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Relevant bibliographies by topics / Prostaglandin-f2-alpha

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Academic literature on the topic 'Prostaglandin-f2-alpha'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Prostaglandin-f2-alpha"

1

Peters, A. "Effects of prostaglandin F2 alpha." Veterinary Record 118, no. 16 (April 19, 1986): 466–67. http://dx.doi.org/10.1136/vr.118.16.466-b.

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Young, I. "Effects of prostaglandin F2-alpha." Veterinary Record 118, no. 19 (May 10, 1986): 543–44. http://dx.doi.org/10.1136/vr.118.19.543-a.

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Barnard, J. W., R. A. Ward, and A. E. Taylor. "Evaluation of prostaglandin F2 alpha and prostacyclin interactions in the isolated perfused rat lung." Journal of Applied Physiology 72, no. 6 (June 1, 1992): 2469–74. http://dx.doi.org/10.1152/jappl.1992.72.6.2469.

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To characterize the interactions between prostaglandin F2 alpha and prostacyclin in controlling tone in the pulmonary circulation, isolated rat lungs were ventilated, perfused with blood, and subjected to challenge by prostaglandin F2 alpha in increasing doses. The pulmonary resistance was evaluated using occlusion techniques that separate the resistance into segments of large and small arteries and veins. The total vascular compliance was evaluated using outflow occlusion. Resistance increased after prostaglandin F2 alpha, and this resistance change was primarily in the small artery segment. The maximum resistance increase by prostaglandin F2 alpha (Rmax,PGF2 alpha), calculated from the Michaelis-Menton equation, was 16.6 +/- 3.6 cmH2O.l-1.min.100 g-1 for total vascular resistance with a concentration required to produce 50% Rmax (K0.5) of 5.26 +/- 3.57 nM. The Rmax,PGF2 alpha for small artery resistance was 13.5 +/- 2.4 cmH2O.l-1.min.100 g-1 with a K0.5 of 2.35 +/- 1.57 nM. The vascular compliance decreased during vasoconstriction by prostaglandin F2 alpha, and the maximum decrease in compliance (Cmin,PGF2 alpha) was -0.43 +/- 0.12 ml/cmH2O with a K0.5 of 2.84 +/- 2.99 nM. At each dose of prostaglandin F2 alpha, prostacyclin was administered in increasing doses to reverse the vasoconstriction caused by prostaglandin F2 alpha. For each concentration of prostaglandin F2 alpha, prostacyclin almost completely reversed the resistance increases and approximately one-half the compliance decrease. The maximum change in vascular resistance or compliance produced by prostacyclin was dependent on the dose of prostaglandin F2 alpha; yet the K0.5 for prostacyclin was within the picomolar range for all doses of prostaglandin F2 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

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Bedrick, A. D., M. A. Wells, D. L. Ford, and O. Koldovsky. "Intact biliary excretion of gastrically administered prostaglandin F2 alpha in rats: developmental differences." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 6 (December 1, 1987): G787—G792. http://dx.doi.org/10.1152/ajpgi.1987.253.6.g787.

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Tritium-labeled prostaglandin F2 alpha was administered via orogastric tube to bile duct-cannulated suckling and weanling rats to determine if maturational differences were present in the biliary excretion of prostaglandin F2 alpha and metabolites. Animals were killed 2 h after radioactivity administration. Characterization of radioactivity present in bile revealed age-related differences in biliary prostaglandin F2 alpha excretion. Suckling rats had a greater proportion of radioactivity migrating in chromatographic regions of greater polarity than prostaglandin F2 alpha. Compared with the weanling, a significantly greater amount of radioactivity cochromatographed with intact, unmetabolized prostaglandin F2 alpha (33.08 +/- 1.99 vs. 21.38 +/- 1.46). These results indicate that orogastrically administered prostaglandin F2 alpha can be absorbed from the gastrointestinal tract, transported to the liver, and subsequently excreted into bile and detected in an unmetabolized form in suckling and weanling rats. The enterohepatic circulation of milk-derived prostaglandin present in bile may contribute to the overall content of intestinal prostaglandins.

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Ramagopal, M. V., and S. J. Mustafa. "Effect of adenosine and its analogues on calcium influx in coronary artery." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (December 1, 1988): H1492—H1498. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1492.

