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1.
The plasma concentration of 6-keto-PGF1 alpha, the stable degradation product of prostacyclin, was similar in the radial and pulmonary arteries and in the coronary sinus before and after the induction of the anesthesia in patients undergoing coronary artery bypass surgery. After the beginning of the mechanical ventilation and anesthesia the pulmonary vascular resistance decreased although no changes were detected in the plasma levels of 6-keto-PGF1 alpha or TXB2. During the prebypass period after the sternotomy and cannulation of the large vessels the plasma level of 6-keto-PGF1 alpha was increased similarly in the radial and pulmonary arteries and even more in the coronary sinus. During the cardiopulmonary bypass the concentration of 6-keto-PGF1 alpha remained at the increased level as compared to the values before the anesthesia. This indicates that pulmonary circulation is perhaps not the main source of prostacyclin in man. The plasma level of TXB2 was increased during the prebypass period significantly only in the coronary sinus, but during the bypass also in the radial artery. The concentration ratio of 6-keto-PGF1 alpha/TXB2 was increased significantly during the prebypass period in the radial and pulmonary arteries. At the same time the pulmonary vascular resistance was, however, returned to the preanesthesia level and was thus not decreased. The vascular resistance in the systemic circulation was increased during the prebypass period. The plasma level of 6-keto-PGF1 alpha or TXB2 in the radial and pulmonary arteries did not correlate significantly with the total vascular resistance in the systemic and pulmonary circulation, respectively. The vascular resistance in the coronary circulation did not correlate significantly with TXB2 level in the radial artery or coronary sinus. There was, however, a slight positive correlation between the blood flow and the concentration of TXB2 in the coronary sinus (r = 0.76, P less than 0.01). Coronary sinus flow did, however, not correlate with the plasma level of 6-keto-PGF1 alpha in the radial artery or coronary sinus. These results indicate that the detected plasma concentrations of prostacyclin and thromboxane A2 have no significant effects on the total vascular resistance in vivo. 相似文献
2.
We studied the effects of two structurally unrelated inhibitors of the fatty acid cyclooxygenase and of alpha and beta adrenergic blockade on the elevated plasma levels of 13,14-dihydro-15-keto-prostaglandin (PG)E2, 6-keto-PGF1α and thromboxane(TX)B2, the stable derivatives of PGE2, PGI2 (prostacyclin) and TXA2, respectively, in rats with streptozotocin-induced diabetic ketoacidosis (DKA). Meclofenamic acid and indomethacin each produced a significant decrease in the elevated plasma levels of 13,14-dihydro-15-keto-PGE2, 6-keto-PGF1α and TXB2. Phentolamine significantly reduced the plasma level of TXB2 but had no effect on the elevated circulating levels of glucose, free fatty acids, total ketones, 13,14,-dihydro-15-keto-PGE2 or 6-keto-PGF1α. Propranolol significantly reduced the elevated circulating levels of glucose, free fatty acids and total ketones but had no effect on the levels of the three prostaglandin derivatives. The ability of meclofenamic acid and indomethacin to reduce the plasma levels of 13,14-dihydro-15-keto-PGE2, 6-keto-PGF1α and TXB2 confirms that the plasma levels of these three derivatives are elevated in rats with DKA. Since abnormalities in the production of PGI2 and perhaps other cyclooxygenase derivatives may contribute to the pathogenesis of certain important hemodynamic and gastrointestinal features of DKA, cyclooxygenase inhibitors may play a role in the management of selected patients with this disorder. Alpha adrenergic activity is essential for the maintenance of the elevated plasma TXB2 level in rats with DKA. The fall in the plasma TXB2 level during alpha adrenergic blockade appears to reflect inhibition of platelet aggregation and platelet TXA2 production, but other sources of the elevated plasma TXB2 level in DKA are not excluded. Beta adrenergic activity contributes to the maintenance of elevated circulating levels of glucose, free fatty acids and total ketones in experimental DKA but not to the elevated plasma levels of the prostaglandin derivatives. 相似文献
3.
