PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “BLOOD PHOSPHATES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1999

Crude oil exposure affects air-breathing frequency, blood phosphate levels and ion regulation in an air-breathing teleost fish, Hoplosternum littorale.

Exposure of a facultative air breather, Hoplosternum littorale, to 12.5, 25, and 37.5% of the water soluble fraction (WSF) of Urucu crude oil, resulted in a rapid increase in air-breathing frequency (ABF) sustained over the 45 min period of exposure. Following 4 h exposure to a graded increase in WSF up to 50%, there was no significant affect on haematocrit, or plasma [Na+] and [K+]. Crude oil ingestion resulted in some degree of ion regulatory impairment, however results were variable. A single oral dose of 3.0 ml/kg of Urucu crude elevated net whole body Na+ efflux and resulted in a 7% reduction in plasma [Na+] 72 h following ingestion. A single oral dose of 3.0 ml/kg resulted in a significant net whole body K+ efflux and a reduction in plasma [K+] 24 h after ingestion. No mortalities were observed in any exposure regime in this study. An oral dose of Urucu crude oil at 3.0 ml/kg also resulted in a 24% reduction in ATP:Hb ratio (from 0.206 to 0.157) and a 31% reduction in GTP:Hb ratio (0.455 to 0.315) 24 h following ingestion indicating that these fish may be hypoxemic. Taken together, these results indicate that exposure of H. littorale to Urucu crude oil affects gas exchange and ion regulation.

Animals↗
PubMed1976

[Influence of gynecologic surgery on the blood concentration of adenosine phosphate].

Blood concentrations of ATP, ADP and AMP studied before and immediately after incomplicated gynecologic surgery due to not malignant indications showed the following changes: 1. The initial blood concentration values ranged within the physiological limits and were not therefore essentially influenced by gynecologic diseases. 2. There was a short-term non significant increase of ATP blood concentrations after the operation. 3. After more extensive surgical operations there was a significant short-term decrease of ADP and AMP concentrations that however, approached pre-operation values within 24 hours. 4. The values of ATP/ADP and ATP/AMP coefficients increased significantly after the operation but decreased again within 24 hours. It may be concluded that gynecologic surgery itself as well as attendant circumstances do not induce metabolic changes unfavorably influencing the adenosinephophate system in the blood.

Adenosine Diphosphate↗
PubMedDate not supplied

Changes in red blood cell membrane phosphate concentration during blood bank storage.

The change in red blood cell membrane phosphate concentration of standard CPD whole blood stored in Fenwal blood bags at 4 C was measured daily for two weeks. Membrane phosphate concentrations increased rapidly when stored pH fell to 6.95. At the same time, the rate of K+ leakage from the cells increased, and transport of inorganic phosphate across the membrane decreased. It is concluded that gross uptake of phosphorus by the red blood cell membrane during blood bank storage may be in part responsible for physical changes in the membrane.

Adenosine Triphosphate↗
PubMedDate not supplied

Restoration of blood 2,3-diphosphoglycerate levels in multi-transfused patients: effect of organic and inorganic phosphate.

Blood stored in acid-citrate-dextrose (ACD) shows a progressive decrease in 2,3-diphosphoglycerate (DPG) content. Since the decrease in DPG increases hemoglobin oxygen affinity, which in turn may reduce tissue and venous PO2 and peripheral oxygen delivery, many efforts have been made to preserve or restore DPG levels in stored blood. An in vivo rejuvenating technique, employing fructose-1,6-diphosphate (FDP) at a mean dosage of 1 mmol kg-1 day-1 of phosphate, to increase the DPG circulating level in multi-transfused patients is proposed. Eighteen patients, who received at least one-third of their estimated blood volume (3990 +/- 480 (SEM) ml of ACD stored blood) in blood transfusion, were treated: nine with inorganic phosphate, and nine with FDP. Basal DPG was very low in both groups: 12.61 +/- 1.34 (SEM) and 10.42 +/- 0.98 (SEM) mumol g-1, respectively (normal value is 14.5 mumol g-1, at pH 7.40). However, DPG values increased significantly and promptly in patients receiving FDP, whereas in cases of inorganic phosphate administration, it was not significantly raised over the basal value until the third day. Phosphatemia remained normal and constant with FDP, but it rose significantly on the third day of treatment with inorganic phosphate. FDP appears to consistently and rapidly increase DPG levels after transfusion with blood stored in ACD, and to be particularly safe.

2,3-Diphosphoglycerate↗
PubMed1984

Biological aspects of amazonian fishes I. Red blood cell phosphates of schooling fishes (genus Semaprochilodus: Prochilodontidae).

Red blood cell soluble phosphates from Semaprochilodus taeniurus, S. insignis and a possible hybrid jaraqui-açu, from Amazon basin, were studied by column chromatography. The Semaprochilodus school and the jaraqui-açu shows an intermediate percentage of total phosphorus content as GTP but not as ATP. GTP/ATP ratio for jaraqui-açu and S. taeniurus were 1.5 and for S. insignis, 3.0.

Adenosine Diphosphate↗
PubMed2007

Erythrocytes store and release sphingosine 1-phosphate in blood.

The blood constituent sphingosine 1-phosphate (S1P) is a specific ligand for five G-protein-coupled receptors designated S1P(1-5). Expression of the S1P1 receptor on lymphocytes is required for their exit from secondary lymphoid organs, suggesting that S1P serves as a stimulus for maintaining lymphocyte circulation in blood. Despite its potential role in immune surveillance, the regulatory system that controls blood S1P levels is not well understood. This report reveals that erythrocytes constitute a buffer system for S1P in blood. They efficiently incorporated and stored S1P, and protected it from cellular degradation. They also released S1P into plasma, but not into other serum-free media, indicating that S1P release was controlled by a plasma factor. Erythrocytes did not generate S1P since an increase in plasma S1P levels was always accompanied by a decrease in cellular S1P levels. Thrombocytes that were reported to generate and release S1P after activation did not contribute to the observed S1P release in blood. The amount of erythrocytes as well as the proportion of plasma in the medium determined the magnitude of S1P release. Adoptively transferred S1P-loaded and unloaded mouse erythrocytes displayed a normal life span and similar S1P levels 24 h after recovery, indicating that S1P incorporation and release are dynamically regulated in vivo.

Adoptive Transfer↗
PubMed1975

Enzymatic determination of carbamyl phosphate in blood.

A specific assay for determination of carbamyl phosphate (carbamyl P) in blood has been developed using the enzymatic conversion of carbamyl P to citrulline by ornithine carbamyl transferase (OCT). This assay, for evaluation of bioavailability of carbamyl P, is necessary for study of the in vivo and in vitro effects of carbamyl P as an antisickling agent. The recovery of carbamyl P as citrulline was 88 to 92 per cent. Carbamyl P in whole dog blood in vitro decomposed with first-order kinetics with a t-1/2 of 42 minutes, the same as the t-1/2 reported for decomposition of carbamyl P to cyanate in buffers at physiologic temperature and pH. When carbamyl P (190 mg. per kilogram) was injected intraperitoneally into mice, it appeared in the blood, with a maximum concentration of 0.2 mM observed between 1 and 5 minutes after injection, followed by a rapid decrease within 10 minutes. The clearance of carbamyl P from dog blood after intravenous injection was first-order, with a t-1/2 of approximately 2.2 minutes. The rapid disappearance of carbamyl P in vivo may possibly by explained by the action of tissue acyl phosphatases which have been reported to hydrolyze carbamyl P.

Animals↗