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1.
Thromboxane B2 and 6-keto-PGF (6KPGF), the major stable metabolites of thromboxane and prostacyclin, are present in the CNS, where they appear to be mainly produced within and/or acting upon the vascular district. Their concentrations are of few pg/mg protein in rat brain cortex of animals sacrificed by microwave (MW) radiation, procedure which inactivates tissue enzymes and allows the determination of endogenous “basal” levels of eicosanoids. Levels of 6KPGF and especially those of TxB2 increase several fold over the basal values in brain cortex of animals sacrificed by decapitation followed by a few minute interval before analysis (post-decapitation ischemia, PDI). Pretreatment of animals with the vasoactive drug papaverine, resulted in elevation of brain basal levels of 6KPGF and with the carbochromene derivartive AD6 in reduction of basal levels of TxB2, whereas the calcium antagonist nifedipine and dipyridamole did not modify basal levels of the two eicosanoids. Treatments with papaverine and AD6 reduced the accumulation of TxB2 and enhanced that of 6KPGF occurring after PDI, to different extents, both resulting, however, in reduction of the TxB2/6KPGF ratio. Nifedipine instead, decreased the release of both eicosanoids and resulted in elevation of the TxB2/6KPGF ratio, whereas dipyridamole had no effect. In conclusion, the evaluation of the overall effects of drug treatments on the TxB2/6KPGF ratio in cerebral tissue, provided useful informations on the pharmacological modulation of vascular eicosanoids in this district.  相似文献   

2.
The effects of acute (3 g/kg i.p. two hours before sacrifice) and chronic (6% in drinking water and libitum for 15 days) ethanol administration to male rats (200 g body weight) on basal levels and release of TxB2 and 6-keto-PGF1 alpha in brain cortex were studied. Also the effects of chronic ethanol (30 days) on the fatty acid composition of brain cortical tissue and liver phospholipids were investigated. Acute treatment reduced basal levels of 6-keto- PGF1 alpha in brain cortical tissue (rats sacrificed by microwave radiation) and decreased the accumulation of 6-keto-PGF1 alpha in brain cortex after post-decapitation ischemia (PDI). Basal TxB2 levels were also reduced in brain cortex, but TxB2 release during PDI was enhanced. Chronic treatment (15 days) induced changes of TxB2 and 6-keto-PGF1 alpha levels and release during PDI in brain cortex less pronounced than those observed after acute treatment. The reduced effectiveness of chronic ethanol on brain vasoactive eicosanoids suggest adaptation processes. After chronic treatment (30 days), the fatty acid composition of brain cortex total phospholipids were not significantly modified. Changes of eicosanoid production after ethanol were thus independent from modifications of the fatty acid precursor pool(s). Ethanol-induced changes in the production of vascular eicosanoids in the CNS may be of relevance to the action of the compound on the CNS and may also have implications for the clinic.  相似文献   

3.
The production of vasodilatory, antiaggregatory prostacyclin (PGI2) and vasoconstrictory, proaggregatory thromboxane A2 (TxA2) by the placenta was studied in the cases of hypertensive pregnancy complications by superfusing pieces from maternal and fetal sides of placentae of 9 pre-eclamptic, 6 hypertensive and 11 healthy women and measuring the release of 6-keto-prostaglandin F (6-keto-PGF) and thromboxane B2 (TxB2), the breakdown products of PGI2 and TxA2 respectively, from the superfusate. Both sides of the placentae from the controls produced 6-keto-PGF (maternal side 0.5±0.1 ng/g/min dry weight of tissue, mean±SEM; fetal side 0.7±0.2 ng/g/min) and TxB2 (maternal side 2.5±0.4 ng/g/min; fetal side 2.7±0.5 ng/g/min with no correlation between the two. The 6-keto-PGF production was normal in hypertensive complications whereas the TxB2 production was increased on the fetal side of the placentae obtained from the pre-eclamptic (3.7±0.3 ng/g/min: p<0.05) and hypertensive women (4.1±0.4 ng/g/min; p<0.025). This may explain the occurrence of microthrombi and infarctions in placentae of hypertensive women.  相似文献   

