the PMS-HCG treatment is the ovary, and it is strongly suggested that a rapid increase of PGF2alpha in the ovary may play some important role(s) in the ovulatory process.     

Urogenital vasculature and local steroid concentrations in the uterine branch of the ovarian vein of the female tammar wallaby (Macropus eugenii)

The urogenital vasculature of the tammar comprises 4 major paired arteries and veins: the ovarian, the cranial urogenital, the caudal urogenital and the internal pudendal artery and vein. The ovarian artery and vein and their uterine branches which supply the ovary, oviduct and uterus, ramify extensively. Each anterior urogenital artery and vein supplies the caudal regions of the ipsilateral uterus, lateral and median vagina and cranial parts of the urogenital sinus. The caudal urogenital arteries and veins supply the urogenital sinus and caudal regions of the bladder. The internal pudendal artery and vein vascularize the cloacal region, with some anastomoses with branches of the external pudendal vessels. Anastomoses connect the uterine branch of the ovarian artery with the uterine branch of the cranial urogenital and cranial branches of the caudal urogenital arteries, and connect the caudal urogenital and the internal pudendal arteries. Anastomotic connections between the left and right arterial supply also occur across the midline of the cervical regions of the uteri and the anterior lateral vaginae. Similar connections are seen in the venous system. The uterine branch of the ovarian artery ramifies extensively very close to the ovary, giving a plexiform arrangement with the ovarian veins, and also with the uterine venous system on the lateral side of each uterus. This plexiform structure provides an anatomical arrangement which could allow a local transfer of ovarian hormones from ovarian vein into the uterine arterial supply, and thence to the ipsilateral uterus. Progesterone concentrations in plasma from the mesometrial side of the uterine branch of the ovarian vein are markedly higher than in tail vein plasma, especially during the 'Day 5 peak' early in pregnancy, and also at full term. There is also a marked decrease in progesterone concentration from all sites immediately before birth as previously reported for peripheral plasma. These results support the suggestion of a countercurrent transfer mechanism, at least for progesterone, and possibly other hormones, between the ovarian vein and uterine artery. Such a local transfer could explain the different morphological responses of the endometria of the two adjacent uteri during pregnancy in macropodid marsupial species.     

The involvement of hypophyseal‐gonadal and hypophyseal‐adrenal axes in arsenic‐mediated ovarian and uterine toxicity: Modulation by hCG

This study evaluated the involvement of hypophyseal‐gonadal and hypophyseal‐adrenal axes as a possible mechanism of sodium arsenite toxicity in ovary and uterus by the coadministration of hCG. Subchronic treatment of 0.4 ppm of sodium arsenite/(100 g body weight day) via drinking water for seven estrous cycles significantly suppressed the plasma levels of leutinizing hormone, follicle‐stimulating hormone, and estradiol along with sluggish ovarian activities of Δ⁵,3β‐hydroxysteroid dehydrogenase and 17β‐hydroxysteroid dehydrogenase followed by a reduction in gonadal tissue peroxidase activities in mature female rats at diestrous phase. Noticeable weight loss of the ovary and uterus along with prolonged diestrous phase and increased deposition of arsenic in the plasma and in these reproductive organs were also demonstrated following the ingestion of arsenic. Follicular atresia and thinning of the uterine luminal diameter were evident after sodium arsenite treatment. Effective protection of gonadal weight loss, suppressed ovarian steroidogenesis, and altered ovarian and uterine peroxidase activities were noticed when 1.0 IU hCG/(100 g body weight day) is given in arsenic‐intoxicated rats. Normal estrous cyclicity was restored toward the control level after hCG coadministration, though the elimination of elementary arsenic from the plasma and gonadal tissues was impossible. A significant recovery in the restoration of ovarian and uterine histoarchitecture was prominent after hCG treatment. Adrenal hypertrophy and steroidogenic arrest of the adrenal gland along with altered level of brain monoamines in the midbrain and diencephalons following arsenic intoxication were also ameliorated after hCG coadministration. © 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 24:29–41, 2010; Published online in Wiley InterScience ( www.interscience.wiley.com ). DOI 10.1002/jbt.20309     

Effect of prostaglandin F2α on uterine or ovarian secretion of prostaglandins E and F2α in vivo in 90–100 day hysterectomized, intact or ovariectomized pregnant ewes

