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Journal articles on the topic 'Sulproston'

Author: Grafiati

Published: 11 January 2025

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1

Kunz. "Erfahrungen mit der vorzeitigen Schwangerschaftsbeendigung im zweiten Trimenon am peripheren Spital." Praxis 93, no. 27 (June 1, 2004): 1135–42. http://dx.doi.org/10.1024/0369-8394.93.27.1135.

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Das Ziel dieser in den Jahren 1992 bis 98 durchgeführten Untersuchung war, die Wirkung und Nebenwirkungen der intravenösen Gabe von Sulproston zur Abortinduktion im zweiten Trimenon zu erfassen. 160 Patientinnen wurden hospitalisiert. Davon wurden drei hysterektomiert, drei abortierten nach Zervix-Priming mit Prostin E2-Gel (0.25 mg/ml) und 154 erhielten repetitiv eine Infusion mit Sulproston (Nalador® 500 µg, 3 A/1000 ml NaCl 0.9%, 250 µg/h (gleich ca. 4.17 µg/gleich ca. 55 Tropfen/Min.) während sechs Stunden. Das mittlere Induktions-Abort-Intervall betrug 16 h 56 Min., 53% der Aborte traten innerhalb von 12 h, 95% innerhalb von 48 h ein. Zwei Induktionen waren erfolglos. Bei zwei Frauen traten atonische Blutungen auf. Diese Untersuchung zeigte, dass Sulproston-Infusionen geeignet sind zur Abortinduktion im zweiten Trimenon. Nebenwirkungen sind selten. Besonders beachtet werden müssen Blutungskomplikationen.

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2

Rath, W., N. Dennemark, H. D. Gödicke, and E. Schwab. "Präoperatives Zervixpriming mittels intrazervikaler Applikation eines neuartigen Sulproston-Gels." Archives of Gynecology 238, no. 1-4 (September 1985): 731–32. http://dx.doi.org/10.1007/bf02430179.

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3

Schönegg, W., J. Wessel, and K. Schmidt-Gollwitzer. "Erfahrungen mit intravenöser Sulproston-Applikation bei massiven postpartalen Blutungen." Geburtshilfe und Frauenheilkunde 47, no. 11 (November 1987): 789–91. http://dx.doi.org/10.1055/s-2008-1036047.

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4

Kulka, P. J., P. Quent, A. Wiebaick, D. Jäger, and M. Strumpf. "Myokardinfarkt nach Therapie einer atonen Nachblutung mit Sulproston - Fallbeschreibung und Literaturübersicht." Geburtshilfe und Frauenheilkunde 59, no. 12 (December 1999): 634–37. http://dx.doi.org/10.1055/s-1999-15641.

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5

Rath, W., D. Meyer, D. Harder, R. Hilgers, and W. Kuhn. "Zervixpriming beim Schwangerschaftsabbruch im I. Trimenon mittels intrazervikaler Applikation von Sulproston-Gel." Geburtshilfe und Frauenheilkunde 45, no. 01 (January 1985): 51–56. http://dx.doi.org/10.1055/s-2008-1036206.

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6

Kulenkampff, D., W. Rath, and W. Kuhn. "Gemeprost Vaginal-Suppositorien versus intrazervikale Sulproston-Gel-Applikation zum Zervixpriming im I. Trimenon." Geburtshilfe und Frauenheilkunde 54, no. 03 (March 1994): 174–78. http://dx.doi.org/10.1055/s-2007-1023576.

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7

Schulz, B. O., H. Wiechell, and F. Oberheuser. "Abruptio im 1. Trimenon-Cervixdilatation mit Sulproston i.m. oder i.m.c. in Klinik und Praxis." Archives of Gynecology 238, no. 1-4 (September 1985): 733–35. http://dx.doi.org/10.1007/bf02430181.

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8

Rath, W., E. Schwab, D. H. Harder, and W. Kuhn. "Tonometrische und tokographische Untersuchungen zum zervixselektiven Priming mit Sulproston-Gel beim Schwangerschaftsabbruch im I. Trimenon." Gynäkologisch-geburtshilfliche Rundschau 28, no. 1 (1988): 15–29. http://dx.doi.org/10.1159/000270567.

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9

Findeklee, Sebastian. "Fallbericht 39-jährige III. Gravida, III. Para mit Inversio uteri nach Steißgeburt." Zeitschrift für Geburtshilfe und Neonatologie 224, no. 01 (February 4, 2019): 38–41. http://dx.doi.org/10.1055/a-0828-8696.

