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1.
《Prostaglandins, Leukotrienes and Medicine》1987,26(2):115-122
Although several investigators have attempted to measure the plasma levels of prostacyclin (PGI2) and thromboxane A2 (TXA2) in diabetes and normal subjects, their results have been controversial. In this study, we measured plasma PGI2 and TXA2 levels in diabetic patients and normal subjects. The plasma PGI2 and TXA2 were determined by RIA as 6-keto-PGF1a and TXB2, respectively. The plasma levels of 6-keto-PGF1a were significantly reduced in diabetics with microangiopathy (52.5 ± 18.9 pg/ml, mean ± SE, p<0.05) compared with those of normal subjects. Diabetics as a whole also showed lower levels of 6-keto-PGF1a than normal subjects (57.8 ± 26.1 vs. 70.2 ± 20.7 pg/ml), though this was not significant statistically. The plasma 6-keto-PGF1a levels did not significantly correlate with either age of the patients or duration of diabetes in diabetics. Interestingly, however, hemoglobin Alc significantly correlated inversely with 6-keto-PGF1a levels in diabetics without microangiopathy (r=−0.60, p<0.05). The plasma levels of TXB2 in diabetics were significantly higher than those of normal subjects (155.2 ± 69.5 vs. 108.0 ± 30.0 pg/ml, p<0.05). These data suggest that an imbalance of circulating PGI2 and TXA2 may contribute to the development of diabetic microangiopathy. 相似文献
2.
Pekka Uotila Mathias Suyes Hannu Heikkil Jouko Jalonen 《Prostaglandins & other lipid mediators》1984,28(4)
The plasma concentration of 6-keto-PGF1α, 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-PGF1α or TXB2. During the prebypass period after the sternotomy and cannulation of the large vessels the plasma level of 6-keto-PGF1α 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-PGF1α 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-PGF1α/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-PGF1α 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 < 0.01). Coronary sinus flow did, however, not correlate with the plasma level of 6-keto-PGF1α 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
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.
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
5.
The formation of prostacyclin (PGI2) and thromboxane A2 (TXA2) (measured as the stable metabolites 6-keto-PGF1α and TXB2) during stimulation with vasoactive autocoids was registered in human umbilical arteries perfused
. Responses were registered within 3–4 minutes after addition of the subtances. Both angiostensin I and II were found to increase the formation of PGI2 while depressing that of TXA2. Serotonin increased the formation of TXA2 but not that of PGI2. Both PGE2 and PGF2α stimulated the PGI2 formation. The TXA2 mimetic U46619, increased PGI2 production, whereas PGI2 slighlty increased the formation of TXA2. All responses were found to be completely inhibited by indomethacin. 相似文献
6.
S. Nigam R. Becker U. Rosendahl J. Hammerstein C. Benedetto M. Barbero T.F. Slater 《Prostaglandins & other lipid mediators》1985,29(4):513-528
Peripheral plasma concentrations of 6-keto-PGF1α and TXB2 were measured in patients with benign and malignant tumours of the breast, in patients with nongynecological disease,a nd in healthy female controls. The values were significantly higher in female patients with maligants tumours of the breast than in healthy controls (146 ± 28 vs 13 ± 2.5 pg/ml for 6-keto-PGF1α p<0.01 and 78 ± 17 vs 11 ± 2 pg/ml for TXB2, p<0.01). Benign tumours of the breast were also associated with significantly raised plasma levels of 6-keto-PGF1α and TXB2 compared to normal controls (52 ± 5 vs 13 ± 2.5 pg/ml for 6-keto-PGF1α, p < 0.01 and 26 ± 5 vs 11 ± 2 pg/ml for TXB2, p < 0.05). The high levels of 6-keto-PGF1α and TXB2 were not found to be correlated with clinical and histopathological data. The surgical removal of the primary tumour has apparently no effect on the plasma concentration of 6-keto-PGF1α and TXB2 over a follow-up period of 9 days after operation. The lack of alterations in the ratio of TXB2: 6-keto-PGF1α in the cancer patients and other subjects studied before and after surgery is indicative of the regulatory power of metabolic systems to preserve the homeostatic balance. 相似文献
7.
Modulation of the platelet thromboxane A2 and aortic prostacyclin synthesis by dietary selenium and vitamin E 总被引:1,自引:0,他引:1
Mohsen Meydani 《Biological trace element research》1992,33(1-3):79-86
Vitamin E and selenium (Se) interact synergistically as an important antioxidant defense mechanism. Se, an essential component
of glutathione peroxidase (GSH-Px) and vitamin E decompose fatty acid hydroperoxides and hydrogen peroxides generated by free
radical reactions. Vitamin E and GSH-Px may modulate arachidonic acid metabolism and the activity of cyclooxygenase enzymes
by affecting peroxide concentration. The balance between arterial wall prostacyclin (PGI2) production and platelet thromboxane (TX)A2 directly influences platelet activity. In order to elucidate the differential role of dietary vitamin E and Se in aortic
PGI2 and platelet TXA2 synthesis, 1-mo-old F344 rats were fed semipurified diets containing different levels of vitamin E (0, 30, 200 ppm) and Se
(0, 0.1, 0.2 ppm) for 2 mo. Thromboxane B2 (TXB2) and 6-keto-PGF1α, were measured by radioimmunoassay (RIA) after incubation of whole blood and aortic rings at 37°C for 10 and 30 min, respectively.
