Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

These studies were directed toward determining effects of selected vasoactive compounds on oxygenated erythrocytes. Considering the major circulatory effects that small changes in blood flow might initiate in sickle cell anemia patients, erythrocytes from individuals with this disease and from one person with the trait condition were included. PGA1, PGE1, and PGE2 significantly increase filtration times in normal erythrocytes (AA-type hemoglobin) at 10(-11) M by this method. From studies of the effects of L-epinephrine, D,L-isoproterenol, PGA1, PGA2, PGE1, PGE2, PGF1alpha and PGF2alpha on red blood cell filterabilities, the following observations and conclusions appear to hold: (1) Erythrocytes from different individuals (or from the same individual at different times) vary greatly in responses to these compounds. Effects of vasoactive compounds upon red cell filterability may be positive, negligible or negative. Decreased filterability (positive effect) was seen more frequently than increased. (2) Effects are observed with all compounds on some erythrocyte preparation at every concentration tested (10(-5), 10(-7), 10(-9), 10(-11) M). (3) Where epinephrine showed significant positive effect, PGA2 and PGE2 did also when tested. The reverse was not always true. (4) For PGA and PGE analogs, the subscript 2 analogs affected filterability more frequently. (5) When significant average effects for a group of donors were produced by a given compound at a particular concentration, these effects were positive for the donors studied.
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PMID:Examination of the filterability of oxygenated erythrocytes (containing normal, trait or sickle cell disease type hemoglobins) in the presence of L-epinephrine, D,L-isoproterenol or prostaglandins (PG) A1, A2, E1, E2, F1alpha or F2alpha. 84 33

It is recognized that the lung extracts norepinephrine and 5-hydroxytryptamine from the pulmonary circulation and that this process is affected by cardiopulmonary bypass. Since alterations in the lung's processing of vasoactive substances may be a mechanism of pulmonary injury sustained during operation, we investigated the lung's ability to extract or metabolize prostaglandin A1 (ga1) and prostaglandin E1 (PGE 1). Sixteen patients undergoing cardiac surgery were studied. In five patients, just before going on bypass, a 10 ml of blood was withdrawn at a constant rate, simultaneously from the pulmonary artery and left atrium. In 11 patients, 3H-PGE1 was injected just prior to bypass and, in five of these, again after coming off bypass. Extraction was calculated from tritium activity in the samples. Metabolites were quantitated by thin-layer chromatography after being identified by marker compounds run simultaneously in each chromatogram. The pulmonary extraction of PGA1 was 11.3 +/- 2.3% and there were no detectable metabolites in left atrial blood. Before bypass the extraction of PGE1 was 42.3 +/- 14.3% and after bypass 24.8 +/- 10.0% (P less than 0.005; Student's paired t test). PGE1 was extensively metabolized with 79.7 +/- 7.1% of total radioactivity appearing in the left atrium as metabolites before bypass and 89.1 +/- 2.0% appearing after bypass. This study indicates that PGA(1) is not metabolized by the lung and is only slightly extracted. On the other hand, PGE(1) is extensively extracted and metabolized. While the rate of metabolism is not significantly affected by cardiopulmonary bypass, the extractiom before bypass was significantly greater than after bypass.
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PMID:Fate of prostaglandins E(1) and A(1) in the human pulmonary circulation. 87 Oct 15

This study determined the difference in rate of degradation between pure polymers of lactic acid (pla), glycolic acid (PGA), and various ratios of copolymers of these two substances. Fast-cured and slow-cured polyglycolide was compared with copolymers of glycolide/lactide intermixed in ratios of 75:25, 50:50, and 25:75, as well as pure polylactide. A total of 420 rats were implanted with carbon-14 and tritium-labeled polymers in bone and soft tissue. At intervals of 1, 2, 3, 5, 7, 9, and 11 months, groups of five animals with the implants in bone and five with the implants in the abdominal wall were sacrificed. The implant area as well as tissue from the liver, spleen, kidney, lung and some muscle tissue was analyzed for radioactivity along with the urine and feces collected throughout the experiment. Half-lives of the different polymers and copolymers were calculated from the radioactivity present in the implant area for each time interval. Half-life of the polymers and copolymers decreased from 5 months for 100% PGA to 1 week with 50:50 PGA:PLA copolymer and rapidly increased to 6.1 months for 100% PLA. Fast-cured PGA had a half-life in tissue of 0.85 months. No difference in rate of degradation was seen in soft tissue or bone. No significant radioactivity was detected in urine, feces, or tissue samples. From this study, it is concluded that control of degradation rate of the implant could best be attained by varying the composition of PLA and PGA between 75% and 100% PLA along with a corresponding 25% to 0% PGA. This would provide a half-life range of the implant of from 2 weeks to 6 months.
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PMID:Degradation rates of oral resorbable implants (polylactates and polyglycolates): rate modification with changes in PLA/PGA copolymer ratios. 89 90