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In the present study, we have investigated the changes in calcium influx during the relaxing responses to adenosine and its analogues. Calcium-45 influx was measured in bovine coronary artery rings in the presence of prostaglandin F2 alpha (10(-5) M) and KCl (50 and 100 mM). Prostaglandin F2 alpha and KCl caused increases in calcium influx. Prostaglandin F2 alpha produced a further contraction when added to rings maximally contracted with KCl (100 mM or higher), suggesting two different mechanisms for prostaglandin F2 alpha- and KCl-induced contractions. Similarly, a greater calcium influx was observed when prostaglandin F2 alpha was mixed with KCl (50 or 100 mM). At all the concentrations tested, adenosine and its analogues [5'-(N-ethyl-carboxamidoadenosine, NECA; N6-(L-2-phenylisopropyl)adenosine, L-PIA] significantly inhibited prostaglandin F2 alpha-induced increases in calcium influx. However, only higher concentrations of adenosine, NECA, and L-PIA inhibited 100 mM KCl-induced calcium influx. Previous treatment with 8-phenyltheophylline blocked the inhibitory actions of adenosine, NECA, and L-PIA on calcium influx. The inhibition of calcium influx by adenosine, NECA, and L-PIA correlated well with their relaxing ability in the presence of prostaglandin F2 alpha. The data suggest that prostaglandin F2 alpha-induced calcium influx was more sensitive to the action of adenosine and its analogues than the calcium influx induced by high K+ depolarization.

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Cocnata, Christina L. "Use of Prostaglandin F2 Alpha for Cyclophosphamide-Induced Hemorrhagic Cystitis." Journal of Pharmacy Technology 10, no. 5 (September 1994): 204–6. http://dx.doi.org/10.1177/875512259401000504.

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Objective: To examine the use of prostaglandin F2 alpha in treating cyclophosphamide-induced hemorrhagic cystitis. Data Sources: An English language literature search using MEDLINE 1982–1993 and bibliographic reviews of related textbooks and review articles. Study Selection: Articles containing pertinent information regarding the therapeutic use and effects of prostaglandin F2 alpha as a treatment for cyclophosphamide-induced hemorrhagic cystitis in humans. Data Extraction: Resources were evaluated and information was extracted independently. Data Synthesis: A review of human cases suggests that intravesical administration of prostaglandin F2 alpha may be an effective bedside therapy for cyclophosphamide-induced hemorrhagic cystitis. Adverse reactions are limited primarily to local effects. The optimal dosage regimen of intravesical prostaglandin F2 alpha is not clearly established. Conclusions: Patients with intractable vesical hemorrhage secondary to cyclophosphamide administration may benefit from bedside intravesical instillation of prostaglandin F2 alpha. Information in the literature regarding prostaglandin bladder irrigation is scarce, and confined to case reports. Clinical studies are needed to endorse and/or refute the efficacy of intravesical instillation of prostaglandin F2 alpha as a treatment modality for hemorrhagic cystitis.

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Diczfalusy, U., and S. E. Alexson. "Peroxisomal chain-shortening of prostaglandin F2 alpha." Journal of Lipid Research 29, no. 12 (December 1988): 1629–36. http://dx.doi.org/10.1016/s0022-2275(20)38412-1.

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Shigematsu, S., H. Niwa, and T. Saikawa. "Vasospastic angina induced by prostaglandin F2 alpha." Heart 69, no. 4 (April 1, 1993): 364–65. http://dx.doi.org/10.1136/hrt.69.4.364.

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Norman, RJ, and K. Reddi. "Prostaglandins in dysfunctional labour; evidence for altered production of prostaglandin F2 alpha." Reproduction, Fertility and Development 2, no. 5 (1990): 563. http://dx.doi.org/10.1071/rd9900563.

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Dysfunctional labour was studied in relation to prostaglandin concentrations in amniotic fluid and production by fetal membranes. Initial clinical validation of the model established the presence of hypokinetic labour with no evidence of obstruction to the fetal progress. Prostaglandin F2 alpha (PGF2 alpha) and 13, 14 dihydro-15-keto-prostaglandin-F2 alpha concentrations in the amniotic fluid were low despite relatively normal concentrations of prostaglandin E2. Membranes removed from patients with the condition released very low concentrations of PGF2 alpha from the amniotic side with no alteration on the choriodecidual side of the membrane. Studies of free and phospholipid-associated arachidonic acid indicated normal release of arachidonic acid in dysfunctional labour. No changes in amniotic fluid-related inhibitors and stimulators of prostaglandin synthetase were detected. It is suggested that PGF2 alpha production is impaired in dysfunctional labour and that this prostaglandin is primarily involved in the progress of labour.

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Flint, AP, HN Jabbour, and AS Loudon. "Oxytocin stimulates uterine prostaglandin F2 alpha secretion in red deer Cervus elaphus." Reproduction, Fertility and Development 6, no. 2 (1994): 269. http://dx.doi.org/10.1071/rd9940269.

