Prostaglandin F levels in endometrial jet wash specimens during the normal human menstrual cycle

The Gravlee endometrial jet wash technique has been used to collect uterine fluid in normal human volunteers for Prostaglandin F analysis throughout the human menstrual cycle. Uterine washings so obtained demonstrated a cyclicity in prostaglandin F content with low concentrations found during the proliferative phase and a 3–4 fold rise occurring during the secretory phase. Menstrual fluid prostaglandin F content collected with the jet wash technique gave the highest total concentrations.     

Prostaglandin levels in endometrial jet wash specimens in patients with dysmenorrhea before and after indomethacin therapy

A patient with functional primary dysmenorrhea of over two years duration was subjected to the endometrial jet wash technique during the period of active menstrual flow. Prostaglandin F analysis of the jet washings revealed significantly elevated levels during menstruation over normal control levels. Following indomethacin therapy, jet wash prostaglandin F levels were dramatically reduced and the patient became asymptomatic. A cause and effect relationship between prostaglandin F and dysmenorrhea is suggested by these studies     

Prostaglandin levels in endometrial jet wash specimens in patients with dysmenorrhea before and after indomethacin therapy.

A patient with functional primary dysmenorrhea of over two years duration was subjected to the endometrial jet wash technique during the period of active menstrual flow. Prostaglandin F analysis of the jet washings revealed significantly elevated levels during menstruation over normal control levels. Following indomethacin therapy, jet wash prostaglandin F levels were dramatically reduced and the patient became asymptomatic. A cause and effect relationsship between prostaglandin F and dysmenorrhea is suggested by these studied.     

Prostaglandins in fetal tracheal and amniotic fluid from late pregnant sheep

Concentrations of prostaglandin E (PGE), prostaglandin F (PGF) and 13,14-dihydro-15-keto-prostaglandin F (PGFM) have been measured in fetal tracheal and amniotic fluid from chronically catheterized sheep during late pregnancy. Amniotic fluid contained significantly greater concentrations of these prostaglandins than tracheal fluid (p less than 0.01); there was no correlation between the level of prostaglandins found in each fluid. In tracheal fluid concentrations of PGE and PGFM exceeded those of PGF (P less than 0.01) whereas no significant differences were found in amniotic fluid. The levels of prostaglandins in these fluids were similar in ewes bearing hypophysectomized fetuses.     

Prostaglandin F in monkey uterine fluid during the menstrual cycle and following steroid treatment

Prostaglandin F levels were determined in monkey uterine fluid collected daily from a silicone tubing collection system surgically installed in adult female rhesus monkeys. Sampling was obtained from intact and ovariectomized — hormone treated monkeys. During the primate menstrual cycle, uterine fluid prostaglandin F levels showed a cyclic pattern in concentration with highest values recorded during the 18–20th day of the cycle. Estrogen treatment to the ovariectomized female elicited a striking and marked increase in uterine fluid prostaglandin F levels while progesterone treatment had little effect. These results suggest that the presence of uterine fluid prostaglandin F is estrogen dependent and may be causely related to the control of menstrual cyclicity.     

Fetal viability does not affect the onset of stretch-induced labor and the increase in amniotic fluid prostaglandin F2 alpha and plasma prostaglandin F2 alpha metabolite levels.

The role of the fetus in the onset and progress of stretch-induced labor and in the change in amniotic fluid prostaglandin F2 alpha and plasma prostaglandin F2 alpha metabolite levels was evaluated in six normal pregnant women (group 1) and six women whose fetuses had been dead for more than one week (group 2). The uterus was distended by a balloon inflated with physiologic saline. Regular uterine contractions occurred, and increased in all patients. Within 21 hours, all patients delivered a normal baby in group 1 and a macerated fetus in group 2. There was no significant difference in induction-delivery interval between the two groups. Both groups showed a significant and similar range of increases in the levels of amniotic fluid prostaglandin F2 alpha and plasma prostaglandin F2 alpha metabolite during treatment (P less than 0.001). Thus, the fetus has no functional role in the onset and progress of stretch-induced labor or in the rise of amniotic fluid prostaglandin F2 alpha and plasma prostaglandin F2 alpha metabolite levels.     

Radioimmunoassay of progesterone, 17-hydroxyprogesterone, estradiol-17beta and prostaglandin F in human corpus luteum.

