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T Tulassay

Publications and source records attributed to T Tulassay.

At least 55 records · Page 3Linked to original sources

Postasphyxial reoxygenation reduces the activity of Na+/K+-ATPase in the erythrocytes of newborn piglets.

The aim of our study was to determine whether the impairment of Na+/K+ pump is detectable in erythrocytes during hypoxia and reoxygenation. Acute asphyxia was induced in 10 newborn piglets for 1 h by bilateral pneumothorax. The Na+/K+-ATPase activity, Na+, K+ and ATP content of RBCs were determined in baseline condition (paO2: 60.4 +/- 9.3 mm Hg), at the end of the hypoxic period (1 h) (paO2: 30.2 +/- 10.3 mm Hg), then hourly during the reoxygenation phase (2, 3, 4 h) (paO2: 54.8 +/- 9.0, 56.1 +/- 8.7, 57.2 +/- 9.6 mm Hg). The Na+/K+-ATPase activity was constant during the first 3 h. However, it decreased at 4 h (676 +/- 168 versus baseline 833 +/- 141 U, p < 0.05). The highest ATP content was measured also at this point (4.32 +/- 0.57 versus baseline 3.27 +/- 0.45 mmol/l RBC, p < 0.01). The Na+ content was lower at 1 and 2 h (14.0 +/- 1.8; 13.8 +/- 1.2 versus baseline 15.7 +/- 1.2 mmol/100 g Hb, p < 0.05), but later it became normal. Plasma monovalent cationic levels and intracellular K+ content did not alter during the experiment. Our results indicate that the deterioration of enzyme activity occurs within the same time-frame that previously described morphological alterations in brain tissue develop, so the RBC Na+/K+-ATPase activity might reflect the progress of posthypoxial brain damage.

Adenosine Triphosphate↗

[Mineral content in bones of children with symptomless celiac disease and gluten-free diet].

Osteoporosis is a complication of adult celiac disease. The gluten-free diet improves but does not normalize bone mineral density. Only few and conflicting data are known about the influence of the disease and diet on bone mineralization in children. The aim of this study was to evaluate the radial bone mineral content (BMC) and density (BMD) in children and adolescents who are asymptomatic on gluten-free diet. The BMD and BMC values of non-dominant radius midshaft in ninety-one children (53 girls and 38 boys, mean age: 11.7 years, mean duration of disease: 8.7 years) were determined by single photon absorptiometry. At the diagnosis and at least three years after gluten-free diet, serum calcium, phosphorous and albumin concentrations and alkaline phosphatase activities were determined in all, and additionally intact parathormone concentrations in 16 patients. The mean BMC Z-score value in the entire study population did not differ from the value of normal age-matched population (mean Z-score: -0.27), but in female adolescent group was significantly lower than the normal value (mean Z-score: -1.04, p < 0.01). In contrast, the mean BMC Z-score value was significantly higher than in normal value in girls (mean Z-score: +1.36, p < 0.001), in boys (mean Z-score: +0.53, p < 0.02) as well as in the total patients group (mean Z-score: +1.01, p < 0.001). The diameter of radius midshaft was significantly smaller in all age group than the normal mean value. Serum laboratory parameters of asymptomatic patients were in the normal range. The serum parathormone value in treated patients was significantly lower than in untreated celiac children (mean +/- SD: 3.77 +/- 1.07 versus 7.89 +/- 2.54, p < 0.01), but significantly higher compared to controls (2.89 +/- 0.9, p < 0.05). The data indicate that the gluten-free diet alone is not able to normalize bone mineralization in children. The significant increase of serum parathormone level in treated asymptomatic patients may be explained by the lower calcium content of gluten-free diet. The authors suppose that low calcium supply in children similarly to adult patients can lead to increased parathormone secretion, which can cause the retardation of bone growth even in treated patients with celiac disease.

Adolescent↗

Somatostatin induces vasodilatation in the cat mesenteric artery via endothelium-derived nitric oxide and prostaglandins.

