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Effect of parathyroid hormone on total phosphate and inorganic phosphate in blood, plasma, and urine of domestic fowl.

Previous work has shown that parathyroid hormone causes the kidneys of domestic fowl to secrete inorganic phosphate (Pi) into the urine. Secreted Pi is not derived directly from plasma Pi. The objective of the present study was to determine if direct or indirect correlations exist between the urinary Pi excretion rate and the concentration of phosphate in plasma or whole blood. Parathyroid hormone dissolved in gelatin carrier vehicle was injected into immature domestic fowl to cause net renal Pi secretion. Control birds were injected with carrier vehicle alone, resulting in net Pi reabsorption. Urine, plasma, and whole blood samples obtained during net Pi secretion were compared with samples obtained during net Pi reabsorption. Each sample was assayed for total and inorganic phosphate. Neither time course nor point by point comparisons of individual samples provided any evidence that secreted Pi is derived from organic phosphate in plasma or whole blood. These experiments suggest that phosphate pools within the kidneys may serve as a source for the Pi that is secreted in response to parathyroid hormone.

Animals↗

Platelet concentrates stored in plasma for 72 hours at 22 degrees C prepared from buffycoats of citrate-phosphate-dextrose blood collected in a quadruple-bag saline-adenine-glucose-mannitol system.

A method is described to prepare platelet concentrates from the buffycoat of citrate-phosphate-dextrose (CPD) blood in a closed four-bag system and to store the platelets in autologous plasma under sterile conditions. After separation of the blood into plasma, buffycoat and leukocyte- and thrombocyte-poor red cell concentrate, saline-adenine-glucose-mannitol (SAGM) was added to the red cells. Next the platelets were concentrated in plasma by a second centrifugation and were transferred to the 600-ml bag that previously contained the SAGM. The platelets were stored for 72 h at 22 degrees C on a platform rotator at 1 cycle per second. The mean volume of the platelet concentrates (n = 12) was 61 ml, with an average platelet content of 72 X 10(9). The mean leukocyte contamination was only 17 X 10(6); erythrocytes were not detected. The aggregation of the platelets with 1 microM of ADP was normal. After 72 h of storage, the mean pH was 7.1 +/- 0.1. The PO2 always remained above 17 mm Hg. No loss of thrombocytes had occurred during storage. The platelets had retained their discoid shape. The aggregation response to ADP had disappeared, however. The in vivo viability of the platelets was determined in 8 healthy volunteers. Autologous platelets, stored for 72 h at 22 degrees C, were labeled with 51 Cr and reinfused [43 (+/- 9)% recovery at 15 min after reinfusion]. The mean survival time in vivo of the platelets was 6.8 (+/- 0.7) days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine↗

Estimation of galactose-1-phosphate in blood spotted on filter paper.

A method is described for the enzymic estimation of galactose-1-phosphate (Gal-1-P) in blood which has been applied to filter paper and allowed to dry. The successful clinical management of patients with galactosemia depends upon exclusion of galactose from their diet. Earlier studies demonstrated that red cell Gal-1-P is a sensitive indicator of exposure of such patients to galactose. These earlier methods, however, required venipuncture, preparation of washed, packed red cells, and shipment of the sample in dry ice to a central laboratory. With the present method, capillary blood can be drawn by a nonphysician, applied to filter paper and mailed in a conventional envelope at ambient temperature. From this sample, the Gal-1-P content of the red cells can be determined, if the hematocrit is known. These conveniences should allow estimates of Gal-1-P at a frequency more appropirate for optimal dietary control.

Child↗

Changes in pyridoxal phosphate and pyridoxamine phosphate in blood, liver and brain in the pregnant mouse.

A decrease in plasma pyridoxal-5'-phosphate (PLP) occurs during pregnancy in humans and experimental animals for reasons that are not known. To determine if mice also develop decreased plasma PLP concentrations during pregnancy, and if plasma PLP levels in pregnancy reflect tissue levels of PLP and pyridoxamine-5'-phosphate (PMP), we measured PLP concentrations in plasma, erythrocytes and whole blood, and liver and brain PLP and PMP in control and pregnant mice. Mice were fed a nonpurified diet containing 8.13 mg pyridoxine-HCl/kg. The PLP analyses were performed in our newly developed apotryptophanase method in which the substrate S-benzyl-L-cysteine is hydrolyzed to benzyl mercaptan, reacted with Ellman's reagent and measured spectrophotometrically. During pregnancy, plasma PLP levels decreased 50% below control levels, but erythrocyte and whole blood PLP levels increased 2.9- and 1.6-fold, respectively. Liver PLP and PMP decreased 25%, in parallel with plasma PLP, but brain PLP and PMP concentrations were unchanged during pregnancy. These results suggest that metabolism or utilization of vitamin B-6 is altered in pregnancy, and that plasma PLP concentrations alone may not be a good indicator of nutritional status in pregnancy.

Animals↗

NMR determination of myocardial pH in vivo: separation of tissue inorganic phosphate from blood 2,3-DPG.