Radioimmunoassay procedures have been adapted for the assay of progesterone, 17-hydroxyprogesterone, estradiol-17beta, and prostaglandin F in human corpus luteum. The method utilises a single homogenisation and extraction of the tissue followed by fractionation of the steroids on alumina, and separation of the prostaglandins of the F series from the E and A series on silica gel, prior to radioimmunoassay. An attempt has been made to validate the method for the progestins by comparison with results after fractionation of the progestins on Sephadex LH-20, for estradiol-17beta by comparison with values obtained with competitive protein-binding, and for prostaglandin F by comparison with values after additional purification. The results showed that peak concentrations of the three steroids in corpora lutea from women during the luteal phase of the menstrual cycle were comparable to those found in corpora lutea from women in early pregnancy. However, in six out of fourteen corpora lutea from non-pregnant women, prostaglandin F levels were higher than those found in corpora lutea from seven women in early pregnancy, i.e. 13-46 ng/g compared with 1-7 ng/g. Of the above six corpora lutea, four were on days 23-25 of the cycle, at a time when luteolysis would be commencing. The results in this paper support the conclusion that the corpus luteum is a major site of synthesis of the three steroids examined, although the site of synthesis of prostaglandin F is still equivocal.     

Central venous concentrations of immunoreactive prostaglandins E,F, and 6-keto-prostaglandin F1 in eclampsia.

Concentrations of prostaglandins E, F, and 6-keto-prostaglandin F1 alpha were estimated in central venous blood and amniotic fluid in 21 women with eclampsia and 16 healthy pregnant controls. Central venous blood concentrations of 6-keto-prostaglandin F1 alpha and prostaglandin E were significantly lower in patients than controls before delivery and remained reduced for at least 48 hours after delivery. Low concentrations of prostaglandins E and 6-keto-prostaglandin F1 alpha are probably directly related to the pathogenesis of eclampsia.     

Gonadotropin-releasing hormone in third ventricular cerebrospinal fluid of the heifer during the estrous cycle

The release profile of GnRH in cerebrospinal fluid (CSF) and its correlation with LH in peripheral blood of ovary-intact heifers during the estrous cycle were investigated. A silicon catheter was placed into the third ventricle of six heifers using ultrasonography. During the mid-luteal phase, the heifers were injected with prostaglandin F(2alpha) to induce luteolysis. Surges of CSF GnRH (66.7 h after prostaglandin F(2alpha) administration) and peripheral LH (66.3 h) occurred simultaneously and were coincident with the onset of estrus (67.0 h). Duration of elevated GnRH concentration considerably overlapped with the estrous phase in each of the heifers. Mean pulse frequencies of both GnRH and LH were significantly higher during the proestrous and early luteal phases than during the mid-luteal phase, while mean concentration and pulse amplitude of both GnRH and LH were not different between these three phases. Of all the GnRH pulses identified, more than 80% were accompanied by an LH pulse during the proestrous and early luteal phases. However, the proportion of GnRH pulses that were coincident with an LH pulse during the mid-luteal phase decreased to 60%. The results clearly demonstrate that a dynamic (pulse) and longer-term (surge) changes of GnRH release into CSF are physiologically expressed during the estrous cycle in heifers, and the pattern of pulsatile GnRH secretion in heifers depends upon their estrous cycle.     

Endogenous stimulant of prostaglandin endoperoxide synthase activity in human amniotic fluid

In this study we describe the discovery and characterization of a substance in human amniotic fluid that stimulates prostaglandin biosynthesis by a microsome-enriched preparation of bovine seminal vesicles. The stimulatory activity is not retained substantially upon anisotropic ultrafiltration through a filter with a molecular weight exclusion limit of 500. Stimulation of prostaglandin biosynthesis by this substance is time- and concentration-dependent; maximal stimulation of approx. 200% being observed within 20 min of commencing incubation with 1 ml-equivalent of stimulant fraction. Stimulatory activity is demonstrable both in the presence of reduced glutathione (1.3 mM) and L-tryptophan (20 mM), either separately or combined, and in the presence of exogenous arachidonic acid (5-120 microM). In the absence of added cofactors, the stimulatory substance increases the rates of biosynthesis of prostaglandin E2 and prostaglandin F2 alpha to equal extents. The amount of stimulatory substance added to incubations is correlated positively with increased oxygen consumption during incubations. The stimulatory substance is stable to heating at 100 degrees C for 10 min but is inactivated substantially (to less than 20% of original activity) by treatment with pronase. It is concluded that human amniotic fluid contains a substance of relatively low molecular weight, which is proteinaceous in character, that stimulates prostaglandin endoperoxide synthase activity.     