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ZusammenfassungDie Inversio uteri bezeichnet das Umstülpen der Gebärmutter in die Scheide postpartal. Sie ist äußerst selten, aber stellt einen geburtshilflichen Notfall dar. Die Gefahr für die Gebärende besteht in einer Uterusatonie mit dem Verlust großer Mengen Blut in kurzer Zeit. Dies kann, wenn keine rechtzeitige Therapie erfolgt, zum hypovolämischen Schock bis zum Herz-Kreislaufversagen führen. Die Therapie erfolgt durch eine Uterus-Reposition in Vollnarkose mit anschließender manueller Plazentalösung. Anschließend folgen die Kürettage und die Gabe von hochpotenten Uterotonika wie Sulproston. Durch den in der Regel hohen Blutverlust kommt es häufig zu einer Störung des Gerinnungssystems, sodass eine Substitution von Antifibrinolytika wie Tranexamsäure, Gerinnungsfaktoren und/oder Erythrozytenkonzentraten erforderlich wird. Gelingt keine vaginale Reposition des Uterus, so bleiben als Ultima Ratio nur die Reposition per Laparotomie oder die Hysterektomie. Wir berichten über eine 39-jährige III. Gravida, III. Para mit 36+3 Schwangerschaftswochen (SSW), bei der es nach spontaner Steißgeburt bei Placenta accreta zur Inversio uteri kam, die vaginal reponiert werden konnte.

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10

Tabarelli, M., K. Heim, P. Mayr, and Elisabeth Karpellus. "Abortinduktion bei gestörter Schwangerschaft im I. und II. Trimenon durch lokale und systemische Gabe von Sulproston." Gynäkologisch-geburtshilfliche Rundschau 28, no. 2 (1988): 221–24. http://dx.doi.org/10.1159/000270831.

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11

Heine, O. "Präoperatives Zervixpriming im 1. Trimenon: erste klinische Erfahrungen mit einer Kombination von Pluronic F 127 und Sulproston." Geburtshilfe und Frauenheilkunde 48, no. 02 (February 1988): 102–5. http://dx.doi.org/10.1055/s-2008-1035703.

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12

Schmidt, W., Dagmar Rabe, and H. Hendrik. "Abortinduktion im zweiten Schwangerschaftstrimenon. Endozervikale PGE2-Gel-Applikation, intramuskuläre Sulprostonapplikation und kombinierte (endozervikale PGE2-Gel/intramuskuläre Sulproston) Behandlung." Geburtshilfe und Frauenheilkunde 45, no. 04 (April 1985): 261–64. http://dx.doi.org/10.1055/s-2008-1036456.

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13

&NA;. "Sulprostone see Mifepristone/sulprostone." Reactions Weekly &NA;, no. 379 (November 1991): 12. http://dx.doi.org/10.2165/00128415-199103790-00062.

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14

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 709 (July 1998): 11. http://dx.doi.org/10.2165/00128415-199807090-00040.

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15

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 1367 (September 2011): 35. http://dx.doi.org/10.2165/00128415-201113670-00124.

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16

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 845 (March 2001): 11. http://dx.doi.org/10.2165/00128415-200108450-00024.

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17

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 1406 (June 2012): 35. http://dx.doi.org/10.2165/00128415-201214060-00120.

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18

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 394 (March 1992): 8. http://dx.doi.org/10.2165/00128415-199203940-00030.

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19

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 423 (October 1992): 12. http://dx.doi.org/10.2165/00128415-199204230-00054.

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20

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 1281 (December 2009): 31. http://dx.doi.org/10.2165/00128415-200912810-00096.

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21

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 1238 (February 2009): 31–32. http://dx.doi.org/10.2165/00128415-200912380-00090.

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22

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 329 (December 1990): 8. http://dx.doi.org/10.2165/00128415-199003290-00036.

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23

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 341 (March 1991): 11. http://dx.doi.org/10.2165/00128415-199103410-00064.

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24

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 1019 (September 2004): 13. http://dx.doi.org/10.2165/00128415-200410190-00044.

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25

&NA;. "Sulprostone." Reactions Weekly &NA;, no. 488 (February 1994): 10. http://dx.doi.org/10.2165/00128415-199404880-00049.

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26

Hebert, R. L., H. R. Jacobson, D. Fredin, and M. D. Breyer. "Evidence that separate PGE2 receptors modulate water and sodium transport in rabbit cortical collecting duct." American Journal of Physiology-Renal Physiology 265, no. 5 (November 1, 1993): F643—F650. http://dx.doi.org/10.1152/ajprenal.1993.265.5.f643.