Direct vascular effects of somatostatin (ST) were investigated in cat superior mesenteric artery (SMA) segments in vitro. Changes of outer diameter were measured at constant axial length and perfusion pressure. SMA segments in the resting state were not affected by ST, regardless of endothelial integrity. Noradrenaline-preconstricted SMA segments were dilated concentration-dependently by ST (EC50 10(-13) mol/l). At maximal dilatation (by 10(-11) mol/l ST) the preconstriction was diminished to 45 +/- 9% (P<0.001). Perfusion with Triton X-100, or NG-nitro-L-arginine nearly abolished the ST-induced dilatation, while indomethacin treatment partially suppressed it. We conclude that ST dilates preconstricted cat SMA segments mainly via the endothelial release of nitric oxide, and additionally via prostaglandins.

Animals↗

Renal excretion of endothelin in children.

Endothelin (ET) is a peptide with profound vasoconstrictive potential. First isolated from porcine endothelial cell supernatant, it is produced also by smooth muscle, epithelial and circulating cells. Besides vasoconstriction, a wide spectrum of biological activities of ET (via activation of membrane receptors) has been described. These include regulation of other hormones and neurotransmitters, cellular growth and proliferation, bronchoconstriction, and, in the kidney, natriuresis and water diuresis. ET exerts its effects mainly in an autocrine and paracrine fashion. A high concentration of ET is found in urine, compared with plasma originating mainly from the kidney itself. In this review we focus on the role of urinary excretion of ET in children. ET excretion was determined under different physiological and pathological conditions. In premature infants and newborns, the daily excretion of ET (corrected for body surface) was higher than in older children; it was constant, and comparable to the values in healthy adults after the age of 2 years. Renal ET excretion correlated positively with urine flow in both healthy and sick children. Conditions with tubular and/or collecting duct cell damage, such as severe hypoxia, hemolytic-uremic syndrome, renal transplantation, diabetes mellitus, chronic renal failure, and contrast media cytotoxicity were characterized by elevated urinary excretion of ET. In conclusion, the renal excretion of ET is influenced by several factors, probably reflecting the intrarenal ET production. ET has a low specificity with regard to renal injury.

Adolescent↗

X-linked hypophosphatemia: effects of treatment with recombinant human growth hormone.

The impact of recombinant human growth hormone (rhGH) treatment on growth, bone mineral metabolism, and bone mineral density (BMD) was evaluated in six children (3 girls, 3 boys) with familial hypophosphatemic rickets (XLH). Five were prepubertal (aged 6-8.8 years), one 15.3-year-old boy had combined XLH and GH deficiency, but had not been treated with rhGH previously. rhGH was administered daily for 1 year, at a dose of 1 IU/kg per week, combined with 1,25-dihydroxyvitamin D3 and oral phosphate therapy. Z scores for growth velocity and height improved significantly (-2.9 vs. 2.5, P < 0.01, and -2.2 vs. -1.5, P < 0.01, respectively). However, the ratio of Z score for height to that of subischial leg length decreased significantly (0.65 vs. 0.43, P < 0.01), indicating disproportionate growth in favor of the trunk. The height-corrected BMD Z increased slightly (-0.99 vs. -0.94, P < 0.05). A slight increase in serum phosphate occurred (0.78 vs. 0.88 mmol/l, P < 0.02). Tubular reabsorption of phosphate/glomerular filtration rate increased from 0.45 mmol/l to 0.55 mmol at 6 months (P < 0.02), but returned to the initial level at 12 months. These results indicate that children with XLH can benefit from the positive effect of rhGH on growth, however treatment could aggravate the already existing tendency to disproportionate growth. GH production should be evaluated in poorly growing patients with XLH, because it can mask GH deficiency. rhGH can be safely combined with conventional treatment in XLH. Further studies are needed to determine the effect of treatment on final height and maximal BMD.

Body Height↗

Altered erythrocyte sodium-lithium counter-transport and Na+/K(+)-ATPase activity in cystic fibrosis.

