acid-phosphatase has been researched along with Acidosis* in 6 studies
6 other study(ies) available for acid-phosphatase and Acidosis
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Automated determination of blood metabolic acidosis, total acid phosphatase, angiotensin converting enzyme, fructosamine and urinary oxalate and citrate on the ABX Pentra 400.
We have adapted automated assays for quantification of pyruvate (PYR), acetoacetate (AA), and betahydroxybutyrate (BOHB) in plasma, total acid phosphatase (TAP), angiotensin converting enzyme (ACE) and fructosamine (FRUCT) in serum, and oxalate (OXAL) and citrate (CIT) in urine that can be performed on the ABX Pentra 400. The aim of this study was to evaluate the analytical performances of these parameters and to compare data obtained in patient samples with those obtained with the Cobas Mira. Within-run and between-run imprecisions ranged from 0.55 to 14.2 and 0.37 to 11.8%, respectively. Correlations with the Cobas Mira showed r2 coefficients ranging from 0.816 to 0.983 and linear regression slopes from 0.706 to 1.087. The ABX Pentra 400 provides precise and accurate measurement for a wide variety of analytes including PYR, AA, BOHB, TAP, ACE, FRUCT in blood samples and OXAL, CIT in urine. Topics: Acid Phosphatase; Acidosis; Blood Chemical Analysis; Citrates; Fructosamine; Humans; Oxalates; Peptidyl-Dipeptidase A | 2007 |
Changes in renal handling of platinum in cisplatinum-treated rats following induction of metabolic acidosis or alkalosis.
Manipulations of metabolic acid-base status were used in an attempt to modify the renal handling and toxicity of the anticancer drug cisplatinum. Rats were orally pretreated with either tap water (TW), ammonium chloride (AC), or sodium bicarbonate (SB) for 3 days prior to intraperitoneal administration of a high cisplatinum dose (7.5 mg/kg b.w.). Urine was collected daily for 4 days between drug dosing and killing of the animals. AC-pretreated rats did not exhibit the characteristic cisplatinum-induced diuresis and were unable to maintain an acid urinary pH following drug administration. AC rats had a significantly lower, and SB rats a significantly higher, urinary excretion of platinum than did TW rats. Platinum excretion was found to be correlated with urinary pH (r = 0.88) and not urinary volume (r = 0.30). The renal concentration of platinum was greater in AC animals than in SB or TW animals, but no significant difference was observed in liver or plasma concentrations between the groups. Both pretreated groups had equal percent of free vs bound platinum. Proteinuria was more severe in AC-pretreated rats, but histologic evidence of renal tubular damage was present in all the three groups. It is concluded that metabolic acidosis can seriously impair the renal handling of high dose cisplatinum but that metabolic alkalosis offers no evident advantages over nonpretreatment. Topics: Acid Phosphatase; Acidosis; Alkalosis; Animals; Cisplatin; Female; Hydrogen-Ion Concentration; Kidney; Platinum; Proteinuria; Rats; Rats, Inbred Strains; Time Factors | 1982 |
Steroid effect on the release of the lysosomal enzyme acid phosphatase in shock.
The effect of corticosteroids on cellular resistance in shock was studied by serial measurement of the serum concentration of the lysosomal enzyme acid phosphatase in untreated and steroid dogs subjected to hemorrhagic, endotoxin and cardiogenic shock. In each shock category, elevation in serum acid phosphatase was significantly less in steroid treated dogs as compared to untreated animals at corresponding time intervals. This difference was most apparent in endotoxin shock, next in hemorrhagic shock and least in cardiogenic shock. Steroid treatment also reduced the serum lactate increment in hemorrhagic and cardiogenic shock and delayed or reduced the onset and severity of the occurring acidosis, an apparent reflection of the ability of steroids to promote increased tissue perfusion. In addition, steroid treatment increased or prolonged survival in all three shock groups. By showing that glucocorticoids affect a reduction in the release of the lysosomal enzyme acid phosphatase during shock, the study offers direct evidence that steroids enhance cellular resistance to shock stress in the dog. Whether this salutary effect is due solely to the ability of steroids to stabilize cellular membranes or is in part secondary to promoting improved tissue hemodynamics could not be established. The interpretation and clinical application of these results must take into account the possibility of a species specific response. Topics: Acid Phosphatase; Acidosis; Animals; Blood Transfusion, Autologous; Cell Membrane Permeability; Coronary Vessels; Endotoxins; Hemoglobinometry; Lactates; Ligation; Lysosomes; Methylprednisolone; Pyruvates; Shock, Cardiogenic; Shock, Hemorrhagic; Shock, Septic; Time Factors | 1974 |
Interpretation of hyperamylasemia in diabetic coma.
Topics: Acid Phosphatase; Acidosis; Amylases; Blood Glucose; Diabetic Coma; Glucuronidase; Hexosaminidases; Humans; Keto Acids; Lipase; Time Factors | 1973 |
Influence of cellular acidosis and altered cation concentrations on shock-induced mitochondrial damage.
Topics: Acid Phosphatase; Acidosis; Adenosine Triphosphatases; Animals; Calcium; Escherichia coli; Hydrogen-Ion Concentration; Lysosomes; Male; Mitochondria, Liver; Oxidoreductases; Potassium; Rats; Shock, Septic; Sodium; Succinates | 1972 |
The pathophysiology of pulmonary fat embolism.
Topics: Acid Phosphatase; Acidosis; Animals; Blood Volume; Capillary Permeability; Cardiac Output; Dogs; Embolism, Fat; Hemoglobins; Hypoxia; Isoenzymes; Lung; Lysosomes; Oils; Oleic Acids; Pulmonary Circulation; Pulmonary Embolism; Respiratory Dead Space; Shock, Hemorrhagic; Ventilation-Perfusion Ratio | 1971 |