Vitamin E deficiency reduced plasma vitamin E to 5–17% of control-fed rats, and supplementation increased it to 53% of the
control-fed rats. Se supplementation in vitamin E-supplemented animals increased plasma GSH-Px by 17%, compared to vitamin
E-deficient rats. Se and vitamin E supplementation did not have a similar effect on TXB2 and PGI2 synthesis. Se deficiency did not alter platelet TXB2 synthesis, but significantly decreased aortic PGI2 synthesis. It was necessary to supplement with both antioxidants in order to increase, PGI2 synthesis. Se and vitamin E deficient groups had a higher TXB2/PGI2 ratio (0.17±0.08) compared to Se- and vitamin E-supplemented groups (0.03±0.01). These results confirm previous reports in
humans and animals and are in accordance with epidemiological data indicating an inverse relationship between plasma Se and
platelet aggregation. Thus, further suggesting that vitamin E and Se may have a specific role in controlling TXA2 and PGI2 synthesis. 相似文献
8.
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
9.
《Prostaglandins, Leukotrienes and Medicine》1986,21(1):29-35
Acute renal failure (ARF) was induced in 35 week-old conscious female Wistar rats, by intramuscular (IM) injection of glycerol. Intraperitoneal (IP) injection of imidazole, an inhibitor of thromboxane (TXA2) synthesis, partially protected the animals against ARF. This protection was accompanied by a significant decrease in renal TXB2 (the stable chemical metabolite of TXA2) and a significant increase in renal 6-keto-PGF1α (the stable chemical metabolite of PGI2) synthesis. Intraperitoneal injection of captopril (SQ 14225) an angiotensin-converting-enzyme inhibitor, did not protect the animals against ARF. This lack of protection was accompanied by a significant increase in renal TXB2 and a significant decrease in renal 6-keto-PGF1α synthesis. The results suggest that: (a) the renin-angiotensin (R-A) system does not play a role, or has only a secondary one in the development of ARF; (b) thromboxane A2 (the most potent vasoconstrictor and platelet aggregator agent known) is the preponderant agent responsible for the development of this pathological syndrome. 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.
《Prostaglandins, Leukotrienes and Medicine》1987,26(1):75-84
We measured plasma levels of PGI2 as 6-keto-prostaglandin Fla (6-keto-PGFla) and thromboxane A2 (TXA2) as thromboxane B2 (TXB2) in patients with Graves' disease and in normal subjects. The levels of plasma 6-keto-PGFla were significantly elevated and correlated with those of serum T4 and T3, respectively, in hyperthyroid patients with Graves' disease. Significant reduction of 6-keto-PGF1a levels was observed after antithyroid drug therapy. In contrast, the levels of plasma TXB2 were significantly lower in untreated patients with Graves disease than in normal subjects. These data suggest that an elevation of plasma 6-keto-PGF1a may play some additional role in pathophysiology of Graves disease. 相似文献
12.
Kenneth R Knight Peter A Collopy T John Martin Bernard McC O'Brien 《Prostaglandins & other lipid mediators》1987,33(3)
The levels of the stable degradation products of prostacyclin (PGI2) and thromboxane A2 (TXA2): 6-oxo-prostaglandin F1α(6-oxo-PGE1α) and thromboxane B2 (TXB2) respectively were determined in the effluent of the rabbit epigastric skin flap after infusion of exogenous arachidonic acid. The blood to the flap passes through the microcirculation and thus the changes in eicosanoid biosynthesis in this part of the vasculature were recorded. The aim was to use inhibitors of arachidonic acid metabolism to increase the PGI2/TXA2 ratio. This may be potentially beneficial to ischaemic skin flaps by reducing platelet aggregation associated with damaged microvascular endothelium, overcoming vasospasm and increasing microvascular blood flow. Increased PGI2/TXA2 ratios (up to 5-fold) were best achieved using TXA2 synthetase inhibitors such as dazoxiben hydrochloride. These were significantly more potent than the phosphodiesterase inhibitor dipyridamole, and the lipoxygenase inhibitor Bay g6575. No increase in blood flow was achieved. The cyclooxygenase inhibitor indomethacin did slow the blood flow at high concentrations (above 10−5 M), and inhibited both PGI2 and TXA2 synthesis. Approximately 2-fold higher concentrations of dazoxiben hydrochloride and dipyridamole were required to produce the same TXA2 synthetase inhibition in the flap microvasculature
compared with platelets
. 相似文献
13.
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
14.
