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

A luteotropic role for prostaglandins (PGs) during the luteal phase of the menstrual cycle of rhesus monkeys was suggested by the observation that intraluteal infusion of a PG synthesis inhibitor caused premature luteolysis. This study was designed to identify PGs that promote luteal function in primates. First, the effects of various PGs on progesterone (P) production by macaque luteal cells were examined in vitro. Collagenase-dispersed luteal cells from midluteal phase of the menstrual cycle (Day 6-7 after the estimated surge of LH, n = 3) were incubated with 0-5,000 ng/ml PGE2, PGD, 6 beta PGI1 (a stable analogue of PGI2), PGA2, or PGF2 alpha alone or with hCG (100 ng/ml). PGE2, PGD2, and 6 beta PGI1 alone stimulated (p less than 0.05) P production to a similar extent (2- to 3-fold over basal) as hCG alone, whereas PGA2 and PGF2 alpha alone had no effect on P production. Stimulation (p less than 0.05) of P synthesis by PGE2, PGD2, and 6 beta PGI1 in combination with hCG was similar to that of hCG alone. Whereas PGA2 inhibited gonadotropin-induced P production (p less than 0.05), that in the presence of PGF2 alpha plus hCG tended (p = 0.05) to remain elevated. Second, the effects of various PGs on P production during chronic infusion into the CL were studied in vivo. Saline with or without 0.1% BSA (n = 12), PGE2 (300 ng/h; n = 4), PGD2 (300 ng/h; n = 4), 6 beta PGI1 (500 ng/h; n = 3), PGA2 (300 ng/h; n = 4), or PGF2 alpha (10 ng/h; n = 8) was infused via osmotic minipump beginning at midluteal phase (Days 5-8 after the estimated LH surge) until menses. In addition, the same dose of PGE, PGD, PGI, or PGA was infused in combination with PGF2 alpha (n = 3-4/group) for 7 days. P levels over 5 days preceding treatment were not different among groups. In 5 of 8 monkeys receiving PGF2 alpha alone, P declined to less than 0.5 ng/ml within 72 h after initiation of infusion and was lower (p less than 0.05) than controls. The length of the luteal phase in PGF2 alpha-infused monkeys was shortened (12.3 +/- 0.9 days; mean +/- SEM, n = 8; p less than 0.05) compared to controls (15.8 +/- 0.5). Intraluteal infusion of PGE, PGD, PGI, or PGA alone did not affect patterns of circulating P or luteal phase length.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intraluteal infusions of prostaglandins of the E, D, I, and A series prevent PGF2 alpha-induced, but not spontaneous, luteal regression in rhesus monkeys. 227 32

The feasibility of maintaining long-term viability of human venous allografts by cryopreservation has been investigated. Segments of vein were obtained from 85 patients undergoing a stripping operation for varicose veins. The venous segments were immersed in a dimethylsulfoxide 15% solution, deep frozen at -196 degrees C in liquid nitrogen and preserved for a duration of 1 week to 24 months. Light microscopy (n = 126) failed to demonstrate striking differences between control veins and any of the cryopreserved veins. The types of damage observed at scanning electron microscopy included endothelial cell separation, endothelial cell loss, exposed basement membrane and exposed fibrillar collagen, which were graded on a scale. The score for short term (less than 3 weeks) stored veins was 8.1 +/- 0.9 (mean +/- SEM) and did not differ from the long-term (greater than 10 weeks) stored veins score (6.3 +/- 1.0, p NS). The tissue enzymes LDH, GOT, GPT, CPK were measured in the frozen vein groups (n = 115) after thawing to room temperature. Cryopreservation did not alter any of the tissue enzymes measured when compared to controls. Endothelial fibrinolytic activity (FA) of 58 venous segments cryopreserved for a mean duration of 20 months was 6136.4 +/- 292.1 Tissue Activator Units (TAU) and did not differ from FA of 11 controls (5989.1 +/- 696.8 TAU). Synthesis of 6-Keto-PGF1-alpha-2, a stable breakdown product of PGI2, measured in 10 venous segments cryopreserved for 10 months, was significantly higher than in 13 veins stored in saline for 12 hours at 4 degrees C (2.8 +/- 0.4 vs 0.4 +/- 0.1 PG ml-1mg-1min-1, respectively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Viability of long-term cryopreserved human saphenous veins. 232 91

