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

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Published: 4 June 2021
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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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Douglas, M. J., D. F. Farquharson, P. L. E. Ross, and J. E. Renwick. "Cardiovascular Collapse Following an Overdose of Prostaglandin F2 Alpha." Obstetric Anesthesia Digest 9, no. 4 (January 1990): 237. http://dx.doi.org/10.1097/00132582-199001000-00057.

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12

Douglas, M. J., D. F. Farquharson, P. L. E. Ross, and J. E. Renwick. "Cardiovascular Collapse Following an Overdose of Prostaglandin F2 Alpha." Obstetric Anesthesia Digest 10, no. 2 (July 1990): 115. http://dx.doi.org/10.1097/00132582-199007000-00075.

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13

Liang, Z., S. R. Sooranna, N. Engineer, M. Tattersall, S. Khanjani, P. R. Bennett, L. Myatt, and M. R. Johnson. "Prostaglandin F2-alpha receptor regulation in human uterine myocytes." Molecular Human Reproduction 14, no. 4 (February 26, 2008): 215–23. http://dx.doi.org/10.1093/molehr/gan008.

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14

Collins, Danielle, Aisling M. Hogan, Alan W. Baird, and Des C. Winter. "Prostaglandin F2-alpha modulates fluid secretion in human colon." Journal of the American College of Surgeons 209, no. 3 (September 2009): S21. http://dx.doi.org/10.1016/j.jamcollsurg.2009.06.038.

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15

Lepak, N. M., and G. Serrero. "Prostaglandin F2 alpha stimulates transforming growth factor-alpha expression in adipocyte precursors." Endocrinology 136, no. 8 (August 1995): 3222–29. http://dx.doi.org/10.1210/endo.136.8.7628355.

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16

Négrel, R., D. Gaillard, and G. Ailhaud. "Prostacyclin as a potent effector of adipose-cell differentiation." Biochemical Journal 257, no. 2 (January 15, 1989): 399–405. http://dx.doi.org/10.1042/bj2570399.

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The terminal differentiation of Ob1771 pre-adipose cells induced by arachidonic acid in serum-free hormone-supplemented medium containing insulin, transferrin, growth hormone, tri-iodothyronine and fetuin (5F medium) was strongly diminished in the presence of inhibitors of prostaglandin synthesis, namely aspirin or indomethacin. Carbaprostacyclin, a stable analogue of prostacyclin (prostaglandin I2) known to be synthesized by pre-adipocytes and adipocytes, behaved as an efficient activator of cyclic AMP production and was able, when added to 5F medium, to mimic the adipogenic effect of arachidonic acid. Prostaglandins E2, F2 alpha and D2, unable to affect the cyclic AMP production, failed to substitute for carbaprostacyclin. However, prostaglandin F2 alpha, which is another metabolite of arachidonic acid in pre-adipose and adipose cells, able to promote inositol phospholipid breakdown and protein kinase C activation, potentiated the adipogenic effect of carbaprostacyclin. In addition, carbaprostacyclin enhanced both a limited proliferation and terminal differentiation of adipose precursor cells isolated from rodent and human adipose tissues maintained in primary culture. These results demonstrate the critical role of prostacyclin and prostaglandin F2 alpha on adipose conversion in vitro and suggest a paracrine/autocrine role of both prostanoids in the development of adipose tissue in vivo.
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17

Eiler, H., C. S. Armstrong-Backus, and W. A. Lyke. "Desensitization of rabbit myometrium to oxytocin and prostaglandin F2 alpha." American Journal of Physiology-Endocrinology and Metabolism 257, no. 1 (July 1, 1989): E20—E26. http://dx.doi.org/10.1152/ajpendo.1989.257.1.e20.