4.
Prostanoids play an important role throughout all of pregnancy and during the initiation and progress of labor. The human placenta at term produces large quantities of prostanoids, yet little is known of the factors that regulate their biosynthesis. Herein, we report the effect of estradiol or estradiol and progesterone on the basal release of placental prostanoids from fresh human term placental explants using a perifusion system.The basal release of prostaglandin E2 (PGE2, prostaglandin F (PGF), thromboxane (TxB2) and 6-keto-prostaglandin F (6-keto-PGF) increased about 50% from the fifth to the ninth hour in culture, while the release of 13, 14-dihydro-15-keto-PGF (PGFM) remained constant and hCG release decreased. The dose-related effect of estradiol (20–2,000 ng/ml) in the perifusing medium starting at the fifth hour of perifusiOn (i.e., the zero treatment time) effected no change in the release of TxB2, PGF, PGFM or hCG. A biphasic action on the release of 6-keto-PGF,. was observed, i.e. it was significantly decreased when incubated with 20 ng/ml of estradiol, but effected an increase after exposure to 200 ng/ml. The concomitant addition of progesterone (2,000 ng/ml) with estradiol (200 ng/ml) significantly inhibited the stimulatory action of estradiol at this dose. The release of PGE2 was inhibited in a dose-related fashion with increasing dose of estradiol. The addition of progesterone with estradiol (2,000 and 200 ng/ml, respectively) reversed the inhibition of PGE2 by estradiol alone.These data demonstrate that physiologic levels of estradiol affect 6-keto-PGFα and PGE2 release from the human term placenta, but do not significantly alter production of TxB2, PGFM or hCG under these conditions.  相似文献   

5.
We investigated the relationship between glucose levels and platelet thromboxane production or aortic prostacyclin production, using radioimmunoassay (RIA) to measure thromboxane B2 and 6-keto-PGF. We found a direct relationship (p<.05) between plasma glucose levels and thromboxane A2 production by arachidonate stimulated platelets in platelet rich plasma of normal mice. However, when mice were deprived of food overnight, the glucose level fell but the TxB2 production rose significantly. Moreover, mice with streptozotocin diabetes had significantly elevated glucose levels. but normal TxB2 production, which also rose significantly after fasting. Thus in our laboratory both fasting and diabetes nullify or reverse the direct relationship between glucose levels and TxB2 production seen in normal fed mice. This makes it diffisult to ascribe the correlation between glucose and TxB2 levels in normal fed animals to cause and effect. RIA revealed an inverse correlation between glucose levels and 6-keto-PGF production which was highly significant in aortas taken from fasted mice and stimulated for 10 minutes with 0.1mM arachidonate. This inverse correlation was present with either normal or diabetic aortas. Moreover, fasting increased the production of 6-keto-PGF. However there was a significant elevation of 6-keto production by aortas of mice with diabetes of 5–6 weeks duration, compared to aortas of normal mice. Therefore either diabetes in these mice reversed a normal inhibitory effect of glucose on 6-keto production, or else the inverse correlation between glucose levels and 6-keto production does not represent a cause and effect relationship between the two variables.  相似文献   

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-PGF, 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-PGF 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-PGF, PGF 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-PGF, PGF and PGE2, suggesting cyclooxygenase blockade at this dose. The peak 6-keto-PGF 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   

