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awa Stefa
czyk-Krzymowska
1
opek
1
Radomski
1
1 Department of Local Physiological Regulations, Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, Tuwima 10, 10-747 Olsztyn, Poland
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Abstract |
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(Received 31 May 2005;
accepted after revision 6 July 2005; first published online 7 July 2005)
Corresponding author S. Stefaczyk-Krzymowska: Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, Tuwima 10, 10-747 Olsztyn, Poland, Email: skrzym{at}pan.olsztyn.pl
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Introduction |
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(PGF2) was enhanced in endometrial cells of pregnant gilts in comparison to cycling gilts (Zhang & Davis, 1991; Davis & Blair, 1993). The content of PGE2 in the uterine lumen was also elevated between days 11 and 14 of pregnancy (Giesert et al. 1982). The secretion of PGE2 by the embryo and its increased synthesis by endometrial cells of early pregnant gilts suggested an increased role for PGE2 in the reproductive organs during this time.
PGs are involved in the control of numerous processes crucial for the establishment of pregnancy. Experiments performed on several species have shown that PGE2 and PGF2 participate in the following operations: the regulation of the lifespan of the corpus luteum (Mojelono et al. 1977; Akinlosotu et al. 1986); growth and differentiation of endometrial cells (Orlicky et al. 1986; Bützow et al. 1988); uterine blood flow (Ford & Christensen, 1979; Bell et al. 1990); vascular permeability (Keys et al. 1986); spacing of embryos in the uterus (Wellstead et al. 1989); and implantation (Dantzer, 1985; Gupta et al. 1989). The presence of PGE2 receptors in porcine endometrium was demonstrated during early pregnancy (Kennedy et al. 1986), and evidence obtained using indomethacin suggested that synthesis of prostaglandins is necessary for the establishment of pregnancy in the pig (Kraeling et al. 1985).
An increase in uterine blood supply due to relaxation of the porcine uterine artery by PGE2 was also shown (Bell et al. 1990). Moreover, the luteotrophic and antiluteolytic effect of PGE2 in the pig was demonstrated during the oestrous cycle (Akinlosotu et al. 1986, 1988) and early pregnancy (Christenson et al. 1994). Recently, the involvement of PGE2 in the local endocrine regulation of the oestrous cycle and early pregnancy in the pig has been postulated (Zi
cik, 2002; Krzymowski & Stefaczyk-Krzymowska, 2002, 2004).
The permeation of PGF2 from venous blood and lymph flowing out of the uterus to arterial blood and its retrograde transfer to the uterine tissues and uterine cavity, dependent on the reproductive stage in the pig, was demonstrated earlier during the oestrous cycle (Krzymowski et al. 1986; Stefaczyk-Krzymowska et al. 1992; Stefaczyk-Krzymowska, 1996) and early pregnancy (Krzymowski et al. 1987; Stefaczyk-Krzymowska et al. 1990). An experiment performed on unilaterally ovariectomized gilts showed how ovarian hormones influence retrograde transfer of PGF2 (Stefaczyk-Krzymowska et al. 1992). In addition, local transfer of PGF2 to the ovary on particular days of the porcine oestrous cycle and pregnancy was shown (Stefaczyk-Krzymowska et al. 1990). This distribution of PGF2 in the area of the reproductive organs may provide evidence of effective local utilization of prostaglandins. The importance of the locally increased arterial concentration in hormonal regulation within the organ was recently postulated (Einer-Jensen & Hunter, 2005).
This study was designed to establish: (a) whether PGE2 can reach the ovary by a local pathway and what is the contribution of lymphatic vessels to this transfer; and (b) whether PGE2 can permeate from venous and lymphatic vessels of the mesometrium to arterial blood and be delivered to the uterine horn during maternal recognition of pregnancy in gilts.
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Methods |
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All experiments were conducted in accordance with protocol No59/2002/N approved by the local Ethics Committee for Animal Experiments. Crossbred gilts (n= 10) bred on a commercial farm were mated after two controlled oestrous cycles. Fourteen days after mating the gilts were killed by electrical stunning (ENZ-Metalowiec, Bydgoszcz, Poland) and exsanguination. The blood was collected and heparinized (10 iu ml–1). The reproductive tract was excised, placed on ice, quickly transported to the laboratory and used to prepare two isolated uterine horns with ovary and broad ligament. Each isolated preparation consisted of about half of the uterine horn with adjacent ovary and broad ligament.
The general experimental design is illustrated in Fig. 1. Silastic catheters were inserted: (1) (o.d., 2.5 mm; i.d., 2.0 mm) into the uterine artery; and (2) (o.d., 2.0 mm; i.d., 1.6 mm) into the ovarian artery to supply the isolated organs with autologous blood. The third catheter (3) (o.d., 4.0 mm; i.d., 3.0 mm) was inserted into the utero-ovarian vein to collect outflowing venous blood. An additional catheter (4) (o.d., 1.0 mm; i.d., 0.6 mm) was inserted into one of the branches of the uterine artery in the central part of the mesometrium as close as possible to the uterine horn to collect the blood supplying the uterine horn (Fig. 1). Peripheral blood vessels of the uterus and broad ligament and the end of the excised part of the uterine horn adjoining the ovary were ligatured.