We have investigated the uptake and subsequent metabolism of the prostaglandins (PGs) PGE1, PGA1, and PGB1 by rat, guinea pig and rabbit isolated perfused lungs (IPL). Significant species differences were not observed in the uptake or metabolism of any PG on passage through the IPL. However, differences in the uptake of PGA1 and PGB1 and in the metabolism of PGA1 were observed with a given species when the composition of the perfusion medium was varied. The IPL removed minimal amounts (less than 20% of the supply rate) of PGA1, and PGB1 from the circulation when the perfusate contained 4.5% bovine serum albumin (BSA). In the absence of BSA, however, both PGA1 and PGB1 were substantially removed from circulation (approximately 53% of the supply rate) and PGA1 was also metabolized. The composition of the perfusate had no effect on the uptake and metabolism of PGE1 which was always taken up and metabolized to a greater extent than was PGA1 and PGB1. Thus, the apparent species differences previously reported for the pulmonary biotransformation of PGA can result from differences in the perfusion medium used. Our data suggest that both plasma protein binding and a transport system play important roles in determining the selectively of the uptake of PGs by the lung.
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PMID:Uptake and metabolism of prostaglandins by isolated perfused lung: species comparisons and the role of plasma protein binding. 89 17

Plasma prostaglandins were studied by radioimmunoassay on alternate days during the menstrual cycle in fourteen normal women. No cyclic patterns were found for A-like prostaglandins using an assay which measured 13,14-dihydro-PGA. Mean subject values of PGA-like prostaglandin ranged from 367 to 904 pg/ml and varied significantly among women. Prostaglandin E determinations showed an upward trend beginning 8 days before the LH peak. PGE subject means varied significantly and ranged from 182 to 362 pg/ml. Prostaglandin F did not exhibit a cyclic pattern. The average concentration of PGF for individual women ranged from 58 to 153 pg/ml, showing significant variance. The physiologic implications of the results are discussed as well as recommendations for the design of future studies.
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PMID:Plasma prostaglandins in the normal menstrual cycle. 92 52

1. Incubation of rabbit choroid plexus, anterior uvea (iris-ciliary body complex) or slices of kidney cortex in a medium containing tritium-labelled prostaglandin F(2alpha) ([3H]PGF(2alpha) or E1 ([3H]PGE1) results in a four- to thirteenfold concentrative accumulation of 3H activity. 2. Addition of PGF(2alpha, PGF(1) or PGA(1), any one of five PG analogues or a PG precursor, arachidonic acid, at a concentration of 10(-4) M reduced the active accumulation of [3H]PGs by 47-97%. Octanoic acid, at the same concentration, had only a moderate effect on the choroid plexus and no significant inhibitory effect on [3H]PFG(2alpha) accumulation by anterior uvea or kidney cortex. 3. Inhibition was also obtained with 2 mM iodoacetate (under anaerobic conditions) and with 10(-4) M diploretin phosphate, probenecid, iodipamide, indomethacin or dinitrophenol. Perchlorate (10(-4) M) and iodide (10(-4) or 10(-3) M) had no inhibitory effect while 10(-4) M p-aminohippuric acid had a significant inhibitory effect on the kidney cortex at a concentration of 10(-4) M and on the anterior uvea at 10(-3) M. 4. It is concluded that the apparent carrier mediated PG transport systems of the choroid plexus, anterior uvea and kidney cortex are not related to the iodide transport system, but may represent a subcomponent of the iodipamide transport system of these tissues. 5. These results suggest that the systemic distribution and the rate of renal excretion of PGs could be altered by high concentrations of PGs, pharmacologically less active PG analogues, some inhibitors of organic acid transport, and by some inhibitors of PG synthesis and PG action.
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PMID:Inhibition of in vitro concentrative prostaglandin accumulation by prostaglandins, prostaglandin analogues and by some inhibitors of organic anion transport. 93 72

