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The Journal of Physiology Jan 19761. The effects of intraportal and hepatic arterial infusion of prostaglandins E1 and E2 on liver function and circulation was studied in fasting chloralose anaesthetized...
1. The effects of intraportal and hepatic arterial infusion of prostaglandins E1 and E2 on liver function and circulation was studied in fasting chloralose anaesthetized cats. 2. Infusion of the prostaglandins at rates of 0-1, 1-0 and 5-0 mug/kg.min caused a 35-40% increase in bile flow. This may be explained by a decrease in the reabsorption or a secretion of sodium ions by the ductular cells. The canalicular bile production and bile flow. This may be explained by a decrease in the reabsorption or a secretion of sodium ions by the ductular cells. The canalicular bile production and bile acid excretion was not affected by the prostaglandins. 3. Infused at rates of 1-0 and 5-0 mug/kg.min the prostaglandins caused a transient decrease in mean arterial blood pressure and mesenteric vascular resistance. The resistance in the intrahepatic arterioles and low-pressure vessels was not affected. 4. The prostaglandins did not influence the splanchnic uptake of oxygen and ethanol, whereas a slight increase in the splanchnic glucose output occurred. 5. The effects of the two prostaglandins were identical and not related to the route of administration.
Topics: Animals; Bile; Blood Pressure; Erythritol; Ethanol; Glucose; Infusions, Parenteral; Liver; Oxygen Consumption; Prostaglandins E; Secretory Rate; Vascular Resistance
PubMed: 1255509
DOI: 10.1113/jphysiol.1976.sp011261 -
The Journal of Physiology Jun 19821. At concentrations of 2.8 x 10(-8)-2.8 x 10(-6) M, prostaglandins (PGs; PGE(1), PGE(2) and PGF(2alpha)) had no effect on membrane potential and resistance of smooth...
1. At concentrations of 2.8 x 10(-8)-2.8 x 10(-6) M, prostaglandins (PGs; PGE(1), PGE(2) and PGF(2alpha)) had no effect on membrane potential and resistance of smooth muscles of the guinea-pig mesenteric artery. PGs (2.8 x 10(-8) M) suppressed the contraction evoked by perivascular nerve stimulation, but did not suppress the contraction evoked by direct muscle stimulation.2. PGs (2.8 x 10(-8) M) suppressed the e.j.p.s evoked by repetitive perivascular nerve stimulation but preserved the facilitation process of e.j.p.s evoked by any given stimulus frequency (0.1-1.0 Hz).3. The relationships between e.j.p. amplitudes and [Ca](o) plotted on log scales in the presence or absence of PGE(2) were not parallel. High concentrations of [Ca](o) prevented the inhibitory actions of PGs on the amplitude of e.j.p.s.4. PGE(2) did not suppress the activity of nerve fibres contributing to the generation of e.j.p.5. Indomethacin (10(-6) M) enhanced the amplitude of e.j.p.s and the frequency of miniature e.j.p.s with no change in the membrane potential and resistance of smooth muscles; these actions of indomethacin were suppressed by PGE(2) (2.8 x 10(-8) M).6. Phentolamine (10(-7) M) enlarged and yohimbine (10(-7) M) reduced the amplitude of the first e.j.p. evoked by a train stimulation, but the maximum amplitude of e.j.p., after the facilitation was completed, was in both cases much larger than that observed in the control. The enhancement of the transmission process was also suppressed by PGs (2.8 x 10(-8) M).7. The results indicate that in the guinea-pig mesenteric artery, PGs mainly suppress chemical transmitter release from nerve terminals due to interactions with Ca influx, but not due to interaction with presynaptic alpha-adrenoceptors. Endogenous PG may act as a regulator substance in neuromuscular transmission.