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The desensitizing effects of oxytocin (OT) and prostaglandin F2 alpha (PGF2 alpha) were investigated in the uteri of rabbits. Uterine motility was measured in anesthetized rabbits infused intravenously with either PGF2 alpha (50 micrograms/min) or OT (100 mU/min) alternately. The treatment sequence was saline (30 min), first drug (OT or PGF2 alpha, 90 min), second drug (OT if PGF2 alpha was first drug and vice versa, 90 min), and first drug (repeated) 60 min. Both OT and PGF2 alpha infusions increased motility approximately 200% within 5–10 min. Thereafter, motility decreased linearly to base-line value. Fifty percent desensitization was completed at 35-45 min and 100% at 90 min. A tenfold increase in the infusion rate caused no further increase in motility. However, OT infusion into a PGF2 alpha desensitized uterus (and vice versa) elicited an immediate uterokinetic response. Oxygen consumption and glucose oxidation rate of uterine slices measured at different stages (preinfusion, maximal motility, and desensitized) of uterine motility showed no difference (P greater than 0.05) between the two experimental treatments. It was concluded that either OT or PGF2 alpha infusions specifically desensitized the uterus.
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18

YAMADA, Yutaka. "Effects of Prostaglandin F2.ALPHA. in Early Pregnancy in Swine." Nihon Yoton Gakkaishi 35, no. 2 (1998): 43–46. http://dx.doi.org/10.5938/youton.35.43.

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19

Ocklind, A., S. Lake, K. Krook, I. Hallin, M. Nistér, and B. Westermark. "Localization of the prostaglandin F2 alpha receptor in rat tissues." Prostaglandins, Leukotrienes and Essential Fatty Acids 57, no. 6 (December 1997): 527–32. http://dx.doi.org/10.1016/s0952-3278(97)90555-x.

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20

van Dam, P. A., I. B. Vergote, G. M. Laekeman, G. H. Keersmaeckers, F. L. Uyttenbroeck, and A. G. Herman. "Prognostic value of prostaglandin F2 alpha concentrations in breast carcinoma." Journal of Clinical Pathology 42, no. 10 (October 1, 1989): 1046–48. http://dx.doi.org/10.1136/jcp.42.10.1046.

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21

Tasaki, Yukari, Hwa-Yong Lee, Jian-Ping Cui, Tomas J. Acosta, and Kiyoshi Okuda. "Local Autoamplification System for Prostaglandin F2 Alpha in Bovine Endometrium." Biology of Reproduction 83, Suppl_1 (November 1, 2010): 419. http://dx.doi.org/10.1093/biolreprod/83.s1.419.

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22

Pinto, C. R. F., C. Rubio, B. E. Holland, E. A. Coffman, H. K. Snyder, C. A. Leisinger, and S. Whisnant. "Antiluteogenesis effects of prostaglandin F2-alpha (PGF) in cyclic mares." Journal of Equine Veterinary Science 34, no. 1 (January 2014): 163. http://dx.doi.org/10.1016/j.jevs.2013.10.116.

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23

Watanabe, K., Y. Iguchi, S. Iguchi, Y. Arai, O. Hayaishi, and L. J. Roberts. "Stereospecific conversion of prostaglandin D2 to (5Z,13E)-(15S)-9 alpha-11 beta,15-trihydroxyprosta-5,13-dien-1-oic acid (9 alpha,11 beta-prostaglandin F2) and of prostaglandin H2 to prostaglandin F2 alpha by bovine lung prostaglandin F synthase." Proceedings of the National Academy of Sciences 83, no. 6 (March 1, 1986): 1583–87. http://dx.doi.org/10.1073/pnas.83.6.1583.

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24

Suematsu, E., M. Resnick, and K. G. Morgan. "Change of Ca2+ requirement for myosin phosphorylation by prostaglandin F2 alpha." American Journal of Physiology-Cell Physiology 261, no. 2 (August 1, 1991): C253—C258. http://dx.doi.org/10.1152/ajpcell.1991.261.2.c253.

