Metabolite Measurement as an Index of Prostaglandin Synthesis in Vivo

1980 ◽  
pp. 123-141 ◽  
Author(s):  
A. R. Brash
Keyword(s):  
Prostaglandin Synthesis ◽  
Metabolite Measurement

Histamine tachyphylaxis in canine airways despite prostaglandin synthesis inhibition

1988 ◽  
Vol 65 (5) ◽  
pp. 1944-1949 ◽  
Author(s):  
P. J. Antol ◽  
S. J. Gunst ◽  
R. E. Hyatt
Keyword(s):  
Smooth Muscle ◽  
Dose Response ◽  
Prostaglandin Synthesis ◽  
Response Curves ◽  
Synthesis Inhibition ◽  
High Concentrations ◽  
Alpha Chloralose ◽  
Prostaglandin Synthesis Inhibitors

Tachyphylaxis to aerosolized histamine was studied in dogs anesthetized with thiamylal after pretreatment with prostaglandin synthesis inhibitors. Three consecutive histamine dose-response curves were obtained in nine dogs pretreated with 5 mg/kg indomethacin; two of these nine were also pretreated with 10 mg/kg indomethacin. Seven of the nine dogs were pretreated with 4 mg/kg sodium meclofenamate; four of these seven were also pretreated with 12 mg/kg. All dogs had tachyphylaxis at high concentrations of histamine regardless of inhibitor used. Pretreatment with indomethacin while the dogs were under alpha-chloralose-urethan anesthesia gave similar results. Histamine tachyphylaxis was also studied both in the presence and in the absence of indomethacin in tracheal smooth muscle strips obtained from seven additional dogs. A decrease in the median effective dose to histamine was observed in the indomethacin-treated strips, but tachyphylaxis to histamine remained. We conclude that prostaglandin synthesis inhibition does not reverse histamine tachyphylaxis either in vivo or in vitro. Thus the mechanism of histamine tachyphylaxis remains unexplained.

Arteriolar reactive hyperemia: modification by inhibitors of prostaglandin synthesis

1977 ◽  
Vol 232 (6) ◽  
pp. H571-H575 ◽  
Author(s):  
E. J. Messina ◽  
R. Weiner ◽  
G. Kaley
Keyword(s):  
Skeletal Muscle ◽  
Reactive Hyperemia ◽  
Prostaglandin Synthesis ◽  
Maximum Increase ◽  
Vasoactive Substances ◽  
Wistar Strain ◽  
Duration Of Response ◽  
Local Release ◽  
Hyperemic Response

Several studies implicate endogenously synthesized prostaglandins in the mediation of reactive hyperemic responses in the coronary, renal, and skeletal muscle circulations. We sought additional evidence to involve locally released prostaglandins in the mediation of reactive hyperemia in skeletal muscle at the level of the microcirculation. The cremaster muscle of pentobarbital-anesthetized Wistar-strain rats was prepared for direct in vivo observation and measurement of postocclusive responses of single arterioles. Responses of individual arterioles were reproducible over a 3-h test period. The postocclusion increase in diameter and the duration of response were dependent upon the duration of the occlusion. Repetitive occlusions did not influence arteriolar responsiveness to vasoactive substances. Indomethacin and 5-8-11-14-eicosatetraynoic acid, inhibitors of prostaglandin synthesis, did not affect resting arteriolar diameters; however, both drugs decreased the maximum increase in diameter and duration of the vasodilator response following release of the arteriolar occlusion. These findings suggest that in this microcirculatory bed, prostaglandins contribute little to resting vascular tone; in contrast, temporary arteriolar occlusion elicits the local release of dilator prostaglandins which contribute to the reactive hyperemic response.

scholarly journals The Beneficial Biological Properties of Salicylic Acid

2015 ◽  
Vol 32 (4) ◽  
pp. 259-265 ◽  
Author(s):  
Pavle Randjelović ◽  
Slavimir Veljković ◽  
Nenad Stojiljković ◽  
Dušan Sokolović ◽  
Ivan Ilić ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Well Being ◽  
Biological Properties ◽  
Vital Role ◽  
Prostaglandin Synthesis ◽  
Beneficial Effects ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Anti Inflammatory ◽  
Antiinflammatory Effects

Summary Salicylic acid is a phytochemical with beneficial effects on human well-being. Salicylic acid is a phenolic compound and is present in various plants where it has a vital role in protection against pathogenic agents. Natural sources include fruits, vegetables and spices. The most famous and defined effect of salicylic acid is prostaglandin synthesis inhibition. Salicylic acid has antiinflammatory effects through suppression of transcription of genes for cyclooxygenase. Most of the pharmacological properties of salicylic acid can be contributed to the inhibition of prostaglandin synthesis. Also, it was discovered that salicylic acid has other in vivo cyclooxygenase-independent pathways. Since salicylic acid does not inhibit cyclooxygenase considerably, the anti-inflammatory effect is not a consequence of direct inhibition of cyclooxygenase activity. Because of its fundamental role, it was suggested that inhibition of nuclear factor kappa B by salicylic acid is one of the key anti-inflammatory mechanisms of action for salicylates. One of the most studied properties of salicylic acid is its antioxidative activity. Salicylic acid is a confirmed inhibitor of oxidative stress. Salicylic acid is capable of binding iron. This fact is significant for antioxidative effect of salicylic acid because iron has an important function in the course of lipid peroxidation.

scholarly journals Effect of Aging on Prostaglandin Synthesis: In Vivo and In Vitro Studies