Phosphorus NMR can measure myocardial tissue pH from the chemical shift of inorganic phosphate (Pi) in isolated buffer-perfused hearts, but in vivo the Pi peak originating from the myocardium is obscured by the resonance of 2,3-diphosphoglycerate (DPG) in the blood, making pH difficult to determine. Taking advantage of the fact that most of the interfering DPG is within the cardiac chambers and is rapidly flowing out of the sensitive volume of our coil, we developed a pulse sequence which would separate myocardial Pi signal from interfering DPG. We tested this method on a flow phantom and in living rat heart, using exogenous glycerol phosphate as a blood-pool marker. The results indicated that signal from moving and nonmoving substances could be separated, and derived values for myocardial pH and PCr/Pi ratio were consistent with previous estimates. This method should be useful for studying myocardial acid-base physiology with NMR.

2,3-Diphosphoglycerate↗

Sulfonamide inhibition of bone resorption: lack of a hypophosphatemia.

Calcitonin and acetazolamide inhibit bone resorption in the ureter-ligated rat. Calcitonin treatment results in an ensuing hypocalcemia and hypophosphatemia. Although acetazolamide treatment results in a hypocalcemic response similar to that seen with calcitonin, plasma phosphate concentrations increase or remain unchanged after drug treatment. Data are presented indicating that acetazolamide exhibits two effects that influence blood phosphate. Drug treatment of ureter-ligated rats results in an inhibition of bone resorption which tends to lower blood phosphate concentrations. However, this effect is masked by a drug-induced hypercapnia which results in an increase in plasma phosphate concentrations. Elevation of blood pCO2 also attenuates the hypophosphatemic response to calcitonin.

Acetazolamide↗

Role of erythrocyte organic phosphates in blood oxygen transport in anemic quail.

The effects of two different degrees of experimentally induced anemia and the consequent high percentage of circulating immature erythrocytes on oxygen affinity (pH 7.5 and 41 degrees C), erythrocyte organic phosphates, and Hb fractions have been studied in quail. Blood reticulocytes reached percentages of 24 and 69-87% in the first and second experiments, respectively. Variations in the phosphate levels found during the anemic process were related to the amount of circulating reticulocytes. The erythrocyte [ATP] (brackets indicate concentration) and [ATP]/[Hb] molar ratio increased with the release of reticulocytes and returned to control levels as they matured. The erythrocyte [inositol pentakisphosphate (InsP5)] decreased significantly when circulating reticulocytes showed their highest values, whereas there was hardly any effect on the [InsP5]/[Hb] molar ratio, which changed only slightly. Hb-O2 affinity also exhibited no statistical changes associated with acute anemia. These latter findings indicate that InsP5, at physiological concentrations, is the primary modulator of quail Hb function; the observed rise in [ATP] has no additional influence on Hb-O2 affinity. It is suggested that InsP5 tends to maintain the blood oxygen affinity in both mature erythrocytes and reticulocytes. The main compensatory response at blood level is a rapid bulk reticulocyte release from medulla.

Adenosine Triphosphate↗

Removal of excess inorganic phosphate by haemoperfusion with composite beads.

New composite beads, made by encapsulating hydrous zirconium oxide powder in agarose, are evaluated in vitro and in vivo for the removal of inorganic phosphate from the blood. Phosphate adsorption is rather good and calcium removal can be controlled. Thus, a 250 to 300 ml column is capable of reducing phosphate plasma level by some 5 mg per cent, thus making it attractive for the treatment of acute renal failure. Biocompatibility tests showed that supplementing the standard heparinization procedure by adding some citrate, as ACD, to the extracorporeal circuit greatly improves platelet and leucocyte count. No adverse haemodynamic effects were noted in repeated haemoperfusions of five dogs.

Acute Kidney Injury↗

[Experimental study in treating chronic renal failure with dry extract and tannins of herba ephedra].

The effects of dry extract and tannin of Herba Ephedra on adenine-induced chronic renal failure in rats and their mechanisms of action have been studied. Dry extract of Herba Ephedra in dose of 10 mg, 20 mg and 30 mg/d with adenine (for 24 days) were administered to rats. After inducing renal failure (34 days), it reduced toxins in blood significantly. The action of 30 mg-dose was highly significant, BUN decreased by 37%, creatinine (Cr) 35%, methylguanidine (MG) 76%, guanidinosuccinic acid 83%, blood phosphate 39%, while blood calcium raised for 28%. But in 25mg and 45mg-dose, MG in urine decreased by 49%-65%. The mechanisms of action might be including (1) Inhibiting the production of Cr; (2) Inhibiting the production of hydroxyl free radical, blocking the conversion of Cr into creatol, thereby reducing, the production of MG from creatol. In conclusion, dry extract of Herba ephedra could improve renal function in adenine-induced chronic renal failure in rats, correct Ca and P disorder, and especially inhibit the production of MG. Fraction 2 and fraction 3 of Ephedra tannin had no effect on this renal failure model.

Adenine↗

Creatine phosphate in rat blood platelets.

Creatine phosphate (CP) was found in rat platelets by an assay method devised to increase the specificity and sensitivity. In this method, radioactivity of [14C]ATP was measured after the reaction of CP with [14C]ADP in the presence of creatine kinase. The mean value of the CP content in rat platelets was 24.8 nmoles per 10(9) platelets. Since the molar ratio of CP and ATP was 1:2.6, it is probable that CP plays a role in the energy metabolism of rat platelets.

Adenosine Diphosphate↗