Prostaglandin F2 alpha (PGF2 alpha) is a well-known luteolytic factor in the rat corpus luteum. To investigate a possible luteal origin of PGF2 alpha, measurements of this prostaglandin were performed in different luteal tissues in vivo. Prostaglandin E2 (PGE2) and the stable metabolite of prostacyclin, 6-keto-PGF1 alpha, were assayed simultaneously. Corpora lutea of different ages from 57 pregnant and pseudopregnant rats (mated with sterile males) were rapidly excised, dissected in 0 degree C indomethacin solution, homogenized, and extracted for prostaglandins with solid-phase extraction cartridges. Prostaglandins were determined by radioimmunoassay. Plasma levels of progesterone and 20 alpha-dihydroprogesterone were also monitored. In the adult pseudopregnant rat model, luteolysis occurs at Day 13 +/- 1, and maximal levels of all three prostaglandins were detected on Day 13 of pseudopregnancy: 0.40 +/- 0.02, 2.6 +/- 0.29, and 1.76 +/- 0.24 pmol/mg protein (mean +/- SEM, n=7) for PGF2 alpha, PGE2, and 6-keto-PGF1 alpha respectively. In pregnant rats, on the corresponding day, levels were considerably lower: 0.15 +/- 0.02, 0.90 +/- 0.13, and 0.50 +/- 0.06 pmol/mg protein (mean +/- SEM, n=9, p less than 0.0001), respectively. Luteal levels in pregnant rats showed a continuous decline on Days 13 and 19 for all prostaglandins measured, whereas in pseudopregnant rats an increment of PGF2 alpha was noted between Days 7 and 13 and remained high on Day 19. PGE2 closely followed levels of PGF2 alpha, but at a 5- to 10-fold higher level. The coefficient of correlation between PGF2 alpha and PGE2 in the luteal compartment of both models was 0.87 (p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo levels of prostaglandin F2 alpha, E2 and prostacyclin in the corpus luteum of pregnant and pseudopregnant rats. 238 8

The ability of heparin and prostacyclin to improve streptokinase-induced recanalization was examined in open-chest dogs subjected to thrombotic occlusion of the left circumflex coronary artery. Vessel injury was produced by electrical stimulation of the intimal surface at the site of a noncircumferential fixed stenosis. Animals were divided into three treatment groups as follows: group 1 received intracoronary streptokinase alone (75,000 units/80 min starting 30 min postocclusion; n = 8); group 2 received streptokinase plus heparin (300 units/kg i.v. at 20 min postocclusion; n = 7); group 3 received streptokinase plus heparin plus prostacyclin (500 ng/kg/min, intracoronary, given intermittently during reperfusion; n = 7). Overall, the groups did not differ with respect to preocclusion coronary blood flow (27 +/- 1 ml/min; +/- SEM), the duration of streptokinase infusion required to achieve reflow (15 +/- 2 min), and the percentage of animals recanalized (85%). They did differ in the average rate of reflow, which was greater in group 2 (16 +/- 2 ml/min) and group 3 (20 +/- 4 ml/min) as compared with group 1 (6 +/- 1 ml/min; p less than 0.05). The intermittent reocclusions which persisted during reperfusion in group 1 and 2 dogs were diminished during the periodic infusions of prostacyclin. Thrombus mass at the site of injury was comparable among groups. In contrast, distal circumflex thrombi, about twice the weight of the proximal mass, were observed in all group 1 dogs and were undetectable in group 2 and 3 animals. Transient improvements in contractile force during reperfusion were observed only with groups 2 and 3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Augmentation of streptokinase-induced thrombolysis by heparin and prostacyclin. 241 Jul 16