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The mechanism of contraction of vascular smooth muscle by prostaglandin F2 alpha (PGF2 alpha) was examined by simultaneous measurement of the intracellular Ca2+ concentration [( Ca2+]i), force, and myosin light-chain (MLC) phosphorylation in ferret aorta. In the presence of 2.5 mM extracellular Ca2+, PGF2 alpha (10(-5)M) produced a tonic contraction with a transient spike in [Ca2+]i, followed by a relatively small sustained increase in [Ca2+]i (from a basal level of 2.32 +/- 0.07 x 10(-7) to 2.72 +/- 0.05 x 10(-7) M). In Ca(2+)-free bathing media, PGF2 alpha also produced a tonic contraction with a small spike in [Ca2+]i, indicating a release of Ca2+ from intracellular store sites, followed by no significant increase in [Ca2+]i. Ca(2+)-force curves were constructed by plotting the calibrated steady-state aequorin light signal against the resulting steady-state force. The curve was significantly shifted to the left by PGF2 alpha. PGF2 alpha also shifted the Ca(2+)-phosphorylation curve to the left. These results suggest that PGF2 alpha causes contraction by both elevating [Ca2+]i and decreasing the Ca2+ requirement for MLC phosphorylation. The data are consistent with a mechanism where there is either an increase in activity of MLC kinase or a decrease in phosphatase activity. Additionally, there was a smaller, but statistically significant, effect to increase force at any one phosphorylation level, pointing to the possibility of regulation of contractile force separate from MLC phosphorylation.
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25

Fairclough, RJ, and TM Lau. "Hormonal control of concentrations of endometrial oxytocin receptors in the ewe." Reproduction, Fertility and Development 4, no. 3 (1992): 313. http://dx.doi.org/10.1071/rd9920313.

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Uterine oxytocin receptors have been shown to play a major role in the regulation of uterine prostaglandin F2 alpha release during the oestrous cycle and early pregnancy in sheep. The concentration of endometrial oxytocin receptors increases sharply from around Day 13 of the oestrous cycle to reach a maximum between Days 15 and 16. The high concentration of endometrial oxytocin receptors at this time coincides with the release of endogenous uterine prostaglandin F2 alpha during luteal regression and the maximum uterine prostaglandin F2 alpha response to an oxytocin stimulus. The concentration of uterine oxytocin receptors appears to be regulated by both progesterone and oestradiol. Studies in ovariectomized ewes have shown that initially progesterone lowers the concentration of endometrial oxytocin receptors, but after prolonged treatment with progesterone the concentration of oxytocin receptors increases; this suggests that the uterine-PGF2 alpha response to oxytocin has become refractory to the inhibitory effects of progesterone. The concentration of endometrial oxytocin receptors is also lowered by short-term oestradiol treatment. However, oestrogen treatment of ewes after long-term treatment with progesterone does not result in an increase in the concentration of oxytocin receptors following the cessation of progesterone treatment. On the basis of these and other data it is proposed that in the normal oestrous cycle the concentration of endometrial oxytocin receptors is initially depressed by both oestradiol and progesterone but that the marked increase in the concentration of oxytocin receptors over Days 13-16 of the cycle is due primarily to the withdrawal of the inhibitory influence of progesterone alone. During early pregnancy the release of uterine prostaglandin F is suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)
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26

Erkiliç, Kuddusi, Faruk Ekinciler, Ertuğrul Mirza, Hakki Doğan, and Nurullah Çağil. "Effects of Topically Applied Prostaglandin F2 alpha on Normotensive Human Eyes." Ophthalmic Research 28, no. 6 (1996): 351–55. http://dx.doi.org/10.1159/000267927.

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27

Villumsen, J., and A. Alm. "Prostaglandin F2 alpha-isopropylester eye drops: effects in normal human eyes." British Journal of Ophthalmology 73, no. 6 (June 1, 1989): 419–26. http://dx.doi.org/10.1136/bjo.73.6.419.

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28

Rib�ri, O., I. Sziklai, and J. G. Kiss. "Cyclic nucleotide and prostaglandin F2 alpha contents of otosclerotic auditory ossicles." Archives of Oto-Rhino-Laryngology 242, no. 1 (July 1985): 63–66. http://dx.doi.org/10.1007/bf00464408.

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29

YL, D. "Nitric oxide prevents prostaglandin F2$alpha;-induced preterm labor in rats." Journal of the Society for Gynecologic Investigation 3, no. 2 (March 1996): 331A. http://dx.doi.org/10.1016/1071-5576(96)82993-5.

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30

Dhaliwal, G. S., R. D. Sharma, and G. Singh. "Efficacy of prostaglandin F2-alpha administration for inducing estrus in buffalo." Theriogenology 29, no. 6 (June 1988): 1401–6. http://dx.doi.org/10.1016/0093-691x(88)90021-0.