Topics: Alprostadil; Animals; Dinoprost; Dinoprostone; Guinea Pigs; In Vitro Techniques; Indomethacin; Membrane Potentials; Mesenteric Arteries; Muscle, Smooth, Vascular; Neuromuscular Junction; Prostaglandins; Prostaglandins E; Prostaglandins F; Synaptic Transmission
PubMed: 6288928
DOI: 10.1113/jphysiol.1982.sp014241 -
Fertility and Sterility Feb 1988The aim of the present study was to evaluate the effect of addition of physiologic amounts of different prostaglandins normally present in semen, on sperm motility, on...
The aim of the present study was to evaluate the effect of addition of physiologic amounts of different prostaglandins normally present in semen, on sperm motility, on sperm penetration capacity in cervical mucus in vitro, and on the adenosine triphosphate (ATP) concentration in semen. Semen samples were obtained from volunteers who were attending the fertility outpatient clinic. Sperm motility was measured on a video recorder with a built-in timer, sperm penetration by the Kremer test, and ATP by bioluminescence assay. The addition of 19-hydroxy prostaglandin (PG) E to ejaculates positively stimulated sperm motility and sperm penetration capacity. The opposite effect was observed with 19-hydroxy PGF. PGE1, PGE2, and PGF2 alpha had no effect on either parameter, while PGF1 alpha reduced the sperm motility. The addition of 19-hydroxy PGE to ejaculates increased and the addition of 19-hydroxy PGF reduced semen concentrations of ATP. However, only the last-mentioned effect was statistically significant (P less than 0.05). It is suggested that, in particular, 19-hydroxy PGE and 19-hydroxy PGF are important regulators of sperm motility and that the effect may be mediated via effects on the ATP content in the spermatozoa.
Topics: Adenosine Triphosphate; Dinoprost; Dinoprostone; Female; Humans; In Vitro Techniques; Male; Prostaglandins E; Prostaglandins F; Semen; Sperm Motility; Sperm-Ovum Interactions
PubMed: 3338588
DOI: 10.1016/s0015-0282(16)59723-4 -
Fertility and Sterility Jan 1977Spontaneous isometric contractions of the human fallopian tube were measured in vitro. The tubes were obtained during the follicular phase of the menstrual cycle in 16... (Comparative Study)
Comparative Study
Spontaneous isometric contractions of the human fallopian tube were measured in vitro. The tubes were obtained during the follicular phase of the menstrual cycle in 16 experiments and during the luteal phase in 23 experiments. The area under the curve and the frequency of spontaneous isometric contractions, together with the amount of prostaglandins E and F produced by the tube, were measured. Using each tissue as its own control, the effects of adding indomethacin or papeverine to the tissue both were assessed. Indomethacin, a prostaglandin synthetase inhibitor, significantly reduced the prostaglandin output without affecting the tubal motility. By contrast, papaverine, which is a smooth muscle relaxant but not an inhibitor of prostaglandin synthesis, significantly reduced both motility and prostaglandin output. It is concluded that prostaglandins do not have a direct role in the regulation of the spontaneous motility of the human fallopian tube.
Topics: Fallopian Tubes; Female; Humans; In Vitro Techniques; Indomethacin; Menstruation; Muscle Contraction; Papaverine; Prostaglandins E; Prostaglandins F
PubMed: 832721
DOI: 10.1016/s0015-0282(16)42322-8 -
Prostaglandins Aug 1986Separation and quantification of prostaglandin E1 (PGE1) and prostaglandin E2 (PGE2) were achieved using reverse phase high performance liquid chromatography (HPLC)....
Separation and quantification of prostaglandin E1 (PGE1) and prostaglandin E2 (PGE2) were achieved using reverse phase high performance liquid chromatography (HPLC). Panacyl bromide (p-(9-anthroyloxy)phenacyl bromide) (PAB) derivatives of PGE2 and PGE1 were prepared. Reverse phase HPLC using a linear gradient of 56% to 80% acetonitrile in water containing 0.10% acetic acid gave baseline resolution of the two derivatives. A 3 um diameter particle, C18 column provided good resolution and reproducible recoveries. Human synovial tissue cells were incubated with the precursor fatty acids for PGE1 or PGE2 and stimulated with a crude Interleukin 1 (IL-1) preparation. Cells grown in the presence of dihomogammalinolenic acid (DGLA), the precursor for PGE1, made significantly more PGE1 than cells grown in control medium or in the presence of arachidonic acid, precursor for PGE2. PGE2 synthesis was reduced when DGLA was added to cells (resting or IL-1-stimulated).