Is prostaglandin F2 alpha involved in the increased myometrial contractility of primary dysmenorrhoea?

The concentrations of prostaglandin F2 alpha (PGF2 alpha) and E2 (PGE2) in menstrual fluid collected daily from 13 women with primary dysmenorrhoea and 11 matched controls, were compared with the pattern of uterine contractility during the hour following the menstrual fluid collection. The intra-uterine pressure (IUP) was measured using a micro-transducer catheter and the tracings analysed. On Day 2 the concentration of PGF2 alpha correlated with the peak area, but not with amplitude, duration or rate of contraction. These findings add additional support to the hypothesis that increased production of PGF2 alpha could contribute to the increased uterine contractility in primary dysmenorrhoea.     

Prostaglandin biosynthesis and catabolism in the developing fetal sheep lung.

The prostaglandin biosynthetic and catabolic capacity of homogenates of lungs from fetal sheep of various gestational ages was measured. Prostaglandin biosynthesis was assayed by the deuterium-isotope dilution technique making use of mass fragmentography whereas prostaglandin catabolism was measured by the radioisotope-dilution method described previous (Pace-Asciak, C.R. and Rangaraj, G. (1976) J. Biol. Chem. 251, 3381-3385). Homogenates of lungs from fetuses of all ages tested (40 days to term) formed both prostaglandins E2 and F2alpha; although prostaglandin F2alpha was formed to a greater extent than prostaglandin E2 by the 40 days lung, prostaglandin E2 increased with increasing age until at term the ratio of both prostaglandins approached unity. Total prostaglandin biosynthesis (E2 + F2alpha) rose gradually with age (approx. 3 fold increase between 40 days and term). Prostaglandin F2alpha catabolism occurred mainly by the prostaglandin 15-hydroxy dehydrogenase pathway; this activity was detectable even at 40 days and remained unchanged up to 80 days. Prostaglandin catabolic activity rose sharply at 90 days (approx. 3 fold) with a maximum around 110 days (approx. 4 fold) decreasing back to 40 day levels by term (143 days). The increasing prostaglandin catabolic activity around 90-100 days in this species is discussed in relation to the hemodynamic changes in the lungs starting around this age and the appearance of surfactant. Prostaglandin catabolism might play an important role in the developing organ controlling steady state concentrations of prostaglandins during certain periods of organogenesis.     

The effect of acute hypoxia on prostaglandin release in perfused human fetal placenta

The release of prostaglandin E2 and F2 alpha, thromboxane B2 and 6-keto-prostaglandin F1 alpha was measured in isolated human placental cotyledons perfused under high- and low-oxygen conditions. Also the effect of reoxygenation on prostaglandin production was studied. During the high-oxygen period, prostaglandin E2 accounted for 44% and 6-keto-prostaglandin F1 alpha for 28% of all prostaglandin release, and the rank order of prostaglandin release was E2 greater than 6-keto-prostaglandin F1 alpha greater than thromboxane B2 greater than prostaglandin F2 alpha. Hypoxia had no significant effect on quantitative prostaglandin release, but the ratio of prostaglandin E2 to prostaglandin F2 alpha was significantly increased. After the hypoxic period during reoxygenation the release of 6-keto-prostaglandin F1 alpha was significantly decreased, as was the ratio of 6-keto-prostaglandin F1 alpha to thromboxane B2. Also the ratio of the vasodilating prostaglandins (E2, 6-keto-prostaglandin F1 alpha) to the vasoconstricting prostaglandins (thromboxane B2, prostaglandin F2 alpha) was decreased during reoxygenation period. With the constant flow rate, the perfusion pressure increased during hypoxia in six and was unchanged in three preparations. The results indicate that changes in the tissue oxygenation in the placenta affect prostaglandin release in the fetal placental circulation. This may also have circulatory consequences.     