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Experiment I: local transfer of [3H]PGE2 from venous vessels to the ovary and to arterial blood supplying the uterine horn (n= 9)
Three cannulae (o.d., 1.0 mm; i.d., 0.6 mm) labelled in Fig. 1 as 5, 5' and 5'' were inserted into the small branches of the uterine vein on the broad ligament approximately 1 cm from the junction of the uterine horn and the mesometrium, about 10, 20 and 30 cm from the isthmus of the oviduct (Fig. 1). Then, [5,6,8,11,12,14,15–3H(N)]PGE2 (specific activity 185 Ci mmol–1, Amersham Biosciences UK Limited, Buckinghamshire, UK) at a total dose of 5.5 x 107 d.p.m., corresponding to 49 ng, dissolved in 1.5 ml saline, was infused continuously at a constant rate for 30 min in equal portions into three cannulated venous branches (Fig. 1).
Experiment II: local transfer of [3H]PGE2 from lymphatic vessels to the ovary and to arterial blood supplying the uterine horn (n= 8)
Three injection needles, labelled in Fig. 1 as 6, 6' and 6'' (o.d., 0.5 mm), were connected by cannulae with a microinfusing pump. They were carefully inserted, to avoid all visible blood vessels, into the most superficial layer of the myometrium under the serosa of the uterus along the length of the uterine horn, about 10, 20 and 30 cm from the isthmus of the oviduct approximately 0.5 cm from the junction of the uterine horn and the mesometrium. [3H]PGE2 prepared as described in Experiment I and at the some dose was infused for 30 min in equal portions at three different sites (Fig. 1). The infusion was performed into the most superficial layer of the myometrium under the serosa according to the method used for filling the lymphatic vessels of the reproductive organs with Microfil®, MercoxTM or coloured gelatin (Gawroska et al. 1992, 1997; Jankowska et al. 2001; Doboszyska, 2002). This method of infusion was adopted in a study of the counter-current transfer of PGF2 in porcine mesometrium by Krzymowski et al. (1987). In that study and in the current study, lymphatic vessels draining the mesometrium were visualized with Evans blue injected under the serosa as described by Staples et al. (1982).
Collection of blood, uterine flushing and tissue samples
In Experiments I and II, after blood perfusion started, samples were collected of arterial blood supplying the uterine horn from a cannulated branch of the uterine artery and venous blood flowing out from the isolated organ: control samples (n= 3) and every 5 min from the beginning of [3H]PGE2 infusion for the experimental period of 60 min. The samples were immediately centrifuged and plasma was harvested. When blood perfusion of the isolated preparation was stopped, 50 ml saline was injected into the uterine lumen and uterine flushing samples were collected. Tissue samples of myometrium and endometrium were dissected from three different sites of the antimesometrial surface of the uterine horn. From the broad ligament samples of the muscular layer of the mesometrium (n= 3) (close to the ovary, the central part and close to the uterine body parts of the broad ligament), branches of the uterine artery (n= 2) and branches of the uterine vein (n= 2) from different sites were dissected. Tissue samples of the corpus luteum (n= 3) and stroma of the ovary (n= 2), the muscular layer of the mesovarium (n= 2) and segments of the oviduct adjoining the uterine horn (n= 2) were collected. Corresponding control tissues samples were excised from the reproductive organs of additional untreated animals to estimate the background radioactivity.
Measurement of radioactivity of samples
Duplicate samples (0.5 ml) of blood plasma and uterine flushings were mixed with a scintillation cocktail (10 ml), and [3H]PGE2 radioactivity was quantified by liquid scintillation spectroscopy (LS 5000 TD, Beckman Instruments, CA, USA). The radioactivity of each sample was measured for 10 min using a program with automatic quench compensation. All tissue samples weighing approximately 100 mg were digested (40°C) in 1 ml tissue solubilizer (Soluene 350, PerkinElmer Life and Analytical Sciences, Boston, MA, USA). Then, Ultima Gold cocktail (10 ml, PerkinElmer Life and Analytical Sciences) was added and radioactivity was measured as described for the plasma samples. Mean values (d.p.m.) of the control blood and tissues samples (background samples) were subtracted from the experimental samples. [3H]PGE2 concentration was calculated according to the radioactivity and specific activity of the labelled prostaglandin.