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31

Leighton, B., L. Budohoski, F. J. Lozeman, R. A. J. Challiss, and E. A. Newsholme. "The effect of prostaglandins E1, E2 and F2α and indomethacin on the sensitivity of glycolysis and glycogen synthesis to insulin in stripped soleus muscles of the rat." Biochemical Journal 227, no. 1 (April 1, 1985): 337–40. http://dx.doi.org/10.1042/bj2270337.

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Prostaglandins E1 and E2 increased the sensitivity of glycolysis to insulin in the isolated stripped soleus muscle of the rat, but prostaglandin F2 alpha had no effect. Indomethacin, which inhibits prostaglandin formation, markedly decreased the sensitivity of glycolysis to insulin. These findings suggest that prostaglandins of the E series increase the sensitivity of muscle glycolysis to insulin in vivo.
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32

Kawai, Y., and T. Ohhashi. "Prostaglandin F2 alpha-induced endothelium-dependent relaxation in isolated monkey cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 5 (May 1, 1991): H1538—H1543. http://dx.doi.org/10.1152/ajpheart.1991.260.5.h1538.

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Effects of prostaglandin F2 alpha (PGF2 alpha) on isolated monkey and dog cerebral arteries were investigated to reevaluate PGF2 alpha's possible action on the endothelium. Low concentrations of PGF2 alpha ranging from 10(-11) to 10(-8) M produced a dose-dependent relaxation in the monkey arteries. PGF2 alpha (10(-7) M) produced a transient contraction followed by a small relaxation, whereas higher concentrations (greater than 10(-6) M) of PGF2 alpha induced only contractions. The PGF2 alpha-induced relaxation was not observed in the canine cerebral arteries. The PGF2 alpha-induced relaxation of the monkey cerebral arteries was not affected by treatment with 10(-7) M propranolol, 10(-7) M atropine, or 10(-6) M cimetidine. In monkey cerebral arteries without endothelium, PGF2 alpha in concentrations ranging from 10(-11) to 10(-6) M caused no relaxation. Treatment with 5 X 10(-5) M aspirin, 3 X 10(-5) M NG-monomethyl-L-arginine, and 10(-5) M oxyhemoglobin significantly suppressed the PGF2 alpha-induced relaxation. These results suggest that low concentrations of PGF2 alpha may produce an endothelium-dependent relaxation in monkey cerebral arteries and that the relaxation may be mediated by release of both endogenous vasodilative prostaglandins and endothelium-derived relaxing factor from endothelial cells.
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33

Gilbert, CL, TH Burne, JA Goode, PJ Murfitt, and SL Walton. "Indomethacin blocks pre-partum nest building behaviour in the pig (Sus scrofa): effects on plasma prostaglandin F metabolite, oxytocin, cortisol and progesterone." Journal of Endocrinology 172, no. 3 (March 1, 2002): 507–17. http://dx.doi.org/10.1677/joe.0.1720507.

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In the pig, nest building occurs in the day preceding parturition (gestation=114--116 days). Nest building behaviour can be induced in pregnant, pseudopregnant and cyclic female pigs following injection of prostaglandin F2alpha. Here we investigated behaviour and endocrine changes after the administration of indomethacin, which inhibits cyclo-oxygenase enzymes and thus prostaglandin synthesis. In experiment 1, pregnant primiparous pigs (gilts) were blood sampled through jugular vein catheters every 20 min from 1000 h on day 113 of pregnancy and behaviour was recorded until birth. Two hours after pre-partum nest building began, animals received 4 mg/kg indomethacin (n=7) or control vehicle (n=8) intramuscularly. Indomethacin-treated animals showed less nest building than controls between 1 and 5 h after injection (P<0.05), during which time they were mostly inactive and lay down for longer than controls. From 5 h before birth until birth there was no significant treatment difference in nest building behaviour. There was a tendency for the start of birth to be delayed in indomethacin-treated animals. Plasma 13,14-dihydro-15-keto-prostaglandin F2 alpha (a major metabolite of prostaglandin F2 alpha) rose during pre-injection nest building and then fell following indomethacin treatment, but was not significantly different between groups when behaviour differed. Plasma oxytocin, cortisol and progesterone were not significantly affected by treatment. In experiment 2, indomethacin-treated non-pregnant gilts (n=7) did not show any changes in activity or posture compared with vehicle-treated controls (n=6) between 90 and 150 min after treatment. These results suggested that indomethacin treatment reversibly and specifically inhibits porcine pre-partum nest building by a mechanism that may involve endogenous prostaglandin F2 alpha synthesis inhibition but is independent of circulating oxytocin, cortisol and progesterone concentrations.
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34