Vehicle or 8 or 16 mg of PGF_2α per 58 kg body weight was given intramuscularly to intact, hysterectomized or ovariectomized 90–100 day pregnant ewes in three separate experiments. Both doses of PGF_2α increased PGF_2α in ovarian venous plasma compared with controls at 72 hr post treatment in intact (P≤0.05) but did not in hysterectomized (P≥0.05) 90–100 day pregnant ewes. Concentrations of PGE in ovarian venous blood of intact ewes did not differ (P≥0.05) between treatment groups and were equivalent to concentrations of PGE determined in uterine venous plasma. PGE was decreased in ovarian venous plasma by PGF_2α in hysterectomized ewes (P≤0.07). PGE in uterine venous plasma averaged 6 ng/ml over the 72-hr treatment period in intact and ovariectomized 90–100 day pregnant ewes and was 12 fold greater (P≤0.05) than PGF_2α which averaged 500 pg/ml in uterine venous plasma. Both PGF_2α and PGE increased (P≤0.05) by 64 hr in uterine venous plasma of the 8 mg PGF_2α — treated intact pregnant ewes. A significant quadratic increase (P≤0.05) was observed for PGF_2α and PGE in the vehicle and both PGF_2α treatment groups of intact ewes at the end of the 72-hr sampling period. It is concluded that the uterus and ovaries secrete significant quantities of PGE but little PGF_2α during midgestation. In addition, PGF_2α increased uterine secretion of PGE . PGE may be a placental stimulator of ovine placental secretion of progesterone or PGE may protect placental steroidogenesis from actions of PGF_2α.     

Prostaglandins F in uterine and ovarian venous plasma from nonpregnant and pregnant ewes collected by cannulation

Periodic collections of uterine venous blood were obtained from three nonmated, three pregnant and two mated but nonpregnant ewes in which uterine veins were cannulated with polyvinyl tubing on day 11 postestrus. Frequent sampling was achieved in three of these ewes with additional cannulae in the ovarian veins. Blood samples were collected at 3-hr intervals from 0600 on day 12 to 1800 on day 13 and then at 6-hr intervals through day 15. On day 13, three additional samples at 30-min intervals were collected between 1400 and 1530. Prostaglandins F (PGF) in plasma were quantified by radioimmunoassay.     

Effect of oxytocin on concentration of PGF2 alpha in the uterine lumen and subsequent endometrial responsiveness to oxytocin in pigs

The aim of this study was to determine the effect of oxytocin on PGF2 alpha secretion into the uterine lumen of pigs and subsequent endometrial responsiveness to oxytocin in vitro. Cyclic, pregnant and oestradiol-induced pseudopregnant gilts were injected i.v. with vehicle or 20 iu oxytocin 10 min before hysterectomy on day 16 after oestrus. Concentrations of PGF2 alpha and 13,14-dihydro-15-keto PGF2 alpha (PGFM) were significantly increased in uterine flushings collected at hysterectomy (P < 0.05) in pregnant oxytocin-injected gilts. Concentrations of PGF2 alpha and PGFM were greater (P < 0.001) in pregnant than in pseudopregnant and cyclic gilts, and greater (P < 0.01) in pseudopregnant than in cyclic gilts. The ratio of PGFM:PGF2 alpha tended to be greater in cyclic (P < 0.06) and pseudopregnant gilts (P < 0.1) than in pregnant gilts. At 85 +/- 5 min after oxytocin injection, endometrium from each gilt was incubated for 3 h for determination of phosphoinositide hydrolysis and PGF2 alpha secretion in response to treatment with 0 or 100 nmol oxytocin l-1. Endometrial phosphoinositide hydrolysis in response to 100 nmol oxytocin l-1 in vitro was greater (P < 0.05) in cyclic oxytocin-injected gilts than in cyclic vehicle-injected gilts. Treatment with oxytocin in vitro did not stimulate phosphoinositide hydrolysis significantly in vehicle- or oxytocin-injected pregnant gilts or pseudopregnant gilts. Endometrial PGF2 alpha secretion increased after treatment with 100 nmol oxytocin l-1 in vitro in cyclic vehicle-injected (P < 0.01), cyclic oxytocin-injected (P < 0.01), pregnant vehicle-injected (P = 0.06), pseudopregnant vehicle-injected (P < 0.05) and pseudopregnant oxytocin-injected (P < 0.05) gilts, but not in pregnant oxytocin-injected gilts. The increase in PGF2 alpha in pseudopregnant oxytocin-injected gilts was less (P < 0.05) than that in cyclic oxytocin-injected gilts. These results indicate that oxytocin increases the concentration of PGF2 alpha and PGFM in the uterine lumen during pregnancy and may upregulate endometrial responsiveness to oxytocin during late dioestrus in pigs, but does not have the latter effect during early pregnancy or oestradiol-induced pseudopregnancy.     