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Prostaglandin E2 (PGE2) modulates both water and sodium transport in the rabbit cortical collecting duct (CCD). To determine whether these effects are mediated by separate PGE2 receptors, we compared the effects of PGE2 and its analogue sulprostone in the isolated perfused rabbit CCD. PGE2 increased basal water permeability (hydraulic conductivity), whereas sulprostone did not. PGE2 and sulprostone were equipotent inhibitors of water absorption when it was prestimulated by vasopressin. Pertussis toxin completely reversed the inhibitory effect of sulprostone but only partially reversed the inhibitory effect of PGE2. In contrast, a protein kinase C (PKC) inhibitor, staurosporine, partially reversed the inhibitory effect of PGE2 but had no effect on sulprostone. PGE2 also raised intracellular calcium ([Ca2+]i). This effect is coupled to its capacity to inhibit Na+ absorption. Sulprostone was 10-fold less potent than PGE2 both in raising [Ca2+]i or inhibiting sodium transport. The results suggest sulprostone selectively interacts with a PGE2 receptor coupled to pertussis toxin-sensitive inhibition of water permeability. Sulprostone less potently activates a PGE2 receptor coupled to [Ca2+]i, PKC activation, and sodium transport and completely fails to interact with the PGE2 receptor that stimulates water permeability in the collecting duct. These results suggest distinct PGE2 receptors modulate sodium and water transport in the CCD.

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27

&NA;. "Dinoprost/sulprostone." Reactions Weekly &NA;, no. 1120 (September 2006): 9–10. http://dx.doi.org/10.2165/00128415-200611200-00030.

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28

&NA;. "Norepinephrine/sulprostone." Reactions Weekly &NA;, no. 1398 (April 2012): 32. http://dx.doi.org/10.2165/00128415-201213980-00116.

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29

&NA;. "Mifepristone/sulprostone." Reactions Weekly &NA;, no. 379 (November 1991): 10. http://dx.doi.org/10.2165/00128415-199103790-00049.

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30

&NA;. "Dinoprost/sulprostone." Reactions Weekly &NA;, no. 939 (February 2003): 9. http://dx.doi.org/10.2165/00128415-200309390-00029.

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31

Vostrikov, N. S., V. Z. Vasikov, and M. S. Miftakhov. "Racemic sulprostone." Russian Journal of Organic Chemistry 40, no. 10 (October 2004): 1539–40. http://dx.doi.org/10.1007/s11178-005-0058-5.

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32

Van Mensel, Kristin, Filip Claerhout, Patrick Debois, Marc J. N. C. Keirse, and Myriam Hanssens. "A Randomized Controlled Trial of Misoprostol and Sulprostone to End Pregnancy after Fetal Death." Obstetrics and Gynecology International 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/496320.

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Objective. To compare effectiveness, side effects, and patients' perception of vaginal misoprostolversusintravenous sulprostone for ending pregnancy after fetal death between 14 and 42 weeks gestation.Method. Multicenter randomized controlled trial, using block randomization, central allocation, and prior power analysis.Outcome measures. Induction-delivery interval, gastrointestinal side effects, use of analgesia, pain perception, pyrexia, placental retention, hemorrhage, and women's opinions.Results. Of 176 women aimed for, 143 were randomized over 7 years, of whom 4 were excluded. There was no difference in delivery within 24 and 36 hours: 91.4% and 97.1% with misoprostol ()versus85.5% and 92.8% with sulprostone (). There was no difference in either gastrointestinal side effects, as reported by the women and their caregivers, use of analgesia, women's pain perception, blood loss or placental retention. Hyperthermia 38°C was more common with misoprostol (24.3%) than with sulprostone (11.6%; difference: +12.7%; 95% CI: +1.2% to +25.3%) and related to the total dose used. Acceptability of both induction methods was similar except for freedom of movement, which was substantially in favor of misoprostol (lack of freedom reported with misoprostol in 34.3%versus63.8% with sulprostone; difference: −29.5%; 95% CI: −13.6% to −45.4%).Conclusions. Misoprostol and sulprostone are similarly effective with little difference in side effects except for hyperthermia, related to the dose of misoprostol used, and women's reported lack of mobility with intravenous sulprostone. Effectiveness of both methods increased with gestational age.

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33

Nakao, A., M. L. Allen, W. K. Sonnenburg, and W. L. Smith. "Regulation of cAMP metabolism by PGE2 in cortical and medullary thick ascending limb of Henle's loop." American Journal of Physiology-Cell Physiology 256, no. 3 (March 1, 1989): C652—C657. http://dx.doi.org/10.1152/ajpcell.1989.256.3.c652.

