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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin E biosynthesis and its effect on water permeability were investigated in the toad urinary bladder. Arginine vasopressin (1 mU/ml) increased prostaglandin E (PGE) biosynthesis from 0.5+/-0.1 to 5.0+/-0.4 pmol/min per hemibladder (mean +/-SEM, n= 8, P less than 0.001). Maximal vasopressin-stimulated PGE biosynthesis, 6.4+/-0.2 pmol/min per hemibladder, occurred at vasopressin concentrations in excess of 3 mU/ml. Half-maximal stimulation of PGE biosynthesis occurred at a vasopressin concentration of approximately 0.7 mU/ml, whereas half-maximal stimulation of water flow occurred at a vasopressin concentration of approximately 5 mU/ml. Vasopressin-stimulated PGE biosynthesis did not depend on water flow along an osmotic gradient or upon sodium transport. Thin-layer chromatographic analysis of the lipids released from hemibladders labeled with tritium-arachidonic acid revealed that vasopressin stimulates the release of arachidonic acid from intracellular lipid stores without affecting the percentage of free arachidonic acid converted to PGE. Neither cyclic AMP nor theophylline stimulated PGE biosynthesis although they mimic arginine vasopressin (AVP) in stimulating water permeability. Biosynthesis of PGE was inhibited by mepacrine, a phospholipase inhibitor, and by agents that inhibit arachidonic acid oxygenase. The inhibition of PGE biosynthesis resulted in augmented vasopressin- and theophylline-stimulated water flow, but had no effect on cyclic AMP-stimulated water flow. We interpret these results to mean that endogenous PGE inhibits basal and vasopressin-stimulated adenylate cyclase activity. In contrast to the effects of AVP on permeability and transport, AVP stimulates PGE biosynthesis by a mechanism that does not depend on an increase in cellular cyclic AMP levels. The water permeability response of the toad urinary bladder to vasopressin is inhibited by PGE synthesized by the bladder in response to vasopressin.
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PMID:Vasopressin-stimulated prostaglandin E biosynthesis in the toad urinary bladder. Effect of water flow. 19 20

Prostaglandin E (PGE) release from the anterior calf muscles of anesthetized dogs was measured during and following exercise. Blood flow was held constant at 15.5 +/- 1.6 (SEM) ml.min-1. 100 g-1 and the muscles were stimulated for 20 min at a frequency of 4 Hz. PGE release dropped from a resting level of 11.4 +/- 3.8 ng.min-1.100 g-1 to 6.5 +/- 2.0 ng.min-1.100 g-1 during exercise (P less than 0.05). Following exercise, PGE release slowly returned to and eventually exceeded the resting level over a 60-min period. Return of vascular resistance to control was even more prolonged. Indomethacin (5 mg/kg) caused 1) an increase in resting resistance (40%), 2) a drop in PGE release (48% at rest), and 3) a more rapid return of vascular resistance to control following exercise. PGE release does not appear to contribute to the vasodilation during exercise, but can account for the portion of vascular resistance recovery not blocked by indomethacin. The remaining prolonged vasodilation could be explained by another as yet unidentified vasodilator(s). This preparation exhibits tonic prostaglandin release that causes a vasodilation at rest.
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PMID:Prostaglandin E release from dog skeletal muscle during restricted flow exercise. 43 26

Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age- and sex-matched controls (p less than 0.02). PGF 2 alpha--excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p less than 0.001), while the increase in PGF 2 alpha-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167% +/- 11, SEM) than in the normotensive (386% +/- 46) group (p less than 0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
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PMID:[Reduced urinary prostaglandin E2-excretion and diminished responsiveness of plasma renin activity in patients with essential hypertension (author's transl)]. 45 71

We have previously shown that the prostaglandin analogue 15(R)15 methyl-prostaglandin E2 methyl ester (Me-PGE2) when administered at a dose of 50 microgram per kg significantly inhibits aspirin-induced gastric mucosal erosions in the rat. In this study we have investigated the effect of cimetidine under similar circumstances. Cimetidine in a dose of 50 mg per kg significantly inhibited gastric mucosal erosions induced by aspirin (192 mg per kg) in the rat, reducing the incidence from 70% of 20 rats to 9.5% of 21 rats, the mean lesion score was reduced from 9.3 +/- 2.1 (mean +/- SEM) to 0.4 +/- 0.3. We then compared the effect of the above doses of Me-PGE2 and cimetidine on gastric erosions induced by aspirin (192 mg per kg) with the hourly addition of 160 mM HCl. The incidence of erosions in the aspirin + HCl group was 100% of 20 rats (mean lesion score 27.4 +/- 2.4). This was not significantly reduced by cimetidine, the incidence being 90% of 20 rats (mean lesion score 19.7 +/- 3.4). The incidence of erosions in the presence of Me-PGE2 was significantly less than that in both the other groups, 13% of 23 rats, (mean lesion score 3.1 +/- 0.8) P less than 0.01 in both instances. These results suggest that, whereas cimetidine protects the gastric mucosa through acid inhibition, Me-PGE2 appears to have a protective effect independent of acid inhibition.
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PMID:Cimetidine and prostaglandin: evidence for different modes of action on the rat gastric mucosa. 64 13