7.
Prostaglandins are involved in the modulation of various central functions (neurotransmitters and hypothalamic hormone release, thermoregulation, cerebro-vascular tone) and their levels increase in pathological situations [subarachnoid hemorrhage (SAH), stroke, convulsive disorders, etc.]. This study, using sensitive and specific antibodies, examined levels of four eicosanoids, Prostaglandins E2 and F(PGE2, PGF); and the metabolites of PGI2, 6-keto-prostaglandin F (6-keto-PGF1α) and of thromboxane A2, thromboxane B2 (TxB2), in the cerebrospinal fluid (CSF) obtained atraumatically from three species (human, canine, and feline). An assessment of the methodologic procedures (extraction and radioimmunoassay) was carried out. Human lumbar cerebrospinal fluid was shown to contain PGF (15–44 pg/ml), 6-keto-PGF (undetectable to 39 pg/ml), and TxB2 (un-detectable to 28 pg/ml), whereas PGE2 was undetectable (>18 pg) in all cases. In both animals species the eico-sanoid concentrations were 3-to 30-fold higher than humans for every prostaglandin examined. Although the prostaglandin profile for a given species remained constant (cat, PGE2:6-keto-PGF:TxB2:PGF; dog, TxB2:PGE2:6-keto-PGF:PGF), the absolute levels were found to be lower in the pentobarbital-anesthetized animals than in conscious cats. The correspondence of the prostaglandin profiles found in cerebrospinal fluid with the profiles reported in the literature in brain homogenates for the same species supports the hypothesis that cerebrospinal fluid levels of prostaglandins reflect the relative rates of synthesis in neural tissue.  相似文献   

8.
The administration to male rats of 5 en % fish oil (FO) as supplement to a diet containing 5 en % corn oil (CO), selectively and markedly decreased arterial parameters (6-keto-PGF formation and platelet antiaggregatory activity) assessed in isolated aortic segments perfused with autologous platelet rich plasma (PRP). Platelet parameters (ADP-induced aggregation, TxB2 formation in thrombin-stimulated PRP and sensitivity to exogenous PGI2) were instead minimally affected. Eicosapentaenoic acid (EPA, 20:5 n-3) did not accumulate in plasma, platelet and aorta lipids and arachidonic acid (AA, 20:4 n-6) levels declined markedly only in the plasma compartment. When FO was given alone at the same 5 en % level, both arterial and platelet parameters were similarly affected. EPA accumulated in plasma cholesterol esters and was present in appreciable concentrations also in platelets and aortic walls. AA levels declined markedly in plasma lipids and appreciably also in platelet and aorta lipids. It is concluded that a) arterial and platelet parameters are differentially affected by FO administration depending upon the presence of n-6 polyunsaturated fatty acids in the diet, b) 6-keto-PGF production by arterial tissues does not seem to be related to changes of PG precursor fatty acid levels in the phospholipid fraction.  相似文献   

9.
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-PGF, with lesser amounts of PGE2, PGF and thromboxane B2. Biosynthesis of all prostanoids increased during incubation of the pariental pericardium of each species with arachidonic acid, but 6-keto-PGF was still the major metabolite. When slices of dog heart were incubated with arachidonic acid (1 μg/ml) the rates of 6-keto-PGF formation by the pariental pericardium was much greater than that of the myocardium and endocardium. Epicardial slices appeared to be intermediate in 6-keto-PGF 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-PGF, 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-PGF remained the predominant metabolite. In contrast, intravenous infusion of isoproterenol selectively increased the release of 6-keto-PGF 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   

10.
We assessed the effect of a specific thromboxane synthetase inhibitor (an imidazole derivative) on pulmonary hemodynamics and the concentrations of TxB2 (TxA2), 6-keto-PGF (PGI2), and PGF 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-PGF (PGI2) and PGF 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   

11.
Sex differences in eicosanoid production in platelets and vessel walls have been studied in control and n-6 fatty acid supplemented rats. In platelet rich plasma (PRP) of control female rats, arachidonic acid (AA) levels in phospholipids (PL), thromboxane B2 (TxB2) formation following collagen stimulation and aggregatory responses to collagen were higher than in PRP of male rats. 6 keto PGF release from PRP-perfused isolated aortas were the same for both sexes, but the antiaggregatory activity of the wall was higher in males than in females, in association with a greater sensitivity of male platelets to prostacyclin.The administration of n-6 fatty acid supplements increased AA level in PL, TxB2 production and aggregation only in male platelets. Production of 6 keto PGF and the antiaggregatory activity of aortic walls were reduced after dietary treatment in males, but biochemical and functional parameters were not correlated in females.The results indicate complex sex-related differences in fatty acid metabolism and eicosanoid production, and in responses to n-6 dietary fatty acids in platelets and the vascular system in the rat.  相似文献   