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We have examined the regulation by prostaglandin E2 (PGE2) of hormone-induced adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cells isolated by immunodissection from both the medullary and cortical thick ascending limb of Henle's loop of rabbit kidney. At concentrations greater than 10(-8) M, PGE2, but not sulprostone (16-phenoxy-17,18,19,20-tetranor-PGE2 methylsulfonilamide), caused cAMP accumulation in both cortical and medullary thick limb cells. However, at concentrations of less than or equal to 10(-8) M, both PGE2 and sulprostone inhibited arginine vasopressin (AVP)-, calcitonin-, and glucagon-induced cAMP accumulation in medullary thick ascending limb (mTAL) cells. In cortical thick limb (cTAL) cells, sulprostone also inhibited AVP-, calcitonin-, and parathyroid hormone (PTH)-induced cAMP accumulation. The inhibitory effects of PGE2 and of sulprostone were blocked by pretreatment of mTAL and cTAL cells with pertussis toxin. Membranes prepared from mTAL cells exhibited a [3H]PGE2 binding activity that was stimulated on addition of the stable guanosine 5'-triphosphate (GTP) analogue, 5'-guanosine gamma-thiotriphosphate (GTP gamma S); moreover, sulprostone inhibited [3H]PGE2 binding. Our results suggest that PGE2 can function via a prostaglandin E receptor linked to a guanine nucleotide regulatory protein, Gi, to attenuate hormone-induced cAMP formation in both mTAL and cTAL cells of rabbit kidney.

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34

Chen, F. G., K. F. Koh, and Y. S. Chong. "Cardiac Arrest Associated with Sulprostone Use during Caesarean Section." Anaesthesia and Intensive Care 26, no. 3 (June 1998): 298–301. http://dx.doi.org/10.1177/0310057x9802600312.

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Sulprostone, a synthetic prostaglandin with potent uterotonic action, has been shown to have a low complication rate in a large series. We present a case in which a bolus intravenous injection of sulprostone 30 μg was administered to treat postpartum haemorrhage during caesarean section. The 38-year-old patient with no previous cardiac or smoking history developed complete heart block, ventricular fibrillation and subsequent asystole. Cardiopulmonary resuscitation was successful after 45 minutes. Post resuscitation there was no myocardial infarction and she had complete neurological recovery. We postulate that the bolus of sulprostone resulted in possible coronary spasm that resulted in cardiac arrest.

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35

Aoi, Masako, Eitaro Aihara, Masato Nakashima, and Koji Takeuchi. "Participation of prostaglandin E receptor EP4 subtype in duodenal bicarbonate secretion in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 1 (July 2004): G96—G103. http://dx.doi.org/10.1152/ajpgi.00038.2004.

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We examined, by using a specific PGE receptor subtype EP4 agonist and antagonist, the involvement of EP4 receptors in duodenal HCO3− secretion induced by PGE2 and mucosal acidification in rats. Mucosal acidification was achieved by exposing a duodenal loop to 10 mM HCl for 10 min, and various EP agonists were given intravenously 10 min before the acidification. Secretion of HCO3− was dose-dependently stimulated by AE1-329 (EP4 agonist), the maximal response being equivalent to that induced by sulprostone (EP1/EP3 agonist) or PGE2. The stimulatory action of AE1-329 and PGE2 but not sulprostone was attenuated by AE3-208, a specific EP4 antagonist. This antagonist also significantly mitigated the acid-induced HCO3− secretion. Coadministration of sulprostone and AE1-329 caused a greater secretory response than either agent alone. IBMX potentiated the stimulatory action of both sulprostone and AE1-329, whereas verapamil mitigated the effect of sulprostone but not AE1-329. Chemical ablation of capsaicin-sensitive afferent neurons did not affect the response to any of the EP agonists used. We conclude that EP4 receptors are involved in the duodenal HCO3− response induced by PGE2 or acidification in addition to EP3 receptors. The process by which HCO3− is secreted through these receptors differs regarding second-messenger coupling. Stimulation through EP4 receptors is mediated by cAMP, whereas that through EP3 receptors is regulated by both cAMP and Ca2+; yet there is cooperation between the actions mediated by these two receptors. The neuronal reflex pathway is not involved in stimulatory actions of these prostanoids.

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36

Vio, Carlos P., Mariana Quiroz-Munoz, Catherina A. Cuevas, Carlos Cespedes, and Nicholas R. Ferreri. "Prostaglandin E2 EP3 receptor regulates cyclooxygenase-2 expression in the kidney." American Journal of Physiology-Renal Physiology 303, no. 3 (August 1, 2012): F449—F457. http://dx.doi.org/10.1152/ajprenal.00634.2011.