A. Jawerbaum A.M. Franchi E.T. Gonzalez V. Novaro M.A.F. de Gimeno 《Prostaglandins & other lipid mediators》1995,50(1)
The relationship between high glucose concentrations and arachidonic acid metabolism in uterine tissue from control and diabetic ovariectomized rats was evaluated. Uterine tissue from diabetic rats produced amounts of PGE2 and PGF2α similar to controls, while a lower production of 6-keto-PGF1α (indicating the production of prostacyclin) and a higher production of TXB2 (indicating the generation of TXA2) was found in the diabetic group. A group of diabetic rats was treated with phlorizin to diminish plasma glucose levels. Phlorizin treatment did not alter production of PGE2, PGF2α, and 6-keto-PGF1α in the diabetic group. A diminished production of TXB2 was found in the treated diabetic uteri when compared to the non-treated diabetic group. Moreover, a positive correlation between plasma glucose levels and uterine TXB2 generation was observed. When control uterine tissue was exposed in vitro to high concentrations of glucose (22 mM) and compared to control tissue incubated in the presence of glucose 11 mM alterations in the generation of PGE2, PGF2α, and 6-keto-PGF1α were not found, but a higher production of TXB2 was observed and values were similar to those obtained in the diabetic tissue. Alteration in the production of the prostanoids evaluated were not observed when diabetic tissue was incubated in the presence of high concentrations of glucose. These results provide evidence of a direct relationship between plasma glucose levels and uterine production of TXA2. 相似文献
4.
Anders
lund Hans Kindahl Ernst Oliw ke Lindgren Jan Bertil Larsson 《Prostaglandins & other lipid mediators》1980,19(5):791-803
Abortion or delivery were induced by extra-amniotic instillation of Rivanol during the second trimester in twelve patients and during the third trimester in two patients with fetal death and one patient with fetal acrania. Serial sampling of amniotic fluid was performed through a transabdominal catheter and the levels of free arachidonic acid (AA), prostaglandin F2α (PGF2α), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1α (6-keto-PGF1α) and thromboxane B2 (TXB2) were determined. The levels of AA, PGF2α, PGE2, 6-keto-PGF1α and TXB2 in amniotic fluid increased significantly during induction with the exception of AA in fetal death which was high and remained constant during induction. Furthermore, PGF2α, 6-keto-PGF1α and TXB2 were all significantly correlated to AA.These observations suggested that free AA is released during Rivanol-induction of abortion and labour giving an increased synthesis of PGF2α, PGE2 prostacyclin and thromboxane A2 in the fetal membranes and the decidua but not in the fetus. This increase might be relevant for the initiation and progress of abortion and labour in these patients. 相似文献
5.
Bovine gastric mucosal and muscle microsomes synthesize prostaglandins and thromboxane B2 (TXB2) from arachidonic acid (AA). TXB2 and 6-keto-prostaglandin F1α (6-keto-PGF1α) were the major products synthesized by pylorus, body, and cardiac region of the gastric mucosa. Gastric muscle mainly synthesized 6-keto-PGF1α. TXB2 and 6-keto-PGF1α synthesis occurs at an appreciable rate from endogenous precursors but more rapidly with added arachidonate. Prostaglandins E2, F2α and D2 were synthesized in smaller amounts under the conditions studied. 相似文献
6.