Isolation of two novel E prostaglandins in human seminal fluid

cis-8,11,14,17-[1-14C]Eicosatetraenoic acid was incubated with microsomes of ram seminal vesicles and 1 mM glutathione for 3 min at 37 degrees C. The main metabolite was identified as 17,18-dehydroprostaglandin E1 by capillary column gas chromatography-mass spectrometry. Human seminal fluid was analyzed for the presence of 17,18-dehydroprostaglandin E1 and prostaglandin E3. Whereas prostaglandin E3 could be demonstrated by capillary gas chromatography-mass spectrometry, 17,18-dehydroprostaglandin E1 could not be found under these conditions. However, human seminal fluid contained two compounds with a similar polarity on reversed phase high performance liquid chromatography as 17,18-dehydroprostaglandin E1 and prostaglandin E3. The two compounds were identified as 18,19-dehydroprostaglandin E1 and 18,19-dehydroprostaglandin E2 by gas chromatography-mass spectrometry, by UV analysis after conversion to the corresponding prostaglandin B compounds, and by ozonolysis. The amount of each of the two prostaglandins in human seminal fluid seemed to be in the same order of magnitude as the amount of prostaglandin E3.     

Effect of prostaglandin F2alpha on cells of the mammary gland alveoli in mice

In studies on lactating laboratory mice an influence of prostaglandin F2 alpha on the value of transepithelial potential difference and resistance of the alveolar secretory epithelium in the mammary gland, was studied. Prostaglandin F2 alpha did not affect initial level of transepithelial potential difference and resistance in alveoles. In all experiments with the preliminary application of prostaglandin F2 alpha in different concentrations (1 x 10(-5)-1 x 10(-11) M) was registered a reliable increase in an amplitude (before 31 +/- 2%) and duration (before 43 +/- 3%) to return reactions on oxytocin. Prostaglandin F2 alpha caused a reduction of transepithelial resistance in the alveolar secretory epithelium of first phase to return reaction on oxytocin on 28 +/- 22%. The data obtained indicate a possibility of participation of prostaglandin F2 alpha in development of certain stages of shaping a composition of milk.     

Prostaglandin production by horse embryos and the effect of co-culture of embryos with endometrium from pregnant mares

Embryos, endometrial biopsies, and uterine lavage fluid were collected from pregnant and non-pregnant mares 14 days after ovulation. Embryos were cultured for 20.5 h with and without endometrial tissue from pregnant mares, and endometrial tissue was cultured alone. Endometrial content of PGF tended to be higher (P = 0.06) in non-pregnant than in pregnant mares, but the amount of PGF released from tissue during culture was similar for pregnant and non-pregnant mares. Lavage fluid from non-pregnant mares also tended (P = 0.08) to contain higher concentrations of PGF. Coincubation of embryos with endometrium from pregnant mares significantly (P = 0.01) lowered concentrations of PGF in medium. Tissue concentrations and release of PGE-2 and 6-keto-PGF-1 alpha were similar in endometrial samples from pregnant and non-pregnant mares and prostaglandin production was unaffected by the presence of an embryo during incubation. Horse embryos released all three prostaglandins during a 20.5-h incubation.     

Evaluation of potential risks of abrasive water jet osteotomy in-vivo]

Since the 80's the water jet scalpel is an established tool in some surgical fields. It is used in particular in visceral surgery for preparation of parenchymatous organs. By the addition of biocompatible abrasives, this technique is able to effectively machine hard biological tissues. Free defined cutting geometries can be realised in a non contact process. Therewith this method has crucial advantages compared to conventional osteotomy techniques and gives new impulses to the development in endoprosthetics and correction osteotomies of hollow bones. In the presented work the new developed abrasive water injection jet (AWIJ) was used the first time for in-vivo osteotomies. Aim of this study was the detection of potential thrombembolic effects and wash in effects of the cutting fluid. Hollow bones of the fore and hind leg of 20 house pigs were treated with the new cutting technique. Intraoperative documentation of relevant vital parameters was performed by a multi monitoring system. Thrombembolic effects during the osteotomy were detected by transthoracic Doppler ultrasonography and transesophagale echocardiography. The hollow bones were prepared in consideration of the vascularisation's protection especially in respect to the venous flow. Thrombembolic effects with temporary haemodynamic respectively respiratory consequences could be detected exclusively by using the so called "3-component jet", which consists of 90 vol % of air. The usage of an abrasive suspension enables the airfree dosing of dry soluable abrasives. Thrombembolic effects could not be monitored in this case. Intramedullary fluid in-wash effects as well as resulting electrolytic disorders could not be proven. For abrasive waterjet osteotomies with 3 component jet a relevant risk of thrombembolic effects could be shown. This knowledge has also to be considered for abdominal and neurosurgical applications in the future. Due to the usage of an abrasive suspension this risk can fully be avoided.     