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Cyclooxygenase-2 (COX-2) is constitutively expressed and highly regulated in the thick ascending limb (TAL). As COX-2 inhibitors (Coxibs) increase COX-2 expression, we tested the hypothesis that a negative feedback mechanism involving PGE2 EP3 receptors regulates COX-2 expression in the TAL. Sprague-Dawley rats were treated with a Coxib [celecoxib (20 mg·kg−1·day−1) or rofecoxib (10 mg·kg−1·day−1)], with or without sulprostone (20 μg·kg−1·day−1). Sulprostone was given using two protocols, namely, previous to Coxib treatment (prevention effect; Sulp7-Coxib5 group) and 5 days after initiation of Coxib treatment (regression effect; Coxib10-Sulp5 group). Immunohistochemical and morphometric analysis revealed that the stained area for COX-2-positive TAL cells (μm2/field) increased in Coxib-treated rats (Sham: 412 ± 56.3, Coxib: 794 ± 153.3). The Coxib effect was inhibited when sulprostone was used in either the prevention (285 ± 56.9) or regression (345 ± 51.1) protocols. Western blot analysis revealed a 2.1 ± 0.3-fold increase in COX-2 protein expression in the Coxib-treated group, an effect abolished by sulprostone using either the prevention (1.2 ± 0.3-fold) or regression (0.6 ± 0.4-fold vs. control, P < 0.05) protocols. Similarly, the 6.4 ± 0.6-fold increase in COX-2 mRNA abundance induced by Coxibs ( P < 0.05) was inhibited by sulprostone; prevention: 0.9 ± 0.3-fold ( P < 0.05) and regression: 0.6 ± 0.1 ( P < 0.05). Administration of a selective EP3 receptor antagonist, L-798106, also increased the area for COX-2-stained cells, COX-2 mRNA accumulation, and protein expression in the TAL. Collectively, the data suggest that COX-2 levels are regulated by a novel negative feedback loop mediated by PGE2 acting on its EP3 receptor in the TAL.

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37

Hao, Shoujin, AnnMarie DelliPizzi, Mariana Quiroz-Munoz, Houli Jiang, and Nicholas R. Ferreri. "The EP3 receptor regulates water excretion in response to high salt intake." American Journal of Physiology-Renal Physiology 311, no. 4 (October 1, 2016): F822—F829. http://dx.doi.org/10.1152/ajprenal.00589.2015.

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The mechanisms by which prostanoids contribute to the maintenance of whole body water homeostasis are complex and not fully understood. The present study demonstrates that an EP3-dependent feedback mechanism contributes to the regulation of water homeostasis under high-salt conditions. Rats on a normal diet and tap water were placed in metabolic cages and given either sulprostone (20 μg·kg−1·day−1) or vehicle for 3 days to activate EP3 receptors in the thick ascending limb (TAL). Treatment was continued for another 3 days in rats given either 1% NaCl in the drinking water or tap water. Sulprostone decreased expression of cyclooxygenase 2 (COX-2) expression by ∼75% in TAL tubules from rats given 1% NaCl concomitant with a ∼60% inhibition of COX-2-dependent PGE2 levels in the kidney. Urine volume increased after ingestion of 1% NaCl but was reduced ∼40% by sulprostone. In contrast, the highly selective EP3 receptor antagonist L-798106 (100 μg·kg−1·day−1), which increased COX-2 expression and renal PGE2 production, increased urine volume in rats given 1% NaCl. Sulprostone increased expression of aquaporin-2 (AQP2) in the inner medullary collecting duct plasma membrane in association with an increase in phosphorylation at Ser269 and decrease in Ser261 phosphorylation; antagonism of EP3 with L-798106 reduced AQP2 expression. Thus, although acute activation of EP3 by PGE2 in the TAL and collecting duct inhibits the Na-K-2Cl cotransporter and AQP2 activity, respectively, chronic activation of EP3 in vivo limits the extent of COX-2-derived PGE2 synthesis, thereby mitigating the inhibitory effects of PGE2 on these transporters and decreasing urine volume.

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38

&NA;. "Sulprostone: Myocardial infarction: case report." Reactions Weekly &NA;, no. 795 (April 2000): 11. http://dx.doi.org/10.2165/00128415-200007950-00037.

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39

Goureau, O., Z. Tanfin, S. Marc, and S. Harbon. "Diverse prostaglandin receptors activate distinct signal transduction pathways in rat myometrium." American Journal of Physiology-Cell Physiology 263, no. 1 (July 1, 1992): C257—C265. http://dx.doi.org/10.1152/ajpcell.1992.263.1.c257.