A. Edlund W. Bomfim L. kaijser C. Olin C. Patrono E. Pinca . Wennmalm 《Prostaglandins & other lipid mediators》1981,22(2):323-332
The pulmonary formation of prostacyclin (PGI2), as reflected by the difference in concentration of pulmonary and systematic arterial radioimmunoassayed 6-keto-PGF1α, was determined in six healthy waking subjects. The systematic arterial 6-keto-PGF1α levels were low (50 pg/ml), and no evidence of pulmonary formation and release of the compound was noted. In other experiments systemic arterial 6-keto-PGF1α levels were determined in patients prior to and during artificial ventilation, as well as during and after occlusion of the pulmonary circulation (extra-corporeal circulation, ECC). The arterial 6-keto-PGF1α concentration prior to artificial ventillation was 17±4 pg/ml, i.e. within the range observed in the healthy subjects. During artificial ventilation the arterial levels of 6-keto-PGF1α increased to 191±21 pg/ml, suggesting that pulmonary formation of PGI2 was stimulated. In the patients subjected to ECC with occluded pulmonary circulation the arterial content of 6-keto-PGF1α was stabilised at an elevated level (120−170 pg/ml). Following re-establishment of the pulmonary circulation the arterial concentrations of 6-keto-PGF1α increased markedly, to 284±50 pg/ml. It is suggested that the basal pulmonary formation of PGI2 in man is low or non-existent, and that enhanced formation of the compound in the lungs is a consequence of intervention with normal pulmonary ventilation or perfusion. 相似文献
7.
Paulette Mehta Jawahar Mehta Fulton Crews Louis Roy Nancy Ostrowski Christine Horalek 《Prostaglandins & other lipid mediators》1982,24(6):743-749
There is growing evidence that blood vessels generate TXA2 in addition to PGI2. We examined effluents from continously perfused human umbilical vein and supernatants from umbilical vein rings for TXB2 and 6-keto-PGF1α measurements (stable metabolites of TXA2 and PGI2, respectively). TXB2 and 6-keto-PGF1α were identified in all samples. 6-keto-PGF1α to TXB2 ratio was higher in intact vein effluents than in the venous ring supernatants (112:1 and 28:1, respectively, P<0.01). Arachidonate stimulation increased 6-keto-PGF1α and TXB2 levels similarly in the intact vein effluent. In contrast, stimulation of the venous rings resulted in a relatively larger increase in TXB2 than in 6-keto-PGF1α. This caused 6-keto-PGF1α to TXB2 ratio to decline (p<0.01). The identity of TXB2 was confirmed in several different ways. These data suggest that 1) human umbilical veins produce TXA2 in addition to PGI2, 2) TXA2 release is more by venous rings than by the intact vein probably reflecting contribution from non-endothelial layers, and 3) arachidonate stimulation causes relatively greater release of TXA2 than of PGI2 from the venous rings, whereas release of PGI2 and TXA2 is similar from the intact vein. 相似文献
8.
R.D. Nolan G.J. Dusting J. Jakubowski T.J. Martin 《Prostaglandins & other lipid mediators》1982,24(6):887-902
Cyclo-oxygenase products of arachidonic acid metabolism formed by the pericardium and epicardial surface of dog heart were identified and quantitated by radioimmunoassay after separation by high-pressure liquid chromatography. Pieces of pariental pericardium, of dog, ox and rat, when incubated
produced mainly 6-keto-PGF1α, with lesser amounts of PGE2, PGF2α and thromboxane B2. Biosynthesis of all prostanoids increased during incubation of the pariental pericardium of each species with arachidonic acid, but 6-keto-PGF1α was still the major metabolite. When slices of dog heart were incubated with arachidonic acid (1 μg/ml) the rates of 6-keto-PGF1α formation by the pariental pericardium was much greater than that of the myocardium and endocardium. Epicardial slices appeared to be intermediate in 6-keto-PGF1α formation. The hearts of anesthetized dogs were also irrigated
with Krebs' solution, and during the first 5 min of epicardial irrigation the pericardial fluid leaving the heart again contained high levels of 6-keto-PGF1α, with lesser amounts of the other prostanoids. Addition of arachidonic acid (3 μg/ml) to the irrigating fluid caused an increase in all measured prostanoid levels, although 6-keto-PGF1α remained the predominant metabolite. In contrast, intravenous infusion of isoproterenol selectively increased the release of 6-keto-PGF1α from the irrigated heart. It is concluded that the pericardium and epicardium continuously release prostacyclin into the pericardial fluid, and that the increased release of this substance observed when cardiac workload increases derives mainly from these membranous sources. This raises the interesting possibility that pericardial prostacyclin might influence coronary vascular tone and chemoreflexes which arise from the epicardium during myocardial ischemia. 相似文献
9.