Patients with cystic fibrosis (CF) exhibit normal concentrations of sodium and chloride in spite of the disturbance of Cl- and Na+ transport in epithelial cells. To characterize compensatory mechanisms in the regulation of sodium homeostasis, erythrocytes of 13 CF patients were analysed for sodium-lithium counter-transport (SLC), Na+/K(+)-ATPase activity and intracellular sodium content. Values were compared to those of healthy controls. Patients with CF had normal serum sodium and chloride concentrations and renal excretions of these ions were within the physiological range. Intracellular sodium concentration was similar in the CF and the control group (6.8 +/- 2.2 vs 5.7 +/- 1.0 mmol/l RBCs). Red blood cells' SLC and Na+/ K(+)-ATPase activity were elevated in CF patients (381 +/- 106 mumol/h/l RBCs vs 281 +/- 64; p < 0.01) and (445 +/- 129 mumol ATP mg prot/h vs 322 +/- 84, p < 0.01). Our study demonstrates that transmembrane cation transport systems are highly activated in CF. The increased sodium transport may be part of a compensatory mechanism of sodium homeostasis in children with CF.

Adolescent↗

Direct renovascular effect of somatostatin in the dog.

Recently, effects of somatostatin on the renal function have been described and the vasoactive properties of the peptide were proposed to contribute to this action. However, the available data on its effect in the renal vascular bed are very controversial. Therefore, we investigated the effect of local intaarterial somatostatin boluses in a wide range of doses (5 x 10(-11) - 5 x 10(-5) g) on the renal blood flow (RBF) in anesthetized dogs. RBF was measured by an electromagnetic flow probe. Somatostatin did not influence blood pressure or heart rate. RBF exhibited a significant, dose-dependent fall (ranging from 11.6 +/- 11.9% to 31.9 +/- 17.3%), with a threshold at a dose of 5 x 10(-10) g. These results offer conclusive evidence for the contribution of somatostatin-induced direct renal vasoconstriction to its renal effects, in addition to the demonstrated modulation of other vasoactive systems and tubular functions.

Animals↗

[Effect of dialysis on Na+/K+-ATP-ase activity in uremic children].

The enzyme Na+/K(+)-ATPase plays a central role in the regulation of transmembrane ionic transports. According to previous reports its activity decreased in uremic state. The activity of Na+/K(+)-ATPase in detergent pretreated erythrocytes was studied in seven uremic children prior to and following the hemodialysis (HD) session. Additionally, the level of endogenous digoxin like factors in the plasma (EDLF) was determined. Before the HD session the Na+/K(+)-ATPase activity decreased compared to the control value (mean +/- SD: 2078 +/- 527 vs 3245 +/- 362 nmol P/ml RBC/h, p < 0.01). Following HD it became normal (3366 +/- 952 nmol P/ml RBC/h, n.s.). Prior to the HD the EDLF level was higher, while after the HD no difference was noted from the control value (0.29 +/- 0.04, p < 0.05; 0.24 +/- 0.04 n. s. vs control; 0.21 +/- 0.04 ng/ml). Before the HD blood pressure was significantly elevated compared to the control (117 +/- 20/92 +/- 18 vs 95 +/- 2/64 +/- 2 Hgmm, p < 0.05). By the end of the HD it became normal (100 +/- 14/79 +/- 11, n.s.). Although no correlation was found between the EDLF level and Na+/K(+)-ATPase activity, a positive significant correlation was found between the changes of enzyme activity and the changes in the systolic (r = 0.83, p < 0.05) and diastolic (r = 0.82, p < 0.05) blood pressure during the HD. Our results indicate, that in uremic children the Na+/K+ pump is inhibited by a dialysable, blood-pressure regulator substance and so the enzyme activity elevates following the HD session. However, decreased blood pressure activates counterregulatory mechanisms, which-to lower extent-inhibit the activity of the pump.

Adenosine Triphosphatases↗

[Normal values of calcium and oxalate excretion in children].

Aim of the study was to establish normal values for calcium/creatinine (Ca/cr) and oxalate/creatinine (Ox/cr) ratio in infants and children. Urine probes of 416 healthy children (25 infants aged 1-7 days and 391 children aged 1 month-14.5 years) were analysed. Oxalate was measured by ion-chromatography. Urinary Ca2+/cr was normally distributed, Ox/cr had log-normal distribution. Ca/cr was the lowest in the first days of life, the highest between 7 month-1.5 years (mean +/- SD = 0.39 +/- 0.28 mmol/mmol), a slight decrease could be observed until 14 years (0.34 +/- 0.18). The highest Ox/cr values were measured during the first month of life (geometric mean/range/ = 133 /61-280 mmol/mmol/), followed by gradual decrease until 14 years (25/6-73/). The measurement of Ca2+/cr and Ox/cr in first morning urine samples is suitable for screening of hypercalciuria and hyperoxaluria. The interpretation of the values requires age specific reference values. Both calcium and oxalate determinations should be the part of the evaluation of patients with hematuria, hypercalciuria or nephrolithiasis.