Yasmin, Shakila, Rukhsana Aziz, Muhammad Hassan, and Mehak Fatima. "TERMINATION OF PREGNANCY." Professional Medical Journal 25, no. 06 (June 10, 2018): 952–58. http://dx.doi.org/10.29309/tpmj/2018.25.06.287.

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Objectives: To compare efficacy of extra-amniotic Foley’s catheter balloon aloneversus combined use of Foley’s catheter balloon and extra-amniotic instillation of prostaglandinF2-alpha in therapeutic termination of second trimester pregnancy. Study Design: Randomizedcontrolled trial. Setting: Department of Obstetrics & Gynecology, Bahawal Victoria Hospital,Bahawalpur. Period: Two years. July 2014 to June 2016. Sample Technique: Non-probability,consecutive sampling technique. Patients & Methods: A total of 256 patients, 16 to 38 years ofage with fetal death or missed abortion on ultrasonography in 2nd trimester (14-24 gestationalweeks) of pregnancy were included in the study. Patients with previous uterine surgery, multiplepregnancies and parity>3 were excluded. Then selected patients were placed randomly intotwo groups i.e. Group A (extra-amniotic Foley’s catheter balloon alone) & Group B (Foley’scatheter balloon along with extra-amniotic instillation of prostaglandin F2-alpha), by using lotterymethod. Outcome variables like efficacy i.e. expulsion of fetus within 24 hours of induction, werenoted. Results: The mean age of women in group A was 24.51 ± 4.77 and in group B was 24.29± 4.48 years. The mean gestational age in group A was 21.65 ± 2.01 weeks and in group Bwas 21.28 ± 1.93 weeks. Efficacy was 103 (80.47%) in group A (extra-amniotic Foley’s catheterballoon alone) and 119 (92.97%) in group B (combined use of Foley’s catheter balloon andextra-amniotic instillation of prostaglandin F2-alpha) with p-value of 0.003. Conclusion: Thisstudy concluded that combined use of Foley’s catheter balloon and extra-amniotic instillationof prostaglandin F2-alpha is better and more efficacious than extra-amniotic Foley’s catheterballoon alone in therapeutic termination of second trimester pregnancy.
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35

Sugatani, J., Y. Masu, M. Nishizawa, K. Sakamoto, T. Houtani, T. Sugimoto, and S. Ito. "Hormonal regulation of prostaglandin F2 alpha receptor gene expression in mouse ovary." American Journal of Physiology-Endocrinology and Metabolism 271, no. 4 (October 1, 1996): E686—E693. http://dx.doi.org/10.1152/ajpendo.1996.271.4.e686.

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In this study we examined regulation by pituitary gonadotropins of the prostaglandin F2 alpha (PGF2 alpha) receptor gene expression in the mouse ovary. Administration of pregnant mare serum gonadotropin (PMSG) to 35-day-old mice in the diestrus phase stimulated the ovary and enhanced the production of progesterone at 1 h PMSG also increased the ovarian PGF2 alpha receptor mRNA level in a time-dependent manner, reaching a sixfold maximum at 1 h. These actions of PMSG were mimicked by human chorionic gonadotropin (hCG), follicle-stimulating hormone (FSH), and cholera toxin, all of which elevate intracellular adenosine 3',5'-cyclic monophosphate (cAMP). In situ hybridization revealed that PGF2 alpha receptor mRNA was localized to the corpus luteum, but the intensity of staining varied among corpora lutea in the same ovary. Exogenous PGF2 alpha inhibited the PMSG-stimulated progesterone production. These results demonstrate that gonadotropins may induce the expression of the PGF2 alpha receptor gene in luteal cells of the corpus luteum, probably by acting through a cAMP-mediated pathway, and that expression of the PGF2 alpha receptor may be functionally associated with the decrease in serum progesterone level.
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36

Graser, T., and P. M. Vanhoutte. "Hypoxic contraction of canine coronary arteries: role of endothelium and cGMP." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 6 (December 1, 1991): H1769—H1777. http://dx.doi.org/10.1152/ajpheart.1991.261.6.h1769.