Topics: Acetophenones; Alprostadil; Arachidonic Acid; Arachidonic Acids; Cells, Cultured; Chromatography, High Pressure Liquid; Dinoprostone; Humans; Prostaglandins E; Synovial Membrane
PubMed: 3099332
DOI: 10.1016/0090-6980(86)90133-4 -
The Journal of Experimental Medicine Oct 1981Biphasic fevers were induced in sheep with intravascular infusions or injections of 4-10 mug (80-200 ng/kg) of endotoxin, whereas monophasic fevers were obtained with...
Biphasic fevers were induced in sheep with intravascular infusions or injections of 4-10 mug (80-200 ng/kg) of endotoxin, whereas monophasic fevers were obtained with doses of 1-2/mug (20-40 ng/kg). A marked increase in arterial blood pressure invariably accompanied the onset of fever; the latency of responses to the higher and lower doses of endotoxins averaged 26 min and 42 min, respectively. Prostaglandin (PG) assays of plasma from the carotid artery and jugular vein during fever episodes revealed a surge of PGE and PGF coincident with the pressor response and the first phase of fever, but PG were not detected in plasma samples taken throughout the second phase of fever. PG measurements of arterial and venous plasma collected at a distal site (hind limb) showed a similar surge of PGE and PGF in association with the early fever response, indicating that intravascular PG synthesis and release represents a generalized systemic response to circulating endotoxin. Carotid arterial infusions of PGE(2) produced immediate monophasic fevers and pressor responses, whereas PGD(2) infusions produced an immediate pressor effect but no fever. Infusions of PGF(2alpha) or prostacyclin, however, evoked neither fever nor pressor effects. Intracarotid infusions of leukocyte pyrogen (LP) caused monophasic fevers with latent periods of 15-20 min but pressor responses were not seen and neither PGE nor PGF were detected in plasma samples from the carotid artery or jugular vein before or during fever. Indomethacin, a potent inhibitor of arachidonic acid metabolism, blocked fever responses to endotoxin and to LP. These findings implicate PGE as the mediator of the early phase of endotoxin fever and imply a role for another pyrogenic metabolite ofarachidonic acid in the mediation of the second phase of fever, i.e., the phase associated with circulating LP. It is possible that both pyrogenic metabolites are generated within the vascular compartment, reaching thermoregulatory centers of the brain by transfer across the blood-brain interface.
Topics: Animals; Blood Pressure; Body Temperature; Carotid Arteries; Endotoxins; Female; Fever; Indomethacin; Injections, Intra-Arterial; Injections, Intravenous; Interleukin-1; Jugular Veins; Prostaglandins E; Prostaglandins F; Proteins; Sheep
PubMed: 7288365
DOI: 10.1084/jem.154.4.1212 -
The Journal of Physiology Apr 1984In an attempt to elucidate the possible roles of endogenous prostaglandins on the neuro-effector transmission in the dog trachea, effects of a prostaglandin antagonist...