12.
The pulmonary formation of prostacyclin (PGI2), as reflected by the difference in concentration of pulmonary and systematic arterial radioimmunoassayed 6-keto-PGF, was determined in six healthy waking subjects. The systematic arterial 6-keto-PGF 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-PGF 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-PGF 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-PGF 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-PGF was stabilised at an elevated level (120−170 pg/ml). Following re-establishment of the pulmonary circulation the arterial concentrations of 6-keto-PGF 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   

13.
The bony reaction after implantation of uncemented ceramics is of special interest. Therefore porous and dense hydroxylapatite and aluminium oxide ceramics were implanted in rat femurs. One group received no surgical manipulation and another with a sham procedure where no ceramics were implanted served as controls. After 6 and 10 days the rat femurs were harvested and the release of PGE2 and 6-keto-PGF was measured with specific radioimmunoassays. Decrease in the release of PGE2 from day 6 to day 10 was present in all three implants. In contrast, 6-keto-PGF increased from day 6 to day 10. Comparing the ceramic types an increase in 6-keto-PGF release was seen in the porous hydroxylapatite group. These prostaglandin (PG) release patterns after ceramic implantation are similar to those of fracture healing, but aluminium oxide seems to be inert, while hydroxylapatite, especially the porous type, stimulates 6-keto-PGF release.  相似文献   

14.
The endogenous formation of prostaglandin (PG) D2, E2, F, and 6-keto-PGF was determined in homogenates of mouse, rat, and rabbit brain, and of rat cerebral blood vessels, using gas chromatography mass spectrometry. In all species tested, 6-keto-PGF could be identified in the brain homogenates, but was a minor component in relation to other PGs. In contrast 6-keto-PGF was the most abundant PG in the blood vessels, being present in about 40-fold higher levels than in the brain tissue. PGD2 was the most abundant PG in rat and mouse brains, but was below detection limits in the analyzed blood vessels. These studies indicating differential metabolism of PG endoperoxides in nervous and vascular tissue, provide a biochemical basis for further studies on the role of the PGs in brain circulation and neuronal activity.  相似文献   

15.
Two groups of 40 volunteers were given a dietary supplement consisting of 135 g of mackerel or meat (control) paste per day for 6 weeks. Compliance was about 80% in both groups and the daily intake of 20:5(n−3) and 22:6(n−3) from the mackerel supplement was about 1.3 and 2.3 g, respectively. In collagen-activated platelet rich plasma, the potency of blood platelet to produced HHT from arachidonic acid (AA) clearly reduced in the mackerel group, whereas the formation of HHTE from timnodonic acid (TA) increased slightly. Changes in the formation of HHT and HHTE, measured by HPLC, correlated significantly with those of TxB2 and TxB3, respectively, measured by GC/MS. Changes in the formation of the lipoxygenase products HETE (ex AA) and HEPE (ex TA) were qualitatively similar to that seen for the cyco-oxygenase products, but quantitatively the responses were smaller. Formation of ir TxB2 in clotting blood significantly reduced in the mackerel group. In collagen-activated, citrated whole blood, TxB2 formation tended to be reduced in the mackerel-supplemented volunteers. Mackerel consumption was associated with the formation of considerable amounts of PGl3, as judged from the appearance of 2,3-dinor-Δ 17-6-keto-PGF in urine. The amount of the major metabolite of PGl2, 2,3-dinor-6-keto-PGF was not reduced, or even increased. The daily amount of tetranor prostaglandin metabolites in the urine did not change significantly, which indicates that mackerel supplementation did not alter the formation of prostaglandins E and F.  相似文献   