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Attempts were made to identify prostaglandin (PG) receptors in rat myometrium, according to the differential rank order of potencies displayed by the natural PGs and their analogues, both at the level of second messenger generation and contraction. In estrogen-treated rat myometrium, PGs [iloprost = PGI2 greater than PGE2 much greater than 16,16-dimethyl (DM)-PGE2; sulprostone = misoprostol = 0] induced adenosine 3',5'-cyclic monophosphate generation, indicating the contribution of a PGI2 receptor. The generation of inositol phosphates was stimulated by PGs (PGF2 alpha greater than PGD2 much greater than PGE2 = DM-PGE2 much greater than iloprost greater than sulprostone = misoprostol = 0), reflecting a PGF2 alpha-receptor-mediated process, which was insensitive to pertussis toxin (PTX). Contractions caused by PGF2 alpha were closely correlated to PGF2 alpha-receptor activation associated with the phospholipase C pathway. By contrast, contractions evoked by PGE2, equally mimicked by sulprostone and misoprostol, were abolished by PTX and were independent of phospholipase C activation. In the pregnant myometrium (day 21), the latter PGE-receptor-mediated mechanism also contributed to contractions caused by PGE2 (less than microM concn). Phospholipase C activation was coupled not only to PGF2 alpha but also to PGE receptors and could be correlated with contractions induced by PGF2 alpha and PGE2 greater than microM concn). All PGs tested were coupled to inhibitory G protein-mediated adenylate cyclase inhibition, displaying an equipotency that did not allow characterization of the inhibitory PG receptors.

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40

Zhang, Zhi-Hua, Yang Yu, Shun-Guang Wei, Yoshiko Nakamura, Kazuhiro Nakamura, and Robert B. Felder. "EP3 receptors mediate PGE2-induced hypothalamic paraventricular nucleus excitation and sympathetic activation." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (October 2011): H1559—H1569. http://dx.doi.org/10.1152/ajpheart.00262.2011.

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Prostaglandin E2 (PGE2), an important mediator of the inflammatory response, acts centrally to elicit sympathetic excitation. PGE2 acts on at least four E-class prostanoid (EP) receptors known as EP1, EP2, EP3, and EP4. Since PGE2 production within the brain is ubiquitous, the different functions of PGE2 depend on the expression of these prostanoid receptors in specific brain areas. The type(s) and location(s) of the EP receptors that mediate sympathetic responses to central PGE2 remain unknown. We examined this question using PGE2, the relatively selective EP receptor agonists misoprostol and sulprostone, and the available selective antagonists for EP1, EP3, and EP4. In urethane-anesthetized rats, intracerebroventricular (ICV) administration of PGE2, sulprostone or misoprostol increased renal sympathetic nerve activity, blood pressure, and heart rate. These responses were significantly reduced by ICV pretreatment with the EP3 receptor antagonist; the EP1 and EP4 receptor antagonists had little or no effect. ICV PGE2 or misoprostol increased the discharge of neurons in the hypothalamic paraventricular nucleus (PVN). ICV misoprostol increased the c-Fos immunoreactivity of PVN neurons, an effect that was substantially reduced by the EP3 receptor antagonist. Real-time PCR detected EP3 receptor mRNA in PVN, and immunohistochemical studies revealed sparsely distributed EP3 receptors localized in GABAergic terminals and on a few PVN neurons. Direct bilateral PVN microinjections of PGE2 or sulprostone elicited sympathoexcitatory responses that were significantly reduced by the EP3 receptor antagonist. These data suggest that EP3 receptors mediate the central excitatory effects of PGE2 on PVN neurons and sympathetic discharge.

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Kato, Shinichi, Eitaro Aihara, Katsuhide Yoshii, and Koji Takeuchi. "Dual action of prostaglandin E2 on gastric acid secretion through different EP-receptor subtypes in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 1 (July 2005): G64—G69. http://dx.doi.org/10.1152/ajpgi.00397.2004.

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We examined the role of prostaglandin E (EP) receptor subtypes in the regulation of gastric acid secretion in the rat. Under urethane anesthesia, the stomach was superfused with saline, and the acid secretion was determined at pH 7.0 by adding 50 mM NaOH. The acid secretion was stimulated by intravenous infusion of histamine or pentagastrin. Various EP agonists were administered intravenously, whereas EP antagonists were given subcutaneously 30 min or intravenously 10 min before EP agonists. PGE2 suppressed the acid secretion stimulated by either histamine or pentagastrin in a dose-dependent manner. The acid inhibitory effect of PGE2 was mimicked by sulprostone (EP1/EP3 agonist) but not butaprost (EP2 agonist) or AE1–329 (EP4 agonist). The inhibitory effect of sulprostone, which was not affected by ONO-8711 (EP1 antagonist), was more potent against pentagastrin- (50% inhibition dose: 3.6 μg/kg) than histamine-stimulated acid secretion (50% inhibition dose: 18.0 μg/kg). Pentagastrin increased the luminal release of histamine, and this response was also inhibited by sulprostone. On the other hand, AE1–329 (EP4 agonist) stimulated the acid secretion in vagotomized animals with a significant increase in luminal histamine. This effect of AE1–329 was totally abolished by cimetidine as well as AE3–208 (EP4 antagonist). These results suggest that PGE2 has a dual effect on acid secretion: inhibition mediated by EP3 receptors and stimulation through EP4 receptors. The former effect may be brought about by suppression at both parietal and enterochromaffin-like cells, whereas the latter effect may be mediated by histamine released from enterochromaffin-like cells.