Effects of 10 ppm nitrogen dioxide (NO2) exposure on the contents of prostaglandins (PGs) and thromboxane (TX) B2 in broncho-alveolar lavage (BAL) of rats were studied. In the BAL of normal rats, the amounts of PGs and TXB2 in the whole lavage were 6-keto-PGF1α (38.0 ± 6.4 ng) > TXB2 (11.8 ± 4.0 ng) > PGF2α (5.7 ± 1.6 ng) PGE (0.5 ± 0.3 ng). Rats were exposed to NO2 for 1, 3, 5, 7 and 14 days. The NO2 exposure decreased in the level of 6-keto-PGF1α by about 35% throughout the exposure. The level of TXB2 was higher in the day 5 exposure group (155%). The contents of PGF2α and PGE first, decreased and then transiently increased on days 3 and 5. PG 15-hydroxy-dehydrogenase activity of lung homogenate decreased correspondingly on day 3 and 5. Then the contents PGF2α and PGE decreased on day 7 and 14.6-keto-PGF1α and TXB2 are stable metabolites of PGI2, a strong bronchorelaxant and TXA2, a strong bronchoconstrictor respectively. Therefore the results suggested that the decrease in 6-keto-PGF1α, a major prostanoid in the BAL and the increase in TXB2 may correlate with broncho constriction by NO2 exposure. 相似文献
10.
Kristian Bjro Torstein Hovig Kjell Torgeir Stokke Sverre Stray-Pedersen 《Prostaglandins & other lipid mediators》1986,31(4)
Four major prostanoids (6-keto-PGF1α, PGE2, PGF2α and TXB2) were measured by specific radioimmunoassays in the outputs from human umbilical vessels perfussed
. As evaluated by scanning electron microscopy (SEM) only few blood platelets were attached to the vessel wall. After an initial flush with decreasing concentrations of all four prostanoids, a stable stage was reached, lasting for 4–5 hours. During this stage the production could be inhibited by indomethacin and only slightly stimulated with arachidonic acid. The TXA2 synthetase inhibitor UK 38485 depressed the TXB2 production, while only slightly affecting the other three prostanoids at very high concentrations. The arteries produced relatively more 6-keto-PGF1α than did the vein. 相似文献
11.
Danshensu, a type of dihydroxyphenyl lactic acid, is one of the most abundant active phenolic acids in the dried root of Salvia miltiorrhizae (Lamiaceae)—widely used traditional Chinese medicine. The effects of danshensu on platelet aggregation and thrombus formation in rats were examined using various methods. It was found that danshensu significantly reduced thrombus weight in 2 experimental thrombosis models; dose-dependent inhibition of adenosine diphosphate (ADP) and arachidonic acid (AA)-induced platelet aggregation occurred in normal and blood stasis-induced rats; Danshensu also significantly mitigated blood viscosity, plasma viscosity and hematocrit levels. Moreover, danshensu significantly inhibited venous thrombosis-induced expression of cyclooxygenases-2 (COX-2) rather than cyclooxygenases-1(COX-1) in the venous walls, down regulated thromboxane B2 (TXB2) and up regulated 6-keto prostaglandin F1α (6-keto-PGF1α), normalizing the TXB2/6-keto-PGF1α ratio. In addition, danshensu did not induce gastric lesions and even had protective effects on aspirin-induced ulcer formation at doses as high as 60 mg/kg. These findings suggest that the antithrombotic and antiplatelet aggregation effects of danshensu are attributed to its highly selective inhibition of COX-2 and ability to normalize the thromboxane A2(TXA2)/prostacyclin(PGI2) balance. These findings suggest that danshensu have great prospects in antithrombotic and antiplatelet therapy. 相似文献
12.