1987 ◽  
Vol 14 (6) ◽  
pp. 1231-1237
Author(s):  
Makito SATO ◽  
Keishi ABE ◽  
Kazuhisa TAKEUCHI ◽  
Ken OMATA ◽  
Minoru YASUJIMA ◽  
...  
Keyword(s):  
Prostaglandin Synthesis ◽  
In Vitro Studies

scholarly journals Interleukin-1beta suppresses the ventilatory hypoxic response in rats via prostaglandin-dependent pathways

2017 ◽  
Vol 95 (6) ◽  
pp. 681-685 ◽  
Author(s):  
Nina P. Aleksandrova ◽  
Galina A. Danilova ◽  
Viacheslav G. Aleksandrov
Keyword(s):  
Ventilatory Response ◽  
Prostaglandin Synthesis ◽  
Respiratory Neurons ◽  
Hypoxic Ventilatory Response ◽  
Hypoxic Response ◽  
Interleukin 1Beta ◽  
Spontaneously Breathing ◽  
The Brain ◽  
Ventilatory Response To Hypoxia

We investigated the effect of the major inflammatory cytokine interleukin-1beta (IL-1β) on the ventilatory response to hypoxia. The goal was to test the hypothesis that IL-1β impairs the hypoxic ventilatory response in vivo by indirectly inhibiting respiratory neurons in the brainstem via prostaglandins. Thus, IL-1β was delivered by cerebroventricular injection, and the ventilatory hypoxic response was assessed in anesthetized, spontaneously breathing rats pretreated with or without diclofenac, a nonspecific inhibitor of prostaglandin synthesis. We found that the slope of the ventilatory response to hypoxia decreased almost 2-fold from 10.4 ± 3.02 to 4.06 ± 0.86 mL·min−1·(mm Hg)−1 (–61%) 90 min after administration of IL-1β (p < 0.05). The slope of tidal volume and mean inspiratory flow also decreased from 0.074 ± 0.02 to 0.039 ± 0.01 mL·(mm Hg)−1 (–45%, p < 0.05), and from 0.36 ± 0.07 to 0.2 ± 0.04 mL·s−1·(mm Hg)−1 (–46%, p < 0.05), respectively. Pretreatment with diclofenac blocked these effects. Thus, the data indicate that IL-1β degrades the ventilatory hypoxic response by stimulating production of prostaglandin. The increase of cerebral levels of IL-1β, which is induced by the activation of immune cells in the brain, may impair respiratory chemoreflexes.

Renal excretion of prostaglandins E2 and F2alpha in diabetes insipidus rats.

1978 ◽  
Vol 235 (6) ◽  
pp. E624
Author(s):  
M J Dunn ◽  
H P Greely ◽  
H Valtin ◽  
L B Kintner ◽  
R Beeuwkes
Keyword(s):  
Prostaglandin E2 ◽  
Diabetes Insipidus ◽  
Negative Feedback ◽  
Renal Excretion ◽  
Renal Tubule ◽  
Substantial Reduction ◽  
Feedback System ◽  
Prostaglandin Synthesis ◽  
Prostaglandin F2alpha

On the assumption that the antagonism between prostaglandin E2 and vasopressin might represent a negative feedback system, we evaluated the hypothesis that vasopressin stimulates, in vivo, the renal production of prostaglandins. For these studies we used Brattleboro homozygous rats with diabetes insipidus and Long-Evans rats for controls, Brattleboro homozygotes show a substantial reduction in the renal excretion of prostaglandin E2 and prostaglandin F2alpha. Homozygotes excreted 39 +/- 5 ng/24 h prostaglandin E2 and 40 +/- 4 ng/24 h prostaglandin F2alpha, compared to 217 +/- 40 and 221 +/- 18 ng/24 h, respectively, in control rats (P less than 0.001). Therapy of homozygotes with vasopressin tannate in oil resulted in a prompt increase in the urinary excretion of prostaglandin E2 and prostaglandin F2alpha. 1-Desamino-D-arginine vasopressin, a nonpressor analogue of vasopressin, also enhanced the renal production of prostaglandin E2. We conclude that vasopressin (antidiuretic hormone) stimulates renal production and excretion of prostaglandin E2 and prostaglandin F2alpha in vivo. It is possible that this increment of prostaglandin synthesis serves a negative feedback function by modulating the action of vasopressin on the renal tubule.

Potentiation of Pressor Effects of Noradrenaline and Potassium Ions in the Rat Mesenteric Arteries by Physiological Concentrations of Angiotensin II: Effects of Prostaglandin E2 and Cortisol

1977 ◽  
Vol 53 (3) ◽  
pp. 233-239 ◽  
Author(s):  
K. Kondo ◽  
M. S. Manku ◽  
D. F. Horrobin ◽  
R. Boucher ◽  
J. Genest
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Potassium Chloride ◽  
Prostaglandin Synthesis ◽  
Mesenteric Arteries ◽  
Potassium Ions ◽  
Vascular Bed ◽  
Vasoconstrictor Response ◽  
Mesenteric Vascular Bed

1. In the perfused rat mesenteric vascular bed, the effects of angiotensin II, cortisol and prostaglandin E2 on the vascular responses to noradrenaline or potassium chloride were studied. 2. Angiotensin II in subpressor concentrations potentiated the vasoconstrictor response to noradrenaline and potassium chloride. This effect of angiotensin II was inhibited in the presence of indomethacin and prostaglandin E2. 3. Cortisol in physiological concentrations inhibited the potentiating effect of angiotensin II. 4. Prostaglandin E2 enhanced the vasoconstrictor response to noradrenaline. This effect was not abolished by cortisol. 5. These results suggest that some actions of angiotensin II and cortisol in vivo are mediated by the regulation of prostaglandin synthesis or release.

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