Zero extracellular K+ and prostaglandin E release in the guinea-pig taenia coli

Prostaglandin E release rates from isolated strips of guinea-pig taenia coli increased during exposure to zero K+ bathing fluid, from control values of 0.78 +/- 0.11 ng/g per min to levels as high as 29.2 ng/per min. Release rates increased for 40-50 min and then remained constant or fell despite progressive increases in intracellular sodium [Nai+] or fall in intracellular potassium [Ki+]. Readmittance of K+ to the bathing solution resulted in rapid reversal of elevated prostaglandin E release rates. [Nai+] and [Ki+] were markedly more abnormal in strips exposed to zero K+ for 70-201 min compared to 30-min exposures. Upon the readdition of K+ after long zero K+ exposure, the rate of prostaglandin E release fell long before [Nai+] and [Ki+] returned to control levels. After K+ was readded to the bathing solution, the ion concentration of tissues exposed to zero K+ for 30 min returned to normal much more quickly than did those of tissues exposed for the longer time periods, yet the exponential rate constants for fall of prostaglandin E release rate after K+ was added were not significantly different after short or long zero K+ exposure. Thus there was a dissociation between the return of [Nai+] and [Ki+] and the fall of prostaglandin E release rate to control levels. Ouabain augmented prostaglandin E release under conditions where [Ki+] could not fall. Addition of known neurotransmitters present in this tissue to the bathing fluid did not augment prostaglandin E release. Guinea-pig taenia coli strips that had been incubated with [3H]arachidonic acid, constantly released [3H]arachidonic acid and [3H]prostaglandin E and a prostaglandin which cochromatographed with prostaglandin E but could not be converted to prostaglandin B by alkali and was shown to be 6-ketoprostaglandin F1 alpha. Release of [3H]arachidonic acid and [3H]prostaglandin E plus 6-[3H]ketoprostaglandin F1 alpha was increased when strips were exposed to zero K+. Data obtained in this study suggest the augmented prostaglandin E release seen during zero K+ or ouabain is related to increased availability of unbound arachidonic acid at the site of cyclooxygenase in the cell. Augmented prostaglandin E release is apparently not related to alterations in intracellular electrolyte concentrations or release of known neurotransmitters.     

Plasma membrane changes during corpus luteum regression

Structural and biochemical changes were examined in the plasma membrane of luteal cells during corpus luteum regression. Structural alterations as indicated by an increase in the liquid-crystalline to gel phase transition temperature and a decrease in plasma membrane fluidity were observed during luteolysis in microsomes and in plasma membranes prepared from prostaglandin F2 alpha-treated rats, when samples were examined by wide angle x-ray diffraction and fluorescence polarization. In addition, a significant increase in activity of the lipolytic enzyme phospholipase A2 appeared during incubation of plasma membrane samples and dispersed luteal cells at 40 degrees C in the presence of 1.0 mM CaCl2. Similar incubation conditions also produced a drop in human chorionic gonadotropin (hCG) binding in luteal samples from prostaglandin F2 alpha-treated rats. These results indicate that during luteolysis there are important structural changes in the plasmalemma of regressing luteal cells. These alterations appear related to an increase in phospholipase A2 activity and a decrease in hCG receptors. These modifications may account for the decrease in function during corpus luteum regression.     

Differential regulation of prostaglandin production by inhibitors and stimulators in amiotic fluids during normal and dysfunctional labor

The regulatory effect of amniotic fluid factors on prostaglandin production by sheep seminal vesicle prostaglandin synthetase was determined using samples obtained before and after the onset of labor. Variations in the enzymes incubation conditions permitted the effects on both prostaglandin E (PGE) and prostaglandin F (PGF) production to be assessed. Amniotic fluid obtained before the onset of labor and during early labor resulted in a net stimulation of PGE production and no difference was observed between these two groups. Samples obtained before and during early labor had no effect of PGF production. However, when samples obtained late in labor were tested, there was a greater stimulation of PGF and less of PGE compared to early labor suggesting a preference for PGF production rather than PGE in late labo. When samples obtained from patients in dysfunctional labor were compared to normal labor, no difference on the effect of either PGE or PGF production was observed. This implies that the decreased PGF previously described in dysfunctional labor is due to an intrinsic abnormality of the fetal membranes rather than inhibition of prostaglandin production by factors mediated via the amniotic fluid.