3H-oestradiol-17β counter current transfer from the ovarian vein into the ovarian artery in cows

During laparatomy the ovary in the luteal phase with the ovarian pedicle was isolated and transferred under stereomicroscope. The ovary was supplied with blood flowing out of the facial artery through a cannula. ³H-oestradiol-17β or ⁵¹Cr-labelled red blood cells (⁵¹Cr-RBC) were infused for 30 min through the cannula inserted into the ovarian vein 3 cm below the ovary. During and 30 min after the ³H-oestradiol-17β infusion, radioactivity was found both in the ovarian arterial blood near the ovary and in ovarian tissue. When ⁵¹Cr-RBC were infused in the same way as ³H-oestradiol, there was no radioactivity in the arterial blood or ovarian tissue. These experiments indicate the existence of a counter current transfer of ³H-oestradiol-17β from the ovarian vein into the ovarian artery in a cow's ovarian pedicle.     

Natural cytotoxic and antibody-dependent cellular cytotoxic activity of cells in the decidua basales and metrial glands of pseudopregnant rats with deciduomata

Cytotoxic cells are present in the uterine wall of pregnant rats. To determine if the cytotoxic activity arises in response to semen or the products of conception, the profile of cytotoxic activity in deciduomata of pseudopregnant rats was examined. To examine NK activity, Yac-1 cells were used as targets in chromium release cytotoxicity assays and an antibody to Yac-1 cells was included in some assays to determine antibody-dependent cellular cytotoxic (ADCC) activity. Cells from the metrial glands and deciduae of deciduomata of rats at days 10 and 13 of pseudopregnancy did not show NK activity but ADCC activity was present. To examine natural cytotoxic (NC) activity, Wehi 164 cells were used as targets in chromium release cytotoxicity assays. Cells isolated from the metrial glands and deciduae of rats at day 10 of pseudopregnancy were able to kill Wehi 164 cells after 21 h assays, thus demonstrating NC activity. The profile of cytotoxic activity in the uterine wall of pseudopregnant rats with deciduomata is similar to that found in pregnancy and is thus independent of semen or the products of conception.     

Effects of the fetal-placental unit on uterine prostaglandin levels at term in the pregnant rat

Uterine prostaglandins (PGs) increase markedly at term in the pregnant rat. To assess the contribution of the fetal-placental unit (FPU) on uterine tissue and uterine venous blood PG concentrations, each uterine horn of 14 unilaterally pregnant rats at day 21 of pregnancy were compared. In addition, 7 bilaterally pregnant rats were studied. Uterine tissue and uterine venous plasma PGF, PGE, 6-Keto-PGF1 (6KF) and thromboxane B2 (TxB2) and systemic plasma progesterone, estradiol and estrone were determined by radioimmunoassay. Uterine concentrations of PGs (ng/mg DNA) were always greater on the pregnant side of unilaterally pregnant rats (p less than .05) although the PGF levels were elevated to a lesser extent than were PGE, TxB2 or 6KF. However, no differences were detected between uterine tissue from the pregnant side of unilaterally pregnant compared to bilaterally pregnant rats. In addition, no differences were found in uterine venous plasma PGs adjacent or opposite the pregnant uterine horn and in systemic plasma progesterone, estradiol and estrone levels in unilaterally vs bilaterally pregnant rats. These data suggest that the presence of the FPU is associated with an increased capacity of uterine tissue to produce PGE, TxB2 and 6KF, and to a lesser degree PGF, and thus may contribute to the increase in uterine PGs periparturition.     

Progesterone in uterine and arterial tissue and in jugular and uterine venous plasma of sheep

Concentrations of progesterone in uterine and arterial tissue and in uterine and jugular venous plasma were determined. Blood was collected on Days 4 and 9 postestrus from the jugular vein and the first and last venous branches draining each uterine cornu; uterine tissue and arteries were subsequently collected. Progesterone was greater (p less than 0.05) in the cranial third than in the middle or caudal thirds of the uterine horn adjacent to the corpus luteum (CL)-bearing ovary or in any third of the contralateral horn. Progesterone in uterine arterial segments adjacent to the CL-bearing ovary was higher (p less than 0.05) than in contralateral segments. Progesterone was higher (p less than 0.05) in blood from the first venous branch of the cranial third of the uterine cornu adjacent to the ovary with the CL, than in the last branch of the caudal third, or contralateral horn, or in jugular blood. When oviductal veins were resected on Day 9 postestrus, progesterone in the first vein draining the cranial third of the uterine cornu adjacent to the CL-containing ovary was not different (p greater than 0.05) 48 h after resection than in the same vessel in the opposite horn or in jugular blood. We concluded that progesterone and other ovarian products may be delivered to the uterus locally.     