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The effect of severe hypoxia in quiescent or contracted (prostaglandin F2 alpha) canine coronary artery rings with and without endothelium was studied. Hypoxia induced an initial transient relaxation followed by a sustained contraction. The hypoxic contraction in quiescent rings was comparable in rings with and without endothelium. The facilitation of the contraction to prostaglandin F2 alpha was more pronounced in rings with endothelium. Increasing the level of contractions by augmenting the contraction of prostaglandin F2 alpha potentiated the hypoxic contraction in rings with endothelium only. Methylene blue, LY 83583, and nitro-L-arginine reversed the hypoxic facilitation in contracted rings into relaxation, whereas M&B 22948 augmented it. In quiescent coronary preparations, methylene blue reversed the hypoxic contraction into relaxation in preparations with and without endothelium, whereas nitro-L-arginine had the same effect in vessels with endothelium only. SIN-1, nitroglycerin, and dibutyryl guanosine 3',5'-cyclic monophosphate (cGMP) unmasked hypoxic facilitation in rings without endothelium. This was not observed with isoproterenol. The measurement of the level of cGMP revealed an increased level in rings with endothelium compared with those without endothelium under control oxygenation. This difference disappeared during hypoxia due to a decrease of cGMP content in vessels with endothelium. The results suggest that a moderate increase of the cGMP level in vascular smooth muscle is a prerequisite for the occurrence of hypoxia-induced facilitation in contracted canine coronary arteries.
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37

Taniguchi, Ken, Fumie Kizuka, Isao Tamura, and Norihiro Sugino. "Prostaglandin F2-alpha Stimulates Cyclooxygenase-2 Expression and Prostaglandin F2-alpha Synthesis Through NF-kappaB Activation via Reactive Oxygen Species in the Corpus Luteum of Pseudopregnant Rats." Biology of Reproduction 83, Suppl_1 (November 1, 2010): 124. http://dx.doi.org/10.1093/biolreprod/83.s1.124.

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38

Thore, C. R., M. Nam, and D. Busija. "Phorbol ester-induced prostaglandin production in piglet cortical astroglia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R34—R37. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r34.

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We examined effects of phorbol 12,13-dibutyrate (PDB), which activates protein kinase C (PKC), on prostaglandin and leukotriene production in piglet cultured glia derived from cerebral cortex and white matter. Levels of prostaglandins were determined using enzyme immunoassay. Baseline levels in media for prostaglandin F2 alpha (PGF2 alpha) were 730 +/- 116 pg/ml and increased to 1,551 +/- 196 pg/ml at 10(-8) M PDB (P < 0.05) and to 2,182 +/- 190 pg/ml at 10(-6) M PDB (P < 0.05) (n = 16). Little or no 6-keto-prostaglandin F1 alpha, prostaglandin E2, or leukotrienes C4/D4 were produced. PGF2 alpha levels in media did not increase in the presence of the vehicle for PDB (dimethyl sulfoxide) or 4 alpha-phorbol 12,13-didecanoate (PDD; a phorbol ester that does not activate protein kinase C) or when indomethacin (10 micrograms/ml), quinacrine (10(-6) M), or isoquinolinylsulfonylmethyl piperazine (10(-4) M) (an inhibitor of PKC activation) was coadministered with PDB. We conclude that glia can be important contributors of prostaglandins to extracellular-cerebrospinal fluids where they could influence cerebrovascular tone, and that PDB probably increases prostaglandin production via liberation of arachidonic acid by PKC-induced activation of phospholipase A2.
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39

Harker, C. T., P. J. Ousley, C. J. Bowman, and J. M. Porter. "Cooling augments alpha 2-adrenoceptor-mediated contractions in rat tail artery." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 4 (April 1, 1991): H1166—H1171. http://dx.doi.org/10.1152/ajpheart.1991.260.4.h1166.