R. Chahine A. Pham Huu Chanh B. Lasserre V. Dossou-Gbete 《Prostaglandins, leukotrienes, and essential fatty acids》1991,43(4)
The aim of the study was to determine the prostacyclin (PGI2) and thromboxane A2 (TXA2) synthetase activities of myocardial tissue and their variation during ischemia and reperfusion. Regional ischemia was induced by 10 min occlusion of the left anterior descending coronary artery in isolated Langendorff rabbit hearts. Biosynthesis of PGI2 and TXA2 were carried out by using arachidonic acid as substrate and left ventricle microsomes (LVM) from ischemic and non-ischemic areas as sources of PGI2 and TXA2 synthetase. 6-keto-PGF1α and TXB2, stable metabolites of PGI2 and TXA2 respectively, were determined by radioimmunoassay. Experiments carried out under the adopted conditions showed that LVM were able to synthetise PGI2 as well as TXA2 from arachidonic acid. On the other hand, ischemia depressed both PGI2 and TXA2 synthetase activities of cardiac tissue: the depression was more pronounced on TXA2 synthetase than on PGI2 synthetase with no significant difference between ischemic and non-ischemic regions. Moreover, ischemia increased the ratio
indicating therefore that it can facilitate the formation of PGI2. The post ischemic reperfusion of the heart counteracted the decrease in PGI2 synthetase induced by ischemia which returned to the normal level: reperfusion also slightly reversed the decrease in TXA2 synthetase. However, the diminution in TXA2 synthetase of non-ischemic myocardium was attenuated but it remained lower than the normal level. These results suggested that the whole left ventricle is affected by regional ischemia. Furthermore it appears that myocardial TXA2 synthetase is more vulnerable than PGI2 synthetase to a lack of oxygen and nutrients. 相似文献
15.
The influence of platelets and platelet membranes on the generation of prostacyclin (PGI2) and thromboxane A2(TXA2) by isolated rat lung and porcine aortic endothelial cell, as measured by RIA of their stable end-producs, 6-oxo-PGF1α and TXB2 respectively, was studied. After introduction of either aspirin-treated platelets or membranes from aspirin-treated platelets to the perfusate, 1 5-fold increase in the amount of 6-oxo-PGF1α and TXB2 in the perfusate was observed. Treatment of the lung with aspirin produced a 50% reduction in the platelet-stimulated release of PGI2 and TXA2. Treatment of the lung with the phospholipase inhibitor, mepacrine, significantly reduced the platelet-stimulated release of PGI2 and TXA2. Incubation of endothelial cells with untreated platelet membranes did not alter the generation of PGI2. These results suggest that platelet-stimulated release of PGI2 and TXA2 occurs via mechanical stimulation of phospholipase A2, liberating arachidonic acid. 相似文献
16.
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
17.
Aldona Dembiska-Kie Werner Rücker Peter S. Schnhfer 《Prostaglandins & other lipid mediators》1979,17(6):831-838
Metabolism of arachidonic acid (AA) was studied in perfused lungs and kidneys of normal and atherosclerotic rabbits by determination of PGE2, PGF2α and the stable metabolites of PGI2 (6-keto-PGF1α) and TXA2 (TXB2). PGI2 was the main AA metabolite formed by normal lungs and kidneys. Atherosclerosis reduced the formation of PGI2 by about 50 % in both organs. TXA2 formation was similarily decreased in lungs. In kidneys, the decrease in PGI2 formation was accompanied by an increase in PGE2 formation. 相似文献
18.
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
19.
It is known that peroxides, which are increased during Se deficiency because of reduced glutathione peroxidase (GSH-Px) activity,
can influence the prostacyclin I2/thromboxane A2 (PGI2/TXA2) ratio. In this study we analyzed the PGI2 and TXA2 formation of aortas of long-term Se-deficient rats. Despite low GSH-Px activity in the Se-deficient group, the basal PGI2 and TXA2 formation was not different versus control animals (PGI2: 2295 ± 1134 pg/mg vs 2940 ± 1134 pg/mg; TXA2: 3.83 ± 1.06 pg/mg vs 5.67 ± 2.99 pg/mg). However, we checked the capacity of the aortas of Se-deficient rats to compensate
for a suddenly increased peroxide concentration. After peroxide stimulation, the PGI2 release was significantly lower in the Se-deficient group compared to the control group (PGI2: 3507 ± 1829 pg/mg vs 7986 ± 2636 pg/mg). Again, the TXA2 release did not show any differences. The release ratio of PGI2/TXA2 decreased under peroxide stress in Se-deficient animals. Although long-term Se deficiency showed a relatively well-balanced
metabolism under resting conditions, sudden stress, accompanied by an excessive radical production, cannot be compensated. 相似文献
20.
《Prostaglandins and medicine》1978,1(2):151-157
Iris, and to a lesser extent ciliary body , from cat and rabbit produce considerable amounts of prostacyclin (PGI2) after incubation of the tissue with 1-14C arachidonic acid. These tissues also generate PGI2-like material after gentle squeezing. It is likely that major metabolites found previously in iris and aqueous humor actually were 6-keto-PGF1α. It is concluded that PGH2 and PGI2 are synthetized at the same location. PGI2 induces a contraction of the sphincter and dilator and a relaxation of the ciliary muscle if the tissues had been previously exposed to indomethacin. Thromboxane A2 (TXA2) has either no effect or may cause a slight relaxation of the sphincter. 相似文献