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Gil, Daniel W., Cynthia V. Cheevers, Karen M. Kedzie, Cynthia A. Manlapaz, Sandhya Rao, Elaine Tang, and John E. Donello. "α-1-Adrenergic Receptor Agonist Activity of Clinical α-Adrenergic Receptor Agonists Interferes with α-2-Mediated Analgesia." Anesthesiology 110, no. 2 (February 1, 2009): 401–7. http://dx.doi.org/10.1097/aln.0b013e3181943226.

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Background The use of alpha-2 adrenergic agonists for analgesia is limited due to a narrow therapeutic window. Definition of the role of alpha receptor subtypes in alpha agonist mediated analgesia may identify strategies to separate the analgesic from sedative and cardiovascular effects. Methods Analgesic activity of brimonidine, clonidine, and tizanidine was investigated in wild-type C57B/6, alpha-2A, and alpha-2C knockout mice with allodynia induced by N-methyl-D-aspartate or sulprostone. The alpha receptor selectivity of the alpha agonists was assessed using functional in vitro recombinant assays. Results Brimonidine, clonidine, and tizanidine reduced N-methyl-D-aspartate- and sulprostone-induced allodynia in wild-type mice, but not alpha-2A knockout mice. In alpha-2C knockout mice, brimonidine and tizanidine reduced allodynia in both models, whereas clonidine only reduced N-methyl-D-aspartate-induced allodynia. In vitro, clonidine and tizanidine activated alpha-1 and alpha-2 receptors with similar potencies, whereas brimonidine was selective for alpha-2 receptors. In alpha-2C knockout mice with sulprostone-induced allodynia, blockade of clonidine's alpha-1 receptor agonist activity restored clonidine's analgesic efficacy. In wild-type mice, the analgesic potency of intrathecal clonidine and tizanidine was increased 3- to 10-fold by coadministration with the alpha-1A-selective antagonist 5-methylurapidil without affecting sedation. Following intraperitoneal administration, the therapeutic window was negligible for clonidine and tizanidine, but greater for brimonidine. 5-Methylurapidil enhanced the therapeutic window of intraperitoneal clonidine and tizanidine approximately 10-fold. Conclusions Alpha-1A receptor agonist activity can counterbalance alpha-2 receptor agonist-induced analgesia. Greater alpha-2 selectivity may enhance the therapeutic window of alpha-2 agonists in the treatment of pain.

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Kimura, Mitsutoshi, Sachie Osumi, and Masahiko Ogihara. "Prostaglandin E2 (EP1) Receptor Agonist-Induced DNA Synthesis and Proliferation in Primary Cultures of Adult Rat Hepatocytes: The Involvement of TGF-α." Endocrinology 142, no. 10 (October 1, 2001): 4428–40. http://dx.doi.org/10.1210/endo.142.10.8450.

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Abstract We investigated the effects of prostaglandin (EP) receptor subtype agonists on DNA synthesis and proliferation in primary cultures of adult rat hepatocytes to elucidate their mechanisms of action. Maintained in short-term cultures (i.e. 3.5 h) in a serum-free, defined medium, hepatocyte parenchymal cells underwent DNA synthesis and proliferation in the presence of sulprostone (10−6m), PGE2 (10−6m), and 17-phenyl-trinor-PGE2 (10−9m) in a time- and dose-dependent manner. PGE2 was less potent than 17-phenyl-trinor-PGE2 in stimulating hepatocyte mitogenesis. Sulprostone (10−6m) and 11-deoxy-PGE1 (10−6m) showed weak and insignificant stimulation, respectively, for hepatocyte mitogenesis. These effects of PGE2, 17-phenyl-trinor-PGE2, and sulprostone were abolished by treatment with a specific EP1 receptor antagonist, SC-51322, or the PLC inhibitor U-73122. The effects of these EP1 receptor agonists were potentiated by ionomycin and blocked by verapamil. Hepatocyte mitogenesis was almost completely blocked by specific inhibitors of growth-related signal transducers, such as genistein, wortmannin, PD98059, and rapamycin. A monoclonal antibody against TGF-α dose-dependently inhibited PGE2- and 17-phenyl-trinor-PGE2-induced hepatocyte mitogenesis. Treatment with the EP1 receptor agonists significantly increased the secretion of TGF-α, reaching a maximum within 5 min. The increase in TGF-α secretion was blocked by SC-51322, U-73122, somatostatin, and verapamil and potentiated by ionomycin. These results indicate that the proliferative mechanisms of action of EP1 receptor agonists are mediated through an increase in the autocrine secretion of TGF-α, which is dependent on the EP1 receptor/G-protein involved in PLC regulation/PLC/Ca2+ system. The locally secreted TGF-α, in turn, acts as a complete mitogen that stimulates the tyrosine kinase/MAPK pathway in these cells.