16.
To study the role of prostacyclin (PGI2) and thromboxane A2 (TxA2) in uterine tumors, pieces of endometrial cancer (n=12) and leiomyomas (n=12)_were incubated in vitro, and the productions of 6-keto-prostaglandin F1a (6-keto-PGF1a, a hydration product of PGI2) and thromboxane B2 (TxB2, a hydration product of TxA2), measured by radioimmunoassay, were compared to those of corresponding healthy tissues. The production of 6-keto-PGF1a by endometrial cancer (20.8; 1.5–85 ng/mg protein/min, median and interquartile range), by healthy endometrium (25.5; 10.0–55.0), by healthy myometrium (34.9; 25.0–59.9) and by leiomyoma (20.3; 10.2–45.1) was similar. The production of TxB2 was increased by endometrial cancer (55.5; 10.5–155.2, p < 0.02) in comparison with endometrium (9.8; 4.3–35.1), myometrium (3.8; 2.1–8.0) and leiomyoma (1.9; 1.0–3.8). The 6-keto-PGF1a/TxB2 ratio in endometrial cancer (0.9; 0.3–1.5) was smaller (p < 0.02) than that in healthy endometrium (3.3; 1.9–4.8). Thus, TxA2 may be a factor in endometrial cancer.  相似文献   

17.
Urinary excretion of 6-keto-PGF 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-PGF 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-PGF excretion with the onset of labor. During well-established, progressive labor mean values of 6-keto-PGF 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-PGF occurs later in pregnancy than the increase in TXB2 excretion and that labor at term is not associated with marked changes in 6-keto-PGF excretion.  相似文献   

18.
Simultaneous determination of urinary excretion rates of primary unmetabolized prostanoids and their enzymatic metabolites were performed by gas chromatography-mass spectrometry (GC/MS) or tandem mass spectrometry (GC/MS/MS). Changes in kidney function were induced by acute (4 h) volume expansion. Despite marked changes in urine flow, GFR, urinary pH, osmolality, sodium and potassium excretion, only a insignificant or transient rise in the enzymatic prostanoid metabolites (2,3-dinor-6-keto-PGF, PGE-M, 2,3-dinor-TxB2 and 11-dehydro-TxB2) was observed. The excretion rates of the primary prostanoids were elevated in parallel with the rise in urine flow: PGE2 rose (p < 0.05) from 14.2 ± 4.0 to 86.2 ± 20.7, PGF2α from 60.0 ± 4.9 to 119.8 ± 24.0, 6-keto-PGF from 7.2 ± 1.3 to 51.5 ± 17.0, and txB2 from 11.2 ± 3.3 to 13.6 ± 3.6 ng/h/1.73 m2 ( ) at the maximal urine flow. Except for 6-keto-PGF and TxB2, this rise in urinary prostanoid levels was only transient despite a sustained fourfold elevated urine flow. We conclude that urine flow rate acutely affect urine prostanoid excretion rates, however, over a prolonged peroid of time these effects are not maintained. The present data support the concept that urinary levels of primary prostanoids mainly reflect renal concentrations whereas those of enzymatic metabolites reflect systemic prostanoid activity. From the excretion pattern of TxB2 one can assume that this prostanoid represents renal as well as systemic TxA2 activity.  相似文献   

19.
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-PGF 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-PGF 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-PGF. 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-PGF 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   

20.
PGI2 and 6-keto-PGF were converted to 6-methoxime-PGF (6-MeON-PGF) by treatment with methoxyamine HCl in acetate buffer. The formed 6-MeON-PGF was measured by radioimmunoassay. Antisera were raised in rabbits after immunization against 6-MeON-PGF-BSA conjugate. Diluted 1:20.000 to bind 50% of the tracer (3H-6-MeON-PGF, 100 Ci/mmol), the antiserum cross reacted 0.8% with PGE2, 1% with PGF and less than 0.2% with PGD2, PGF, PGF and TXB2. The radioimmunoassay was used to estimate release of PGI2 and 6-keto-PGF from chopped rabbit renal medulla and cortex incubated in Krebs-Ringer bicarbonate buffer (37°C, 30 min). The 6-keto-PGf radioimmunoassay was validated in biological samples by mass fragmentography. The chopped medulla (n=5) released 38±9 ng/g/min and the cortex (n=5) 4.7±2.0 ng/g/min, while the release of immunoreactive PGE2 (iPGE2) and iPGF was 171±26 and 74±13 ng/g/min from the medulla and 4.3±1.3 and 2.7±0.3 ng/g/min from the cortex, respectively. The results confirm previous findings, which indicate that in the renal medulla prostaglandin endoperoxides are mainly transformed to prostaglandins, while in the cortex transformation to PGI2 seems to be of greater importance.  相似文献   

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