Claudia Weber Michael Hller Johan Beetens Fred De Clerck Frank Tegtmeier 《Journal of chromatography. B, Analytical technologies in the biomedical and life sciences》1991,562(1-2)
A method for quantification of 6-keto-PGF1α, 2,3-dinor-6-keto-PGF1α, TXB2, 2,3-dinor TXB2, PGE2, PGD2 and PGF2α in human urine samples, using gas chromatography—negative ion chemical ionization mass spectrometry, is described. Deuterated analogues were used as internal standards. Methoximation was carried out in urine samples which were subsequently applied to phenylboronic acid cartridges, reversed-phase cartridges and thin-layer chromatography. The eluents were further derivatized to pentafluorobenzyl ester trimethylsilyl ethers for final quantification by gas chromatography—mass spectrometry. The overall recovery was 77% for tritiated 6-keto-PGF1α and 55% for tritiated TXB2. Urinary levels of prostanoids were determined in a group of six volunteers before and after intake of the thromboxane synthase inhibitor Ridogrel, and related to creatinine clearance. 相似文献
13.
W.David Watkins Peter C. Hüttemeier D. Kong Myron B. Peterson 《Prostaglandins & other lipid mediators》1982,23(3):273-285
We assessed the effect of a specific thromboxane synthetase inhibitor (an imidazole derivative) on pulmonary hemodynamics and the concentrations of TxB2 (TxA2), 6-keto-PGF1α (PGI2), and PGF2α in pulmonary lymph and transpulmonary blood samples following intravenous administration of E. coli endotoxin (1 μg/kg) in sheep. In control animals the rise in pulmonary artery pressure correlated with increases in plasma and lymph TxB2 concentrations and large transpulmonary concentration gradients of this metabolite were measured. In imidazle treated animals both pulmonary hypertension as well as increases in plasma and lymph TxB2 concentrations were substantially reduced. In contrast, peak concentrations of 6-keto-PGF1α (PGI2) and PGF2α were severalfold higher than those measured in control animals. This suggests a shunting of endoperoxide metabolism towards prostacyclin and primary prostaglandins and documents the specificity of the thromboxane synthetase inhibitor. Out study provides evidence that endotoxin-induced pulmonary hypertension is mediated by pulmonary synthesis of TxA2. 相似文献
14.
T. Yamaguchi R.F. O'Brien W.L. Hanson W.W. Wagner Jr. I.F. McMurtry 《Prostaglandins & other lipid mediators》1989,38(1)
The mechanism by which extracellular alkalosis inhibits hypoxic pulmonary vasoconstriction is unknown. We investigated whether the inhibition was due to intrapulmonary production of a vasodilator prostaglandin such as prostacyclin (PGI2). Hypoxic vasoconstriction in isolated salt-solution-perfused rat lungs was blunted by both hypocapnic and NaHCO3_induced alkalosis (perfusate pH increased from 7.3 to 7.7). The NaHCO3-induced alkalosis was accompanied by a significant increase in the perfusate level of 6-keto-prostaglandin F1α (6-keto-PGF1α), an hydrolysis product of PGI1. Meclofenamate, an inhibitor of cyclooxygenase, counteracted both the blunting of hypoxic vasoconstriction and the increased level of 6-keto-PGF1α. In intact anesthetized dogs, hypocapnic alkalosis (blood pH increased from 7.4 to 7.5) blunted hypoxic pulmonary vasoconstriction before but not after administration of meclofenamate. In separate cultures of bovine pulmonary artery endothelial and smooth muscle cells stimulated by bradykinin, the incubation medium levels of 6-keto-PGF1α were increased by both hypocapnia and NaHCO3-induced alkalosis (medium pH increased from 7.4 to 7.7). These results suggest that inhibition of hypoxic pulmonary vasoconstriction by alkalosis is mediated at least partly by PGI2. 相似文献
15.