Determination of the presence of unaltered [3H]PGE2 molecules in plasma samples by means of specific antibody
To determine whether the radioactivity found in venous blood and arterial blood represented unaltered [3H]PGE2 particles, the following experiments were performed. To the buffer solution with a known amount of [3H]PGE2, highly specific antibodies (Seragen, Inc. Boston, MA, USA) were added to a concentration that bound 60% of radioactive prostaglandin. The antibody cross-reacted with other prostaglandins: PGE1, 3.2%; PGF2, 0.06%; PGA2, 0.2%; 13,14-dihydro-PGE2, 0.15%; and 13,14-dihydro,15 keto-E2, 0.11%. Free and bound prostaglandin was separated with dextran-coated charcoal. Using the same conditions as in the control experiment, the antibodies were added to the samples of plasma containing known levels of radioactivity collected during the experiment from the branch of the uterine artery and the uterine vein.
Determination of endogenous PGE2 concentration in uterine tissues
Samples of the endometrium and myometrium (
2 g) were collected in duplicate from the remaining part of the uterine horn during the preparation of each isolated specimen. Tissues were frozen (–79°C) and dispersed using the homogenizer cooled with liquid nitrogen. Duplicate homogenates (500 mg) were extracted according to the method described by Giesert et al. (1982). The extraction efficiency determined within the assay averaged 68%. The PGE2 concentration was quantified using the radioimmunoassay described by Okrasa et al. (1985). Antibodies were purchased from Sigma-Aldrich Chemie Gmbh (Stainheim, Germany). The specific reactivity of the antiserum was defined as the ratio of the antigen concentration at 50% inhibition of maximum binding. The cross-reactivities obtained were: PGE1, 100%; PGA1, PGA2, PGB1 and PGB2, < 50%; PGF2 and PGF1, < 20%. The sensitivity of the PGE2 assay, defined as 87% of total binding, amounted to 8 pg per tube, while the intra- and interassay coefficients of variation were 6.9 ± 1.1 and 13.8 ± 1.9, respectively.
Statistical analysis
All the data are presented as means ±S.E.M. The concentrations of radioactivity, in particular fragments of the reproductive organ after infusion of radioactive PGE2 into branches of the uterine vein and into lymphatic vessels (Fig. 2), was examined by analysis of variance followed by unpaired t test (Prism GraphPad Software, San Diego, CA, USA). The concentration of radioactivity in tissues collected from different parts of the uterine horn and mesometrium (Fig. 3) was compared by analysis of variance for repeated measurements followed by Bonferroni's t test. The venous effluent of radioactive PGE2 from the isolated preparation and retrograde transfer of [3H]PGE2 into the uterine horn (Figs 4 and 5) were analysed by determining the total area under the respective curves. These data were compared by analysis of variance followed by unpaired t test.
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Results |
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Figure 2 presents the concentration of radioactive PGE2 in selected tissues of the reproductive organ after infusion of [3H]PGE2 into the branches of the uterine vein (Experiment I) or into the lymphatic vessels of the mesometrium (Experiment II). The mean concentration of radioactivity in the corpus luteum and ovarian stroma was 4- and 2.1-fold higher, respectively, after infusion of [3H]PGE2 into lymphatic vessels than into venous vessels. The value differed significantly at P < 0.001. The concentration of radioactivity in the oviduct was 2.6-fold higher and significantly different (P < 0.01) after infusion of [3H]PGE2 into lymphatic vessels than into venous vessels. The above results showed a considerably more effective local transfer of [3H]PGE2 to the ovary and oviduct from the lymphatic vessels than from venous vessels of the mesometrium.
Similarly, a much higher concentration of [3H]PGE2 was found in the uterus after infusion into lymphatic vessels than into venous vessels. The mean concentration of radioactive PGE2 was 4-fold higher in the endometrium and 7-fold higher in the myometrium after its infusion into lymphatic vessels than into venous vessels. Furthermore, the values differed at P < 0.001 for the endometrium and P < 0.01 for myometrium. Retrograde transfer of prostaglandin to the uterine horn was more intensive from lymph than from venous blood. The mean concentration of radioactivity in the mesometrium, showing the accumulation of infused prostaglandin, was 5-fold higher after its infusion into lymphatic vessels than into venous vessels and the difference was significant at P < 0.001.
After infusion into both venous and lymphatic vessels, parts of the uterine horn adjoining and opposite the ovary have different concentrations of [3H]PGE2 in the myometrium (P < 0.05; Fig. 3). Similarly, the concentration of radioactive PGE2 adjoining the ovary or the uterine body parts of the mesometrium was significantly different after its infusion into venous vessels (P < 0.001) and lymphatic vessels (P < 0.05) (Fig. 3).