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Experiments were performed to assess the effects of acute moderate cooling on postjunctional alpha 1- and alpha 2-adrenoceptors in isolated rings of tail arteries from male Sprague-Dawley rats. Rings were contracted with norepinephrine (NE; 10(-9) to 10(-4) M) alone or in the presence of prazosin (Pz; 3 x 10(-7) M) or rauwolscine (Rw; 10(-7) M). NE concentration-response curves were inhibited by alpha 1-blockade (Pz) but not significantly affected by alpha 2-blockade (Rw). In all rings, cooling caused an increase in the slope of the dose-response curve and a significant increase in the concentration of agonist required to evoke contractions, as assessed by that concentration of NE required to evoke a contraction equal to 10% of maximal (EC10). Cooling inhibited contractions evoked by the selective alpha 1-adrenergic agonist phenylephrine (PE) as assessed by EC10 but had no significant effect on the weak contractions elicited by the selective alpha 2-adrenergic agonist B-HT 920. Prior elevation of tone with either KCl or prostaglandin F2 alpha enhanced alpha 2-mediated contractions. These contractions were augmented by cooling, whereas those caused by either KCl or prostaglandin F2 alpha alone were not significantly affected. Our results suggest that alpha 2-adrenoceptor-mediated responses in this blood vessel are dependent on the level of preexisting tone and are potentiated by cooling.
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40

Bode, C., G. Maute, and J. C. Bode. "Prostaglandin E2 and prostaglandin F2 alpha biosynthesis in human gastric mucosa: effect of chronic alcohol misuse." Gut 39, no. 3 (September 1, 1996): 348–52. http://dx.doi.org/10.1136/gut.39.3.348.

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41

McLean, M. P., J. T. Billheimer, K. J. Warden, and R. B. Irby. "Prostaglandin F2 alpha mediates ovarian sterol carrier protein-2 expression during luteolysis." Endocrinology 136, no. 11 (November 1995): 4963–72. http://dx.doi.org/10.1210/endo.136.11.7588230.

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42

Bhattacharaya, Prabha R., Deepak P. Wakharia, Malati M. Andankar, and Puspha Gurtu. "Menstrual Regulation by(15S)-15 Methyl Prostaglandin F2 Alpha by Intramuscular Route." Asia-Oceania Journal of Obstetrics and Gynaecology 10, no. 4 (May 24, 2010): 435–37. http://dx.doi.org/10.1111/j.1447-0756.1984.tb00708.x.

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43

Hankins, G. D. V., G. K. Berryman, R. T. Scott, and D. Hood. "Maternal Arterial Desaturation With 15-Methyl Prostaglandin F2 Alpha for Uterine Atony." Obstetric Anesthesia Digest 9, no. 1 (April 1989): 16. http://dx.doi.org/10.1097/00132582-198904000-00018.

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44

Uchiyama, M., and K. Sakai. "Increased main urinary metabolite of prostaglandin F2 alpha excretion in childhood migraine." Archives of Disease in Childhood 63, no. 3 (March 1, 1988): 342. http://dx.doi.org/10.1136/adc.63.3.342-a.

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45

Douglas, M. Joanne, Duncan F. Farquharson, Peggy L. E. Ross, and Jamie E. Renwick. "Cardiovascular collapse following an overdose of prostaglandin F2 alpha: a case report." Canadian Journal of Anaesthesia 36, no. 4 (July 1989): 466–69. http://dx.doi.org/10.1007/bf03005350.

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46

Graves, R. L., R. G. Lutz, J. W. Riesen, T. A. Hoagland, and C. O. Woody. "Factors influencing estrus and conception in dairy heifers after prostaglandin F2-alpha." Theriogenology 23, no. 5 (May 1985): 733–42. http://dx.doi.org/10.1016/0093-691x(85)90148-7.

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47

Archer, D. F., J. E. Taylor, and T. A. Jacot. "Prostaglandin F2 alpha is a product of the decidualized human stromal cell." Fertility and Sterility 100, no. 3 (September 2013): S298. http://dx.doi.org/10.1016/j.fertnstert.2013.07.1053.

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48

Scott, I. M., R. H. Fertel, and J. A. Boulant. "Leukocytic pyrogen effects on prostaglandins in hypothalamic tissue slices." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 1 (July 1, 1987): R71—R76. http://dx.doi.org/10.1152/ajpregu.1987.253.1.r71.