Urinary excretion of prostaglandin E was measured in seven sick low-birth-weight infants. Four had severe hyaline membrane disease and one had chronic bronchopulmonary dysplasia; all received furosemide. Two infants had patent ductus arteriosus and received indomethacin. Following administration of furosemide, urine volume and the excretion rates of sodium and calcium were significantly increased; such changes were not seen following the administration of indomethacin. Prostaglandin E excretion rate was increased from 0.4 +/- 0.04 to 1.3 +/- 0.2 ng/mg Cr (mean +/- SEM) following administration of furosemide, but decreased in two patients following administration of indomethacin. The present results demonstrate that furosemide enhances urinary excretion of prostaglandin E by mechanisms which may reflect an increase in prostaglandin synthesis, a decrease in prostaglandin renal metabolism, or both. Indomethacin, which is a prostaglandin synthetase inhibitor, decreases the urinary excretion of prostaglandin E. These observations suggest that furosemide therapy in patients receiving indomethacin may be ineffective.
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PMID:Urinary excretion of prostaglandin E following the administration of furosemide and indomethacin to sick low-birth-weight infants. 69 Jul 80

Experiments were performed to evaluate the role of prostaglandin synthesis in the regulation of coronary blood flow in dog hearts. The left main coronary artery was cannulated and flow measured both in otherwise intact animals and in canine heart-lung preparations. Prostaglandin E was measured by radioimmunoassay. Reactive hyperemia (flow after occlusion release) was induced by coronary occlusion for 10, 15, and 20 s and was 39 plus or minus 13 (mean plus or minus SEM), 66 plus or minus 21, and 82 plus or minus 24 ml, respectively. Indomethacin, an inhibitor of prostaglandin synthetase, reduced reactive hyperemia at 10, 15, and 20 s to 15 plus or minus 5, 33 plus or minus 11, and 47 plus or minus 17 ml, respectively (P smaller than 0.05). Meclofenamate, a different prostaglandin synthetase inhibitor, gave similar results. In a second group of five dogs, prostaglandin production of the heart was examined in response to 20-s occlusions. There was a significant increase in prostaglandin production from a basal level of 18.6 plus or minus 4.9 mg/min to 35.3 plus or minus 5.8 ng/min after occlusion of the coronary artery for 20 s (P smaller than 0.05). After indomethacin, this increase in prostaglandin production was not observed and reactive hyperemia was significantly reduced. Thus, prostaglandin synthesis appears to be important to modulating canine coronary blood flow in response to brief periods of coronary occlusion.
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PMID:Regulation of postocclusive hyperemia by endogenously synthesized prostaglandins in the dog heart. 80 95

Cytoprotective effects of the prostaglandins 16,16-dimethyl PGE2 (dmPGE2) and PGF2 alpha tromethamine (PGF2 alpha) were evaluated in the rat model of acute hepatocellular necrosis induced by thioacetamide (TAA). dmPGE2 (100 micrograms/kg SC 8 hourly) did not induce a significant increase in survival when started after the onset of TAA-induced fulminant hepatic failure. However, priming with dmPGE2 (100 micrograms/kg SC 30 min before TAA) reduced TAA-induced elevations in serum ALT (684 +/- 68 (SEM) vs 274 +/- 135 IU/1, p less than 0.01). This phenomenon did not occur if dmPGE2 was administered after TAA or by the IP route. Modulation of TAA-induced centrizonal hepatocellular necrosis by dmPGE2 was associated with a striking increase in centrizonal ballooning of hepatocytes (p less than 0.01), and, as assessed by stereology, less hepatocellular necrosis and degenerative changes. PGF2 alpha, which in contrast to dmPGE2 does not act via cAMP, had no effect on TAA-induced changes in serum ALT or hepatic histology. These findings suggest that dmPGE2 decreases hepatocellular necrosis by activating surface membrane adenylate cyclase and consequently stimulating cAMP. Ballooning of hepatocytes could occur secondary to these membrane events and appears to be a marker of dmPGE2-induced cytoprotection in this model.
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PMID:Modulation of thioacetamide-induced hepatocellular necrosis by prostaglandins is associated with novel histologic changes. 140 79