Figure 4 presents the radioactivity of blood collected from the utero-ovarian vein of pregnant gilts after identical doses of [3H]PGE2 were infused into the small branches of the uterine vein (Experiment I) and into the lymphatic vessels of the mesometrium (Experiment II). The shape of the curves presents a different pattern of radioactivity outflow from the isolated preparation in the two experiments. The highest concentration of radioactive PGE2 in venous blood flowing from the isolated uterine horn was reached during the infusion of [3H]PGE2 into the branches of the uterine vein. This radioactivity dropped immediately after infusion of [3H]PGE2 into venous vessels. When [3H]PGE2 was applied to lymphatic vessels the concentration of the radioactive PGE2 in the blood of the utero-ovarian vein stayed at the same level until the end of the experiment (Fig. 4).
The concentration of radioactivity in arterial blood supplying the uterine horn was significantly greater (P < 0.01) when [3H]PGE2 was infused into the branches of the uterine vein than into lymphatic vessels (Fig. 5). However, when [3H]PGE2 was infused into the branches of the uterine vein the radioactivity in arterial blood reached a maximal level only 25 min after [3H]PGE2 infusion began and continued at this level for 30 min after infusion. Such results suggest that effective transfer of radioactive prostaglandin into the arterial blood was not directly caused by the concentration of [3H]PGE2 in the venous blood.
The content of radioactive PGE2 in the uterine flushing averaged 25490 ± 7189 d.p.m. after infusion into venous vessels and 205 099 ± 39 892 d.p.m. after infusion into lymphatic vessels. These values differ significantly at P < 0.001.
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Discussion |
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ska et al. (1991) presented very abundant bands of uterine lymphatic vessels in the pig directed towards the ovary and passing in very close apposition to the vasculature of the ipsilateral ovary; Abdel Rahim et al. (1983) demonstrated a high concentration of PGE2 in uterine lymph during the oestrous cycle in ewes. The lymphatic pathway was suggested earlier for luteolytic action of PGF2 in the pig (Kotwica, 1980) and in sheep (Heap et al. 1985; Bonnin et al. 1999). The above data led us to conclude that the lymphatic pathway was a fundamental mechanism in the local transfer of prostaglandin from the uterus to the ovary and oviduct. The results of the present study were consistent with those presented by Christenson et al. (1994). These authors showed that increased production of PGE2 in the gravid uterine horn in unilaterally pregnant gilts was associated with enhanced function of the ipsilateral ovary. Thus, we thought that direct transfer of PGE2 from the uterine lymph to the ovary and oviduct is the main and most important pathway involved in luteotropic action of this prostaglandin in the pig.
It should be emphasized that the amount of radioactive PGE2 inserted into the uterus during the experiment (total dose 49 ng infused into the entire isolated uterine horn during 30 min) could not considerably elevate the concentration of PGE2 in uterine tissues because the concentration of endogenous PGE2 averaged 16.3 ± 3.0 ng g–1 and 3.4 ± 0.3 ng g–1 in the endometrium and in myometrium, respectively. Radioactive PGE2 added to the reproductive organ competed with endogenous PGs which were involved in the same processes. Thus, [3H]PGE2 might be considered only a marker of the permeation process and its intensity. The mass of PGE2 corresponding to the values of radioactivity estimated in the tissue or plasma samples did not represent the amounts of the hormone (endogenous and radioactive together) transferred into the ovary, oviduct or uterine horn.
The results presented in Fig. 5 demonstrated transfer of [3H]PGE2 from venous blood, uterine lymph and mesovarian tissues into arterial blood. Radioactive PGE2 was then transported into the uterine horn and was present in the endometrium, myometrium and in the uterine flushing. Similarly, local retrograde transfer was shown in our earlier study for PGF2. Retrograde transfer of PGF2 was intensive during the luteal phase of the porcine oestrous cycle (Krzymowski et al. 1986; Stefaczyk-Krzymowska et al. 1992; Stefaczyk-Krzymowska, 1996), and could considerably limit PGF2 outflow from the uterus (Stefaczyk-Krzymowska, 1996). Retrograde transfer of PGF2 was especially intensive during early pregnancy in gilts (when prostaglandins were necessary in the uterus to maintain the pregnancy) (Krzymowski et al. 1987; Stefaczyk-Krzymowska et al. 1990) and in pseudopregnant gilts (Krzymowski et al. 1987). Local transfer of prostaglandins was also considered as a means of regulating oviduct function (Hunter et al. 1983). Moreover, the adjustment of blood and lymphatic circulation in the mesometrial area created the conditions for effective uptake and local retrograde transfer of PGF2, and a possible mechanism was proposed for participation of these processes in the regulation of the oestrous cycle and early pregnancy in the pig (Krzymowski et al. 1987; Stefaczyk-Krzymowska et al. 1990; Krzymowski & Stefaczyk-Krzymowska, 2002, 2004). The results presented in this paper clearly demonstrate that local transfer of PGE2 by the lymphatic pathway may enable effective access of this hormone to target organs and reduce its outflow with venous blood during early pregnancy in gilts.
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References |
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