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Some studies suggest that leukocytic pyrogen (LP) increase hypothalamic prostaglandins which, in turn, affect hypothalamic thermoregulatory neurons to produce fever. The present study used radioimmunoassays to quantitate the ability of guinea pig hypothalamic tissue slices to produce prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), and thromboxane B2 (TxB2). Dose- and time-dependent prostaglandin increases occurred when these slices were perfused with LP media. Steady-state levels of tissue release were reached at 0-3 min for 6-keto-PGF1 alpha, at 6-9 min for PGE2 and PGF2 alpha, and at 12-15 min for TxB2. With the exception of 6-keto-PGF1 alpha, all substances showed continuous dose-response relationships for concentrations ranging from 0.001 to 0.25 LP dilutions. Tissue PGE2, for example, was 0.7 pg X min-1 X mg-1 with the 0.001 LP dilution and 8.7 pg X min-1 X mg-1 with the 0.25 LP dilution. Indomethacin blocked much of the LP-induced prostaglandin increase. Although there is a relationship between hypothalamic LP and prostaglandins in response to physiological LP levels, tissue prostaglandins are several orders of magnitude lower than concentrations necessary to produce fever by hypothalamic microinjection. This suggests that prostanoids, such as PGE2, may not be the sole mediators of fever induced by leukocytic pyrogen.
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49

Sada, K., M. Shirai, and I. Ninomiya. "Effects of prostaglandin F2 alpha and prostacyclin on pulmonary microcirculation in the cat." Journal of Applied Physiology 62, no. 3 (March 1, 1987): 1124–32. http://dx.doi.org/10.1152/jappl.1987.62.3.1124.

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In pulmonary microcirculation, using a new X-ray television system, we measured the effects of prostaglandin F2 alpha (PGF2 alpha) and prostacyclin on the internal diameter (ID), flow velocity, volume flow, and transit times of a contrast medium in small arteries (Ta) and veins (Tv) in anesthetized cats. The ID of the arteries and veins ranged from 100 to 500 micron. PGF2 alpha, 0.3, 1, and 3 micrograms/kg, predominantly decreased ID on the arterial side in a dose-dependent manner but increased flow velocity 27–62%. Consequently, volume flow was kept relatively constant. With PGF2 alpha, Ta and Tv were decreased 18–41% and 4–15%, respectively. Prostacyclin, 2 and 4 micrograms/kg, uniformly dilated the ID of small arteries 9–16% but did not change small veins. With prostacyclin, flow velocity was unchanged or decreased, whereas volume flow was increased significantly, 27–32%. No significant changes of Ta and Tv were observed in response to prostacyclin. When both prostaglandins, PGF2 alpha and prostacyclin, were administered, they canceled each other with respect to the ID of small pulmonary arteries. Prostacyclin also prevented the PGF2 alpha-induced vasoconstriction of the pulmonary venous microcirculation.
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50

Hoeffner, U., C. Boulanger, and P. M. Vanhoutte. "Proximal and distal dog coronary arteries respond differently to basal EDRF but not to NO." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 3 (March 1, 1989): H828—H831. http://dx.doi.org/10.1152/ajpheart.1989.256.3.h828.

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Experiments were designed to analyze the effects of endothelium-derived relaxing factor(s) (EDRF; released basally or on stimulation with acetylcholine) and nitric oxide (NO) on smooth muscle of coronary arteries of different diameter. During contractions of the bioassay ring evoked with prostaglandin F2 alpha, the relaxations caused by basal EDRF were greater in the distal than in the proximal coronary arteries, whereas there was no difference in response to the EDRF released by acetylcholine. During direct superfusion, NO caused similar relaxations in proximal and distal coronary artery rings. Optimal tension, prostaglandin F2 alpha-induced contractions, and relaxations caused by sodium nitroprusside were comparable in both preparations. In rings of proximal and distal coronary artery studied in organ chambers, acetylcholine caused comparable endothelium-dependent, whereas sodium nitroprusside and NO cause comparable endothelium-independent relaxations. These experiments indicate a difference in response of different-sized coronary arteries to basally released EDRF and suggest that the basally released factor differs from NO.
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