Evidence in vitro and in humans suggest that Mg2+ can alter systemic and renal vascular tone. However, the mechanism of these effects is not known. The role of vasodilator prostaglandin release and Ca2+ flux in Mg2+-induced changes in blood pressure and renal blood flow was studied in 10 normal subjects maintained on a fixed 80-mEq Na+ and K+ diet. Magnesium sulfate infused at 200 mg/hr for 3 hours reduced systolic and diastolic blood pressure within 1 hour (from 119 +/- 2 [SEM] to 109 +/- 4 mm Hg systolic; from 74 +/- 3 to 64 +/- 4 mm Hg diastolic; p less than 0.02). This hypotensive response was seen in all subjects and persisted for 3 hours. The pulse rate did not change, but renal blood flow (p-aminohippurate clearance) increased (from 902 +/- 78 to 1108 +/- 130 ml/min/1.73 m2; p less than 0.05). The Mg2+ infusion produced a significant increase in the excretion of the stable prostaglandin I2 (PGI2) metabolite 6-keto-PGF1 alpha (from 96 +/- 12 to 154 +/- 16 ng/g creatinine; p less than 0.01). In contrast, urinary PGE2 was not altered (328 +/- 75 vs 399 +/- 145 ng/g creatinine; p greater than 0.6). To evaluate the functional role of PGI2 release, the cyclooxygenase inhibitors indomethacin (75 mg) or ibuprofen (600 mg) were given before the Mg2+ infusion. Both cyclooxygenase blockers, given in doses that inhibited immunoreactive 6-keto-PGF1 alpha release, completely prevented the Mg2+-induced decline in blood pressure and increased renal blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that prostacyclin mediates the vascular action of magnesium in humans. 243 56

Fourteen patients with mild to moderate essential hypertension were randomized, after a baseline placebo period of 4 weeks, to receive the angiotensin converting enzyme (ACE) inhibitor quinapril or a placebo. During a 12 week, double-blind phase, the dosage of quinapril was increased from 10 to 40 mg twice daily being doubled every 4 weeks. At the end of the baseline period and of each month of the double-blind phase, 12 h overnight urine collections were made and morning blood samples were taken about 12 h after the last dose of medication. During the double-blind phase, blood pressure in the quinapril group (n = 7) decreased from 159 +/- 3/105 +/- 1 to 141 +/- 6/94 +/- 2 mm Hg (mean +/- SEM). Serum ACE activity and plasma angiotensin II concentration were reduced to 4 +/- 1% and 14 +/- 1% of the pretreatment values, respectively. Neither the plasma concentrations nor the urinary excretions of prostaglandin E2, 6-keto-prostaglandin F1 alpha (a prostacyclin metabolite), or thromboxane B2 (a metabolite of thromboxane A2) were affected by quinapril. In the placebo group, blood pressure tended to decline but the biochemical variables remained essentially unchanged. These results indicate that prostanoids are not involved in the antihypertensive action of quinapril, the principal effect of which seems to be inhibition of the renin-angiotensin system.
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PMID:Effects of the converting enzyme inhibitor quinapril (CI-906) on blood pressure, renin-angiotensin system, and prostanoids in essential hypertension. 245 40

There is evidence that cyclooxygenase products of arachidonic acid participate in the control of renin release. In this study we tested the hypothesis that prostaglandin (PG) I2 and/or its metabolite(s), which are synthesized in the afferent arteriole (AF), stimulate renin release by acting directly on the AF while PGE2 stimulates renin release indirectly via the macula densa. AF alone and AF with macula densa attached (AF-MD) were microdissected from rabbit kidneys and incubated in vitro. The renin release rate from a single AF (or an AF-MD) was calculated and expressed as ng AI.hr-1. AF-1/hr (where AI is angiotensin I). When arachidonic acid (0.12 mM) or PGI2 (10 microM) was added to AF, renin release increased significantly (P less than 0.0001) from 1.04 +/- 0.21 to 3.12 +/- 0.86 (x +/- SEM, N = 7), and from 0.45 +/- 0.14 to 1.48 +/- 0.53 (N = 9), respectively. During the recovery period, renin release increased even further, reaching 9.53 +/- 1.76 and 4.50 +/- 1.24, respectively. A PGI2 synthetase inhibitor, 9, 11-azoprosta-5,13-dienoic acid blocked the effect of arachidonic acid. To examine whether the increases in renin release during the recovery period were due to metabolite(s) of PGI2, we tested the effect of both 6-keto-PGE1 (an active metabolite of PGI2) and carba-PGI2 (a synthetic analog that is metabolized differently from PGI2). Six-keto-PGE1 and carba-PGI2 increased renin release only during the experimental period with no further increase during the recovery period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostanoids on renin release from rabbit afferent arterioles with and without macula densa. 250 84