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Patwardhan, A. M., J. Vela, J. Farugia, K. Vela, and K. M. Hargreaves. "Trigeminal Nociceptors Express Prostaglandin Receptors." Journal of Dental Research 87, no. 3 (March 2008): 262–66. http://dx.doi.org/10.1177/154405910808700306.

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Orofacial inflammation is associated with prostaglandin release and the sensitization of nociceptive receptors such as the transient receptor potential subtype V1 (TRPV1). We hypothesized that certain PGE2 receptor subtypes (EP1–EP4) are co-expressed with TRPV1 in trigeminal nociceptors and sensitize responses to a TRPV1 agonist, capsaicin. Accordingly, combined in situ hybridization was performed with immunohistochemistry on rat trigeminal ganglia. We next evaluated the effects of specific EP2 and EP3 agonists (butaprost and sulprostone) in cultured trigeminal ganglia neurons. The results showed that EP2 and EP3 are expressed in trigeminal neurons (58% and 53% of total neurons, respectively) and are co-expressed in TRPV1-positive neurons (64% and 67 % of TRPV1-positive neurons, respectively). Moreover, most of the cells expressing EP2 or EP3 mRNA were of small to medium diameter (< 30 μm). The application of butaprost and sulprostone triggered neuropeptide exocytosis, and butaprost sensitized capsaicin responses. Analysis of these data, collectively, supports the hypothesis that prostaglandins regulate trigeminal TRPV1 nociceptors via activation of the EP2 and EP3 receptors.

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Blikslager, Anthony T., Susan M. Pell, and Karen M. Young. "PGE2 triggers recovery of transmucosal resistance via EP receptor cross talk in porcine ischemia-injured ileum." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 2 (August 1, 2001): G375—G381. http://dx.doi.org/10.1152/ajpgi.2001.281.2.g375.

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16,16-Dimethyl-PGE2 (PGE2) may interact with one of four prostaglandin type E (EP) receptors, which signal via cAMP (via EP2 or EP4 receptors) or intracellular Ca2+ (via EP1 receptors). Furthermore, EP3 receptors have several splice variants, which may signal via cAMP or intracellular Ca2+. We sought to determine the PGE2 receptor interactions that mediate recovery of transmucosal resistance ( R) in ischemia-injured porcine ileum. Porcine ileum was subjected to 45 min of ischemia, after which the mucosa was mounted in Ussing chambers. Tissues were pretreated with indomethacin (5 μM). Treatment with the EP1, EP2, EP3, and EP4 agonist PGE2 (1 μM) elevated R twofold and significantly increased tissue cAMP content, whereas the EP2 and EP4 agonist deoxy-PGE1 (1 μM) or the EP1 and EP3 agonist sulprostone (1 μM) had no effect. However, a combination of deoxy-PGE1 and sulprostone stimulated synergistic elevations in R and tissue cAMP content. Furthermore, treatment of tissues with deoxy-PGE1 and the Ca2+ ionophore A-23187 stimulated synergistic increases in R and cAMP, indicating that PGE2 triggers recovery of R via EP receptor cross talk mechanisms involving cAMP and intracellular Ca2+.

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Hagenaars, M., J. T. A. Knape, and E. M. J. M. Backus. "Pulmonary oedema after high infusion rate of sulprostone." British Journal of Anaesthesia 102, no. 2 (February 2009): 281–82. http://dx.doi.org/10.1093/bja/aen372.

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LAMPATI, L., L. B. COLANTONIO, and E. CALDERINI. "Cardiac arrest during sulprostone administration - a case report." Acta Anaesthesiologica Scandinavica 57, no. 3 (November 27, 2012): 395–97. http://dx.doi.org/10.1111/aas.12022.

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&NA;. "Low dose sulprostone is sufficient to induce labour." Inpharma Weekly &NA;, no. 725 (February 1990): 11. http://dx.doi.org/10.2165/00128413-199007250-00026.

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&NA;. "Successful termination of early pregnancy with mifepristone + sulprostone." Inpharma Weekly &NA;, no. 741 (June 1990): 16. http://dx.doi.org/10.2165/00128413-199007410-00039.

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Christensen, N. J. "Cervical dilatation with Sulprostone prior to vacuum aspiration." Contraception 32, no. 4 (October 1985): 359–65. http://dx.doi.org/10.1016/0010-7824(85)90039-3.

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