Stuart I. Myers R. H. Turnage L. Bartula B. Kalley Y. Meng 《Prostaglandins, leukotrienes, and essential fatty acids》1996,54(6):403-409
Estrogen has been proposed as a negative risk factor for development of peripheral vascular disease yet mechanisms of this protection are not known. This study examines the hypothesis that estrogen stimulates rat aortic endothelial cell (RAEC) release of PGI2. Male Sprague-Dawley rat abdominal aortic 1-mm rings were placed on 35 mm matrigel plates, and incubated for 1 week. The cells were transferred to a Primaria 60-mm dish and maintained from passage 3 in RAEC complete media and experiments performed between passages 4–10. Cells were incubated with Krebs-Henseleit buffer (pH 7.4) containing carrier or increasing concentrations of β-estradiol or testosterone for 60 min. The effluent was analyzed for eicosanoid release of 6-keto-PGF1α (6-keto, PGI2 metabolite), PGE2 and thromboxane B2 (TXB2) by EIA (hormone stimulated — basal). Cells were analyzed for total protein by the Bradford method and for cyclooxygenase-1 (COX-1) and prostacyclin synthase (PS) content by Western blot analysis and densitometry. Testosterone did not alter RAEC 6-keto-PGF1α release, whereas estrogen increased RAEC 6-keto-PGF1α release in a dose-related manner. Estrogen preincubation (10 ng/ml) decreased COX-1 and PS content by 40% suggesting that the estrogen-induced increase in male RAEC PGI2 release was not due to increased synthesis of COX-1 or PS. These data support the hypothesis that estrogen stimulation can increase endogenous male RAEC release of PGI2. 相似文献
16.
Denis R. Morel Peter C. Huttemeier Marek J. Skoskiewicz Tuan Nguyenduy Cynthia Melvin Dwight R. Robinson Warren M. Zapol 《Prostaglandins & other lipid mediators》1987,33(6)
We investigated the effects of a new pyridoquinazoline thromboxane synthetase inhibitor infused before administering
endotoxin into 18 anesthetized sheep with lung lymph fistulas. In normal sheep increasing plasma Ro 23-3423 concentrations were associated with increased plasma levels of 6-keto-PGF1α, a reduced systemic vascular resistance (SVR, r = −0.80) and systemic arterial pressure (SAP, r = −0.92), the mean SAP falling from 80 to 50 mm Hg at the 20 and 30 mg/kg doses. Endotoxin infused into normal sheep caused transient pulmonary vasoconstriction associated with increased TxB2 and 6-keto-PGF1α levels while vasoconstriction and TxB2 increase were significantly inhibited by pretreatment with Ro 23-3423 in a dose-dependent manner. When compared to controls, plasma and lymph levels of 6-keto-PGF1α, PGF2α and PGE2 after endotoxin infusion were increased several-fold by administering Ro 23-3423 up to plasma levels of 10 μg/ml. Doses over 30 mg/kg with blood levels above 10 μg/ml reduced plasma and lymph levels of 6-keto-PGF1α, PGF2α and PGE2, suggesting cyclooxygenase blockade at this dose. The peak 6-keto-PGF1α levels at 60 min after endotoxin infusion in sheep with Ro-23-3423 levels below 10 μg/ml were associated with the greatest systemic hypotension due to a reduced SVR (r = −0.86). After endotoxin infusion the leukotrienes B4, C4, D4 and E4 in lung lymph were assayed by radioimmunoassay and high pressure liquid chromatography and remained at baseline values. 相似文献
17.