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The prostaglandin F2 alpha analogue cloprostenol stimulates ovarian secretion of oxytocin in red deer hinds and Pere David's deer hinds, as in cattle and sheep, but the response of the uterus to administered oxytocin has not been studied in deer. In the present experiment, oxytocin administered intravenously caused an increase in circulating concentrations of 13,14-dihydro-15-keto prostaglandin F2 alpha from 186 +/- 35 to 404 +/- 34 pmol L-1 within 5 min; concentrations in saline-treated hinds were unchanged (150 +/- 12 and 164 +/- 12 pmol L-1 before and after treatment respectively). This suggest that in red deer as in other ruminants, a positive feedback relationship between the corpus luteum and the uterus may operate to stimulate luteolytic episodes of prostaglandin F2 alpha.

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Dissertations / Theses on the topic "Prostaglandin-f2-alpha"

1

Wittke, Miriam Sophie. "Anwendung eines Ovsynch-Programms in einer Milchviehherde: Einflüsse auf die Konzeption und Vergleich mit einem Prostaglandin- F2[alpha]-Programm [Prostaglandin-F2-alpha-Programm]." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/297/index.html.

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Cassidy, Carrie. "Further evidence that prostaglandin F2-alpha is the obligatory eicosanoid in porcine ovulation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0004/MQ44139.pdf.

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Vielhauer, George A. "Cloning and characterization of novel isoforms of the human receptor for prostaglandin F2 alpha." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280571.

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Prostaglandin F2 alpha (PGF₂α) regulates physiological responses including lowering of intraocular pressure, luteolysis, and parturition. FP prostanoid receptors are GPCRs mediating the actions of PGF₂α. mRNA splice variants exist for the ovine FP receptor gene and are designated FP(A) and FP(B). Thus far, receptor heterogeneity for the human FP receptor gene has yet to be established. This dissertation identifies human FP receptor isoforms and their pharmacological significance. Utilizing PCR, a putative human FP(B) (hFP(B)) ortholog from placenta and CX-1 (colon adenocarcinoma) cDNA was identified. These clones produced similar cDNA sequence both containing inverted repeat sequences. However, the mechanism by which the hFP(B) is produced appears different from alternative mRNA splicing and remains unexplained. Pharmacological characterization of the hFP(B) ortholog is ongoing and its significance remains unknown. Additionally, we report the cloning of a FP receptor mRNA splice variant from human heart and placenta cDNA, named human FP sevenless (hFP(S)). The cDNA encoding hFP(S) has a 71 base pair insert that produces a frame shift resulting in a truncated receptor lacking transmembrane-7 and a carboxyl tail. This sequence is identified as a distinct exon localized on the human FP receptor gene. hFP(S) mRNA are expressed in human skeletal muscle, heart and placenta. Immunohistochemical staining showed positive immunoreactivity in vascular endothelium, trophoblast, and decidual cells from placenta. hFP(S) represents the first confirmed alternative splice variant of the human FP prostanoid receptor gene, however, its function is unknown. Pharmacological characterization of hFP(S) demonstrated no significant PGF₂α binding or PGF₂α-mediated inositol phosphate hydrolysis. FLIPR high throughput screening membrane potential assays yielded four potential agonists for hFPS activation that were not observed in (-)293-EBNA cells; oxytocin, PGB₂, AGNA9B9, and AGNA10B10. These potential agonists require further investigation for hFP(S) selectivity and until such data is determined, hFP(S) should continue to be considered an orphan receptor. In conclusion, these studies demonstrate one FP receptor splice variant of the six transmembrane (6TM) nature exists in humans. In addition, preliminary evidence suggests the existence of a hFP(B) receptor ortholog potentially generated from a mechanism other than traditional mRNA splicing and could contribute to the development of colon carcinogenesis.

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Goravanahally, Madhusudan P. "Cellular mechanisms responsible for development of sensitivity of the bovine corpus luteum to prostaglandin F2 alpha." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10427.

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Thesis (Ph. D.)--West Virginia University, 2009.
Title from document title page. Document formatted into pages; contains xvi, 218 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 92-114).

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Kutz, Bryan. "Synchronizing Estrus and Improving Subsequent Production and Performance with Prostaglandin F2 Alpha and Pregnant Mare Serum Gonadotropin." TopSCHOLAR®, 1997. http://digitalcommons.wku.edu/theses/790.