In an attempt to elucidate the possible roles of endogenous prostaglandins on the neuro-effector transmission in the dog trachea, effects of a prostaglandin antagonist (1-acetyl-2-[8-chloro-10, 11- dihydrobenz (b.f) (1.4) oxazepine-10-carbonyl]hydrazine (SC-19220] on the electrical and mechanical properties of smooth muscle cells and on neuro-effector transmission in the smooth muscle layer were studied by means of micro-electrode, double sucrose-gap, and tension recording methods. The levels of prostaglandins in the perfusate from the dog tracheal tissue were also determined using radioimmunoassay. Excitatory junction potentials (e.j.p.s) and twitch tension evoked by electrical field stimulation with short pulse duration (50-100 microseconds), which were abolished by tetrodotoxin (10(-7) M) or atropine (5 X 10(-6) M), showed gradual and continuous reduction in amplitude during superfusion with normal Krebs solution. Reduction in the amplitude of e.j.p.s occurred with no change in the membrane potential or membrane input resistance. SC-19220 (3.1 X 10(-5) M) did not modify the membrane potential, membrane input resistance or the sensitivity to acetylcholine of the smooth muscle cells. Yet, with application of SC-19220 (3.1 X 10(-6) M), gradual and continuous reductions in the amplitude of e.j.p.s and twitch contractions were no longer observed. With an increased concentration (3.1 X 10(-5) M), e.j.p.s and twitch contractions with a constant amplitude were obtained after the initial increase in the amplitude. When the amplitude of twitch contractions was stabilized by treatment with indomethacin (10(-5) M), low concentrations (10(-12) to 10(-10) M) of prostaglandin E2 (PGE2) or prostaglandin F2 alpha (10(-8) to 10(-6) M) markedly suppressed the amplitude of the twitch contractions. In some muscle preparations (ten out of twenty-two preparations examined), SC-19220 (3.1 X 10(-6) to 3.1 X 10(-5) M) produced a sustained contraction of the muscle, which was suppressed by atropine (5 X 10(-6) M) or PGE2 (10(-8) M). Following pre-treatment of the tissue with atropine (5 X 10(-6) M), SC-19220 did not evoke contracture. In the resting condition, 10-40 ng g-1 wet wt. tissue min-1 PGE or PGF was released into the perfusate from the tracheal muscle tissue of the control dog.(ABSTRACT TRUNCATED AT 400 WORDS)
Topics: Acetylcholine; Animals; Atropine; Dibenz(b,f)(1,4)oxazepine-10(11H)-carboxylic acid, 8-chloro-, 2-acetylhydrazide; Dibenzoxazepines; Dinoprost; Dinoprostone; Dogs; Female; In Vitro Techniques; Indomethacin; Male; Membrane Potentials; Muscle Contraction; Muscle, Smooth; Prostaglandins E; Prostaglandins F; Radioimmunoassay; Synaptic Transmission; Tetrodotoxin; Trachea
PubMed: 6145792
DOI: 10.1113/jphysiol.1984.sp015173 -
British Journal of Pharmacology Jan 19881. Acute release of plasminogen activator (PA) was studied in rat isolated hindleg system perfused with Tyrode solution. 2. Leukotriene C4 (LTC4) and LTD4...
1. Acute release of plasminogen activator (PA) was studied in rat isolated hindleg system perfused with Tyrode solution. 2. Leukotriene C4 (LTC4) and LTD4 dose-dependently induced the release of PA, which plateaued at 160 nmol l-1 and 200 nmol l-1, respectively. The amount of PA released was about 1 iu ml-1. The effects of LTC4 and LTD4 were not additive. 3. The PA released was identified as tissue-type PA (t-PA) by quenching experiments using anti-human t-PA IgG, by fibrin autography, and by the dependence of its activity on the presence of soluble fibrin. 4. LTE4 (300 and 450 nmol l-1) and 5-hydroxy-eicosatetraenoic acid (600 nmol l-1) did not induce any t-PA release in the perfusion system used. 5. Release of t-PA induced by LTC4 and LTD4 was inhibited by the leukotriene-receptor antagonist FPL 55712 (10 mumol l-1), whereas FPL 55712 did not inhibit t-PA release induced by platelet-activating factor (Paf-acether). 6. In vivo LTC4 and LTD4 (2 micrograms kg-1 i.v.) also induced an acute increase of t-PA activity in rat blood as evidenced by decreased blood clot lysis times. 7. Prostaglandin E1 and E2, prostacyclin and the stable prostacyclin analogue ZK 36374 at concentrations of 0.1-3.0 mumol l-1 induced little or no t-PA release.