The binding of tritiated prostaglandins (PGA1, PGE1, PGF2alpha, and PGE2) to human and bovine serum albumins was studied by equilibrium dialysis and batchwise gel equilibration with Sephadex G-25. During equilibrium dialysis (36 hours, 4 degrees C), about half of the PGEs, but not PGA and PGF2alpha, were transformed into dehydration products; by contrast, equilibration of the prostaglandins was attained in less than a half-hour by the batchwise use of Sephadex G-25 at 25 degrees C, with no detectable ligand instability. The values of the apparent association constants for albumin-prostaglandin interactions were inversely related to the protein concentration in the assay systems. "True" apparent association constants (NKo) were measured by extrapolation to zero protein concentration. The NKo values were estimated to be 9.4 X 10(4), 2.7 X 10(4), 9 X 10(3) and 6 X 10(3) M-1 for the interaction of human serum albumin with PGA1, PGE1, PGF2alpha and PGE2, respectively. Very similar values were found for the corresponding bovine serum albumin-Prostaglandin interactions. When comparable, the data obtained by both methods were in excellent agreement. Our results were also in agreement with published values for PGA1 and PGF2alpha, both of which are relatively stable in neutral aqueous phase. Batchwise gel equilibration appears to be a useful method, if thermodynamically valid data are desired in the presence of possible ligand and/or "receptor" instability. We conclude that albumin binding probably affords circulating PGA1 a modest protection from its clearance mechanisms.
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PMID:Prostaglandin-macromolecule interactions. I. Noncovalent binding of prostaglandins A1, E1, F2alpha, and E2 by human and bovine serum albumins. 94 73

The effect of angiotensin II on peripheral levels of immunoreactive prostaglandin A2 (IR-PGA) was determined in 17 normal male volunteers. IR-PGA rose from 338 +/-65 (SE) pg/ml to 635+/-142 in response to pressor infusions of angiotensin II (p less than 0.05 on paired analysis). This increase was not observed when indomethacin, 75 mg p.o., was given to 8 patients two hours prior to a repeat infusion. Five patients of the original group were placed on a low sodium diet (10-20 mEg). The response to angiotensin was now exaggerated (278+/-52 pg/ml to 916+/-284). These five patients were kept on a low sodium intake and given indomethacin 50 mg p.o. g 6 hourly for 4 days. There was no significant rise with angiotensin infusion (106+/-31 pg/ml to 120+/-70). Pressor infusions of angiotensin II raise peripheral levels of IR-PGA, and this response is exaggerated by a low sodium diet and blocked by either acute or chronic indomethacin administration. This data supports the concept that vasodilatory prostaglandins may be released by endogenous angiotensin and thus provide a dynamic antagonism to the renin angiotensin system in man.
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PMID:The effect of angiotensin II and indomethacin on immunoreactive prostaglandin "A" levels in man. 94 20

Venous prostaglandins A, E, and F were determined by radioimmunoassay in 10 dogs before and one hour after administration of sodium pentobarbital (35 mg/Kg, iv). In the conscious state, PGA was 0.34 + 0.04 ng/ml (mean +/- SE), PGE 0.20 + 0.01 ng/ml, and PGF 0.25 + 0.03 ng/ml. During pentobarbital anesthesia, these levels were unchanged (p greater than 0.05). Thus, pentobarbital anesthesia had no effect on peripheral venous prostaglandin levels.
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PMID:Pentobarbital anesthesia: lack of effect on venous prostaglandins in dogs. 94 22

The effects of PGA1, PGA2 and PGB1 on the vasculature of the liver and small intestine were studied in 73 dogs. Infusions were made into a branch of the superior mesenteric artery, the hepatic artery, portal vein or femoral vein. They decreased systemic arterial pressure and dilated the hepatic arterial and prehepatic splanchnic (small intestinal) vascular beds, PGA being most active. Dilator response was not decreased by beta-adrenergic blockade. Compounds appear to be inactivated by liver and decreased systemic pressure less when infused directly into liver circulation. Dilator response was transient, particulary in small intestine, and abated or even converted to constriction when infusion was continued for a period of time. Intrahepatic portal venous vasculature appeared to be constricted by PGA.
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PMID:Splanchnic vascular responses to the infusion of prostaglandins A1, A2 and B1. 95 18


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