The possible mode of action of prostaglandins IX-prostaglandin F2alpha involvement in the reversal of ovulation blockade by ergocornine in rats.

A single injection of 1 mg ergocornine methanesulphonate to semispayed rat on day 3 of the cycle was found to block ovulation. However, the animals showed regular compensatory hypertrophy of the remaining ovary. Prostaglandin F2alpha (PGF2alpha) of 2.0 mg/kg bw on days 3 and 4 in the ergocornine-blocked semispayed rats consistently reversed the blocking effect and the animals showed compensatory ovulation and ovarian hypertrophy. It was moreover observed that the ergocornine-treated mated animals did not become either pregnant or pseudopregnant, but returned to normal cycle as usual. Conversely, the animals which had combined regimen of ergocornine and PGF2alpha became pregnant and the number of embryonic swellings in a single horn and their average weight were statistically identical to their experimental controls. The possible involvement of PGF2alpha in the mechanism of follicular rupture has been discussed.     

Levels of prostaglandin F (PGF) in bovine endometrium uterine venous, ovarian arterial and jugular plasma during the estrous cycle (38789).

Prostaglandins F (PGF) were measured in uterine vein, ovarian artery, and jugular vein plasma and in the endometrial tissues at various times during the bovine estrous cycle, and were compared to peripheral plasma progesterone levels. Four groups of heifers at days 1-5, 10-14, 15-17 and 20-0 of the estrous cycle were studied. Low levels of PGF (48 plus or minus 12 ng/g dry tissue were measured in the endometrium on days 1-14 of the cycle. Higher values (131 plus or minus 9.0) were found at days 15 until the day of estrus (p less than 0.001). Similarly, very low levels of PGF were observed in the uterine vein plasma at days 1-14 (0.162) plus or minus 0.044) ng/mlM plus or minus S.E.), whereas on days 15 until the day of estrus the levels ranged from 1.5 to 3.0 ng/ml. The increases in uterine vein PGF on day 15 occurred even while peripheral plasma progesterone levels were still high. However, PGF was not elevated in either the ovarian artery or the jugular vein at any time during the cycle, even when uterine vein levels were greatly elevated. No differences in PGF content were detected in endometrial tissue from uterine horns adjacent or opposite to the functional corpus luteum.     

Local exchange of oxytocin from the ovarian vein to ovarian arteries in sheep

Local transfer of 125I-labeled oxytocin from the ovarian vein to arteries supplying the ovary, the oviduct, and the tip of the uterine born has been investigated. In five sheep, 10 infusions of 125I-oxytocin over a period of 1 h were performed, and the concentration of labeled polypeptide in the peripheral plasma was compared to ovarian arterial plasma. During 2 consecutive infusions into each animal's ovarian vein, blood was collected simultaneously from the following sites: ovarian branch of the ovarian artery (OBOA), tubal branch of the ovarian artery (TBOA), uterine branch of the ovarian artery (UBOA), and from the jugular vein. In all experiments the concentration of 125I-oxytocin in ovarian arterial plasma was higher than in peripheral plasma. The ratio of ovarian artery/jugular vein for 125I-oxytocin was: OBOA 2.8, TBOA 1.8, UBOA 1.6. Based on a 4 ml/min blood flow through ovarian arteries supplying ovary, oviduct, and the tip of the uterine horn, the local transfer of the total amount of oxytocin infused was estimated to be about 1% (range: 0.1-4.4%). Analysis of variance did not reveal significant differences in the exchange ratios between OBOA, TBOA, and OBOA. However, the variances within these groups are significant, presumably because of anatomical variation in the degree of surface contact area between arteries and veins at the ovarian pedicle. It is concluded that polypeptides are locally recirculated to ovaries, oviduct, and the tip of the uterine horn in a higher concentration than is supplied by peripheral blood. This could provide a mechanism for local distribution and concentration of the ovarian peptides that regulate reproductive function.