C.O. Feddersen M.M. Mathias I.F. McMurtry N.F. Voelkel 《Prostaglandins & other lipid mediators》1986,31(5)
Acetylcholine causes pulmonary vasodilation, but its mechanism of action is unclear. We hypothesized that acetylcholine-induced pulmonary vasodilation might be associated with prostacyclin formation. Therefore, we used isolated rat lungs perfused with a recirculating cell- and plasma-free physiological salt solution to study the effect of acetylcholine infusion on pulmonary perfusion pressure, vascular responsiveness and lung prostacyclin production. Acetylcholine (20 ug infused over 1 minute) caused immediate vasodilation during ongoing hypoxic vasoconstriction and prolonged depression of subsequent hypoxic and angiotensin II-induced vasoconstrictions. Both effects of acetylcholine were abolished by atropine pretreatment. The prolonged acetylcholine effect, but not the immediate response, was blocked by meclofenamate, an inhibitor of cyclooxygenase. The prolonged effect, but not the immediate response, of acetylcholine was associated with an increase in perfusate 6-keto-PGF1α concentration. The acetylcholine stimulated increase in 6-keto-PGF1α production was inhibited by meclofenamate and by atropine. Thus, blockade of prostacyclin production corresponded with blockade of the prolonged acetylcholine effect. In conclusion, acetylcholine caused in isolated rat lungs an immediate vasodilation and a prolonged, time-dependent depression of vascular responsiveness. Whereas both acetylcholine effects were under muscarinic receptor control, only the prolonged effect depended on the cyclooxygenase pathway and, presumably, protacyclin synthesis. 相似文献
18.
Lawrence S. Olanoff James A. Cook Perry V. Halushka 《Prostaglandins & other lipid mediators》1985,29(6)
Previous reports have suggested that sulindac is a unique non- steroidal anti-inflammatory (NSAID) agent, because it does not inhibit renal prostaglandin synthesis in doses that inhibit platelet thromboxane B2 synthesis when tested
. NSAIDS are of potential therapeutic benefit in the treatment of septic or endotoxic shock. Therefore, this study was designed to investigate the proposed unique action of sulindac in experimental endotoxemia. In the current study, the effect of sulindac on aortic, portal and renal venous immunoreactive (i) 6-keto-PGF1α levels, the stable metabolite of prostacyclin, was investigated during endotoxemia in the rat. In doses sufficient to reduce the elevation in aortic and portal venous plasma 16-keto- PGF1α levels, sulindac also significantly (p < 0.05) attenuated the elevated renal venous plasma 6-keto-PGF1α levels, compared to the vehicle group. Using lower doses, sulindac failed to reduce the endotoxin associate increased in either aortic or renal venous plasma 16-keto-PGF1α levels. Thus, sulindac failed to demonstrate any selective sparing effect on renal prostacyclin generation during endotoxemia. 相似文献
19.
Prostanoid formation in human umbilical vessels perfused
was assessed at different oxygen tensions. At an atmosphere of 5% oxygen the production rate of prostacyclin (measured as 6-keto-PGF1α) was higher, while those of thromboxane A2 (measured as TXB2), PGE2 and PGF2α were lower than with 20%, 50% and 95% oxygen. The stimulatory effect of angiotensin II on prostanoid production was found to be independent on the prevailing oxygen tension. Vascular formation of prostanoids thus seems to be at least partially affected by the ambient oxygen tension. Though altered oxygen tension does not seen to affect angiotensin induced prostanoid formation, the action of other vasoactive agents influencing vascular formation of prostanoids may respond differently to hypoxia or hyperoxia. 相似文献
20.
Urinary excretion of 6-keto-PGF1α was measured by high pressure liquid chromatography and radioimmunoassay at various stages of pregnancy and labor. In the first trimester of pregnancy, urinary 6-keto-PGF1α concentrations were nor different from those measured before pregnancy, but they showed a significant increase in the second trimester of pregnancy (p <0.001). The levels rose further in the third trimester, although this increase was not statistically significant when compared to levels obtained in the second trimester. There was no evidence for a significance change in 6-keto-PGF1α excretion with the onset of labor. During well-established, progressive labor mean values of 6-keto-PGF1α excretion were about twice as high as before the onset of labor, but the range of values during labor was so wide that there was no statistical difference with values obtained in the second half of pregnancy.It is concluded that the increase in the urinary excretion of 6-keto-PGF1α occurs later in pregnancy than the increase in TXB2 excretion and that labor at term is not associated with marked changes in 6-keto-PGF1α excretion. 相似文献