Topics: Alprostadil; Animals; Autoradiography; Chromones; Dinoprostone; Epoprostenol; In Vitro Techniques; Male; Perfusion; Prostaglandins E; Rats; SRS-A; Tissue Plasminogen Activator
PubMed: 3126847
DOI: 10.1111/j.1476-5381.1988.tb11417.x -
Journal of Biochemistry Jan 1985The effects of prostaglandins (PGs) on the induction of alkaline phosphatase (ALP) were investigated in osteoblastic clone MC3T3-E1 cells cultured in serum-free medium....
The effects of prostaglandins (PGs) on the induction of alkaline phosphatase (ALP) were investigated in osteoblastic clone MC3T3-E1 cells cultured in serum-free medium. Prostaglandin E2 (PGE2) stimulated ALP activity in the cells in a dose-dependent fashion with a maximal effect which was about twice that in the control cells at concentrations of 100-500 ng/ml. Actinomycin D and cycloheximide inhibited the stimulative effect of PGE2 on ALP activity in the cells. PGE2-induced and native ALPs in the cells were of the same type as that in adult mouse calvaria, being heat-labile, L-homoarginine- and levamisole-sensitive, and L-phenylalanine-insensitive. Isobutyl methylxanthine (IBMX), a cAMP phosphodiesterase inhibitor, stimulated the inductive effect of PGE2 on ALP activity at 0.1 mM, at which concentration IBMX alone had little effect on the activity. PGE2 also increased the intracellular cAMP content in a dose-dependent fashion with a maximal effect at 100 ng/ml. PGE1, PGF1 alpha, and PGF2 alpha (primary PGs like PGE2) increased the activity. Our present results suggest that PGs stimulate the differentiation of osteoblasts and are involved in bone formation in vivo, as well as in bone resorption.
Topics: 1-Methyl-3-isobutylxanthine; Alkaline Phosphatase; Alprostadil; Animals; Bone and Bones; Cell Line; Clone Cells; Cyclic AMP; Cycloheximide; Dactinomycin; Dinoprostone; Enzyme Induction; Mice; Osteoblasts; Prostaglandins; Prostaglandins E; Prostaglandins F
PubMed: 2581942
DOI: 10.1093/oxfordjournals.jbchem.a135072 -
The Journal of Physiology May 19781. The gastric juice outputs of acid, pepsin, PGE and PGF, and the plasma concentrations of PGE and PGF have been measured in response to I.V. infusions of pentagastrin,...
1. The gastric juice outputs of acid, pepsin, PGE and PGF, and the plasma concentrations of PGE and PGF have been measured in response to I.V. infusions of pentagastrin, histamine and insulin in the conscious cat. 2. There were significant correlations between the output of gastric acid and gastric outputs of both PGE and PGF during secretion produced by all stimulants. Furthermore, there were similar significant correlations between the gastric outputs of pepsin and both PGE and PGF. However, during insulin stimulation there was significantly more pepsin output per unit PGE or PGF output than during either pentagastrin or histamine stimulation. 3. The correlations between the outputs of gastric acid and both PGE and PGF were similar during pentagastrin and insulin stimulation whereas those between acid and PGE and PGF altered during the infusion of histamine. 4. It is concluded that these data partially, but not entirely, support the hypothesis that local release of prostaglandins may act as a negative feed-back mechanism on gastric acid secretion. 5. Plasma prostaglandin concentration did not correlate with changes in acid or pepsin secretion.
Topics: Animals; Cats; Gastric Juice; Histamine; Insulin; Pentagastrin; Pepsin A; Prostaglandins E; Prostaglandins F; Secretory Rate; Stimulation, Chemical
PubMed: 353256
DOI: 10.1113/jphysiol.1978.sp012316