Devil's Claw (Harpagophytum procumbens), an herbal product being marketed in Canada and in Europe as a home remedy for the relief of arthritic disease, was investigated in healthy humans on eicosanoid production during spontaneously blood clotting. Volunteers took H. procumbens (daily 4 capsules of 500 mg powder containing 3% of total glucoiridoids) for a period of 21 days. The following are the results (mean (SEM)): before H. procumbens intake, prostaglandin (PG)E2 (ng/ml serum): 2.1 (0.4) (n = 25), thromboxane (TX)B2: 147 (27) (n = 25), 6-keto-PGF1 alpha: 4.4 (0.7) (n = 13), leukotriene (LT)B4: 3.4 (0.4) (n = 25); after intake: PGE2: 3.2 (0.6), TXB2: 143 (24), 6-keto-PGF1 alpha: 4.2 (0.9), LTB4: 3.8 (0.6). Each subject serving as her own control, no statistically significant differences were observed between before and after H. procumbens intake. These results indicate that Devil's Claw lacks, at least in healthy humans and under the selected conditions, the biochemical effects on arachidonic acid metabolism of antiarthritic drugs of the non-steroidal antiinflammatory type.
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PMID:A drug used in traditional medicine, harpagophytum procumbens: no evidence for NSAID-like effect on whole blood eicosanoid production in human. 140 65

We evaluated the inhibitory effect of S-1452, a specific thromboxane (Tx) A2 receptor antagonist on the increase of airway responsiveness in 7 dogs after ozone exposure. Airway responsiveness to inhaled methacholine (Mch) was determined by Astograph (7 Hz oscillation technique), and at the same time TxB2, 6-keto-prostaglandin (PG) F1 alpha, PGE2 levels and total cell counts in the bronchoalveolar lavage fluid (BALF) were measured. Ozone exposure was carried out for 2 hr at an ozone level of 3.04 +/- 0.02 ppm (mean +/- SEM). Airway responsiveness to Mch increased significantly after ozone exposure (p less than 0.01), and this hyperresponsiveness was inhibited significantly by pretreatment with S-1452 (p less than 0.02). TxB2 and PGE2 levels in BALF did not change after ozone exposure, but the levels of 6-keto-PGF1 alpha decreased significantly after ozone exposure (p less than 0.05). Total cell counts in BALF increased significantly after ozone exposure (p less than 0.02). The decrease of 6-keto-PGF1 alpha levels and the increase of total cell counts were not affected by pretreatment with S-1452. These results suggest that S-1452 is protective against the increase of airway responsiveness induced by ozone exposure, and that TxA2 plays an important role in the hyperresponsiveness. But hyperresponsiveness may not be induced by hyperproduction of TxA2, but by the relative increase of TxA2 to PGI2.
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PMID:[Inhibitory effect of S-1452, a specific thromboxane A2 receptor antagonist on the increase of airway responsiveness in dogs after ozone exposure]. 153 11

The levels of prostaglandin (PG) E2 and 6-keto-PGF1 alpha (stable metabolite of prostacyclin) in plasma and gastric juice were determined in 113 critically ill children and adolescent, and compared to those registered in a plasma control group of 24 children and a gastric juice control group of 15. The gastric juice concentration of PGE2 is our patients [9.2 +/- 3.1 (SEM) pg/ml] was significantly lower (p = 0.001) than in the control group [81.1 +/- 18.1 (SEM) pg/ml]. There were no differences in plasma levels of PGE2 and plasma gastric juice levels of 6-keto-PGF1 alpha between the patients and the control groups. Children who died had lower plasma levels of PGE2 [6.2 +/- 2.2 (SEM) pg/ml] and gastric juice levels of PGE2 [2.3 +/- 0.8 (SEM) pg/ml] than the survivors (p less than 0.05). The gastric juice concentration of PGE2 was also lower in children who suffered important upper gastrointestinal bleeding, although the difference did not reach statistical significance.
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PMID:Plasma and gastric juice levels of prostaglandins in critically ill children. 161 33


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