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Two-hundred-seventy-two sows were utilized in two trials to evaluate the effects of prostaglandin and pregnant mare serum on reducing weaning to estrus interval, increasing the degree of estrus synchrony and improving fertility at estrus resulting in improved pregnancy rates and subsequent litter performance. Sows were randomly allotted to treatments. In trial 1, sows were assigned to one of three treatments: T1 (n=18; l0mg of PGF2α /hd 24-48 hrs. after parturition), T2 (n=20; lOmg of PGF 2 α /hd at weaning) and controls (n=20). No differences (P>.05) were observed for survival rate and 21D litter wt. among treated and the control sows (83.71 vs. 81.57%; 103.89 vs. 108.36, respectively). As well, WEI, farrowing rate, and subsequent NBA did not differ between treat 1, treat 2, and controls (4.73 vs. 4.81 vs 4.75; 83.33 vs 80 vs 80%; 11.13 vs. 11.06 vs. 10.25, respectively). Trial 2 was performed with two experiments. The first experiment was performed in July 1996. Sows were assigned to one of two treatments: 1) controls ( n=52); 2) Administration of 60mg pregnant mare serum (n=39; injected at weaning). Farrowing rate was higher (P<0001) for PMSG treated sows than controls (100 vs. 63.46%, respectively). PMSG showed no significant (P>.05 effect upon improving number born alive among treated and control sows (11.13 vs. 10.57, respectively); however, there was a trend toward increased litter size among the treated sows. Experiment 2 occurred in February and March 1997. Sows were allotted to one of three treatments: 1) controls (n=42); 2) 60mg pregnant mare serum (n=42; administered at weaning); 60mg pregnant mare serum gamma radiated (n=39; administered at weaning). Data showed no significant difference among PMSG, GR-PMSG and controls for 5d estrus rate and 30d pregnancy rate (83.33 vs. 89.74 vs. 80.95%; 92.86 vs. 97.44 vs. 88.10%, respectively). Evidence from trial 1 showed that the use of prostaglandin did not enhance reproductive performance in swine. In addition, PMSG had little effect on improving fertility at post-treatment estrus and increasing number born alive. Although not statistically significant, trends toward larger litter sizes as well as improved 5d estrus rates and 30d pregnancy rates were evident in the treated sows. However, treatment with PMSG appeared to be effective in improving farrowing rates in the warmer months, perhaps masking the anestrus conditions typically detected during the summer.

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Püschel, Gerhard P., Ursula Hespeling, Martin Oppermann, and Peter Dieter. "Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a." Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2008/1671/.

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Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a-dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 mug/ml) dose-dependently increased prostaglandin D2, thromboxane B, and prostaglandin F2alpha formation in rat liver macrophages (Kupffer cells); (b) the C3a-mediated increase in prostanoid formation was maximal after 2 min and showed tachyphylaxis; and (c) the C3a-elicited prostanoid formation could be inhibited specifically by preincubation of C3a with carboxypeptidase B to remove the essential C-terminal arginine or by preincubation of C3a with Fab fragments of a neutralizing monoclonal antibody. These data support the hypothesis that the C3a-dependent activation of hepatic glycogenolysis is mediated by way of a C3a-induced prostanoid production in Kupffer cells.

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Drillich, Marc. "Vergleich des strategischen Einsatzes von Prostaglandin F2[alpha] [F 2alpha] mit konventionellen Methoden des Fruchtbarkeitsmanagements in zwei Milchviehbetrieben." [S.l.] : [s.n.], 1999. http://www.diss.fu-berlin.de/1999/83/index.html.

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Kurth, Anja. "Feldstudie zur Überprüfung der klinischen Wirksamkeit von Prostaglandin F2[alpha] [F 2 alpha] als Ergänzung zu einer konventionellen Therapie der Retentio secundinarum bei Milchkühen." [S.l.] : [s.n.], 2001. http://www.diss.fu-berlin.de/2001/252/index.html.

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9

Ruijter, Maurice Sébastien de [Verfasser]. "In vitro Proliferationsverhalten humaner und boviner Linsenepithelzellen unter dem Einfluss von Dorzolamid und Prostaglandin F2-alpha / Maurice Sébastien de Ruijter." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1022644793/34.

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Späth, Bruno. "Der Einfluss von Prostaglandin F2-alpha auf HCG-Sekretion und Zellmorphologie menschlichen intra- und extrauterinen Trophoblastgewebes in einem standardisierten Kultursystem." [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=961721995.

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Book chapters on the topic "Prostaglandin-f2-alpha"

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Lauderdale, James W. "Prostaglandin F2 Alpha." In Stud Managers' Handbook, 120–23. CRC Press, 2019. http://dx.doi.org/10.1201/9780429307782-15.

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Papich, Mark G. "Prostaglandin F2 Alpha." In Saunders Handbook of Veterinary Drugs, 689–90. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-323-24485-5.00491-5.

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Papich, Mark G. "Prostaglandin F2 Alpha." In Papich Handbook of Veterinary Drugs, 791–93. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-323-70957-6.00460-x.

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