Direct fetal intravascular transfusion is well tolerated by the human fetus. However, the rapid transfusion of high-hematocrit blood should increase vessel distention and the flow shear force. Each is known to stimulate the release of prostacyclin. We measured prostaglandins E2 and F2 alpha and the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha, by radioimmunoassay before, at the estimated midway point of, and at the completion of 40 umbilical venous transfusions performed because of immune hemolytic anemia. Umbilical venous pressures corrected for amniotic fluid pressure were measured at similar intervals during nine of the procedures. The mean (+/- SEM) length of gestation at transfusion was 29 +/- 1 week, opening hematocrit 23% +/- 1%, and total volume of 70% hematocrit red blood cells transfused 83 +/- 5 ml. 6-Keto-prostaglandin F1 alpha was the principal circulating fetal prostanoid and its concentration was unrelated to gestational age. Intravenous transfusion was associated with an 84% increase in 6-keto-prostaglandin F1 alpha (p = 0.03) and a 68% increase in prostaglandin E2 (p less than 0.05). The rise for each strongly correlated with the rise in the fetal umbilical venous pressure (6-keto-prostaglandin F1 alpha, r = 0.94, p = 0.0005; prostaglandin E2, r = 0.81, p less than 0.03). We conclude that 6-keto-prostaglandin F1 alpha is the principal circulating prostaglandin in the human fetus and that the release of venodilator prostaglandins may be one reason the human fetus can tolerate a large increase in intravascular volume without obvious sequelae.
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PMID:Effect of acute intravascular volume expansion on human fetal prostaglandin concentrations. 251 19

The effect of arachidonic acid and its metabolites on the histamine-stimulated acid production in human isolated parietal cells provenient from endoscopic biopsies was examined. 14C-aminopyrine (14C-AP) accumulation in the parietal cells was used for evaluation of acid production. Histamine dose-dependently increased AP uptake. Histamine stimulation (taken as 100% at 10(-5) M) was significantly inhibited by prostaglandin (PG) E2 to 66 +/- 7% at 10(-8) M, 42 +/- 8% at 10(-6) M, and 13 +/- 10% at 10(-4) M (mean +/- SEM, n = 10). PGF2 alpha, PGD2, and PGI2 showed significant inhibitory effects only at very high concentrations (10(-5)-10(-4) M). Leukotriene (LT) B4 and LTC4 were without effect. The basal acid production (taken as 0%) was lowered significantly by 10(-6) M arachidonic acid to -20 +/- 7.4% (p less than 0.02, n = 10), and the histamine-stimulated (10(-6) M) acid production from 100% to 64 +/- 7.2% (p less than 0.001, n = 10). Aspirin (10(-3) M) increased basal (45 +/- 9.6%, p less than 0.001, n = 10) and histamine-stimulated (10(-6) M) acid production (164 +/- 16.3%, p less than 0.001). It is concluded that PGE2, the major product from arachidonic acid metabolism in the human gastric mucosa, is a significant inhibitor of the histamine-stimulated human parietal cell and may, in humans, play a role as a local physiologic inhibitor of acid secretion.
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PMID:The effect of arachidonic acid and its metabolites on acid production in isolated human parietal cells. 260 6

1. The vasoconstrictor and vasodilator activity of cultured bovine pulmonary artery endothelial cells was measured to determine how exposure to different partial pressures of O2 [PO2 142,42 and 15 mmHg (18.9, 5.6 and 2 kPa)] affects the production of endothelial-derived relaxing and constrictor factors. 2. A de-endothelialized rat aortic ring [maintained at a PO2 of 142 mmHg (18.9 kPa)] was used to bioassay the effluent from a perfused column of bovine endothelial cells grown on microcarrier beads. The endothelial cells were stimulated by 10(-7) mol/l bradykinin given for 1 min at 12 min intervals. 3. At the start, middle and end of the experiment the bovine endothelial cells were exposed to a PO2 of 142 mmHg (18.9 kPa) and when stimulated by bradykinin the perfusate caused respectively a 70 +/- 4%, 63 +/- 6% and 63 +/- 6% (mean +/- SEM) relaxation of an aortic ring which had been pre-contracted by 10(-6) mol/l phenylephrine. At a PO2 of 42 mmHg (5.6 kPa) the relaxation induced by the cells was not significantly altered, but this tailed to zero after 26-38 min exposure of the cells to a PO2 of 15 mmHg (2 kPa). 4. These responses were unaltered by the presence of 10(-5) mol/l indomethacin, suggesting that prostacyclin is not a significant vasodilator in this system. 5. Reduced production of endothelium-derived relaxant factor rather than production of a constrictor factor, or a direct effect on the smooth muscle, may be involved in pulmonary hypoxic vasoconstriction.
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PMID:Pulmonary endothelium-derived relaxing factor is impaired in hypoxia. 260 70


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