Adolescent↗

Altered Na(+)-K+ ATPase activity in uraemic adolescents.

The Na(+)-K+ ATPase enzyme plays an essential role in the regulation of cell composition and volume. Enzyme activity itself is regulated by substrate availability and several hormones. In adult uraemic patients red blood cell Na(+)-K+ ATPase activity is decreased. However, it is unknown if children with uraemia exhibit the same phenomenon. Therefore, in the present study we examined whether endogenous digoxin-like factors (EDLF) and physicochemical membrane properties play a role in the regulation of erythrocyte Na(+)-K+ ATPase activity in uraemic children and adolescents. Healthy age-matched children were used as controls. Enzyme activity was measured in detergent-pretreated red blood cells and erythrocyte ghosts. Na(+)-K+ ATPase activity (2204 +/- 538 nmol Pi ml erythrocyte-1 h-1 in detergent pretreated erythrocytes; 204 +/- 56 nmol Pi mg protein-1 h-1 in ghosts) in adolescents with uraemia was lower compared to controls (3245 +/- 362 nmol Pi ml erythrocyte-1 h-1; 266 +/- 37 nmol Pi mg protein-1 h-1, p < 0.001, p < 0.05, respectively). Plasma levels of EDLF were elevated in uraemic patients (0.30 +/- 0.05 versus 0.21 +/- 0.04 ng ml-1, p < 0.01). Furthermore, the membrane lipid component was decreased in patients with uraemia, while the cholesterol/phospholipid ratio and membrane fluidity were similar in both groups. No correlation was found between the decrease in Na(+)-K+ ATPase and the increase in EDLF concentration and altered membrane lipid components. Our results demonstrate, that similar to the findings of adults, the activity of Na(+)-K+ ATPase is diminished in uraemic adolescent patients, and that uraemia-associated elevation in EDLF and altered membrane components do not play a role in the down-regulation of Na(+)-K+ ATPase. Therefore other factors (presence of other inhibitors and/or reduced number of enzyme molecules) should contribute to the lower activity of the Na(+)-K+ pump.

Adolescent↗

Elevated urinary excretion of endothelin in insulin-dependent diabetes mellitus: no influence of physical exercise.

The urinary excretion of endothelin was measured by radioimmunoassay in children with diabetes mellitus in metabolically stable condition before and after ergometric exercise. Apparently healthy children served as normal controls. The excretion of endothelin, calculated for 24h and the ratio of endothelin/creatinine in urine were also significantly higher in diabetic children compared to normal controls. Physical exercise had no influence on renal endothelin excretion. In diabetic children the volume of diuresis was higher compared to controls. Physical exercise had no influence on diuresis. In a previous study we found a positive correlation between diureses and endothelin excretion. Therefore, the increased endothelin excretion in the diabetic patients may be at least partially the consequence of the higher diuresis values. It cannot be excluded, however, that it may be a sign of altered renal function as well. Furthermore, the present study suggests that in patients with diabetes mellitus elevated sympathetic nerve activity as a result of physical activity does not influence renal endothelin production.

Adolescent↗

Nitric oxide-dependent opposite effects of somatostatin on arterial and venous caliber in situ.

The vascular effects of somatostatin (ST) and its mechanism of action are not well understood. In the present study, we investigated the direct effects of ST on the vascular tone of rat saphenous artery and vein using videomicroangiometry in situ. ST was administered either in superfusion or in infusion. We found opposite effects in arteries and veins: ST (10(-12)-10(-7) M) dilated the artery (outer diameter increased from 533 +/- 28 to 600 +/- 29 microns, administered in superfusion) and contracted the vein (from 709 +/- 26 to 640 +/- 26 microns and from 775 +/- 30 to 708 +/- 60 microns in superfusion and infusion, respectively). These effects of ST were completely abolished after deendothelization (air bolus maintained for 6 min in vessel lumen) and after local infusion of NG-nitro-L-arginine (L-NNA; 10(-4) M), a nitric oxide (NO) synthesis inhibitor. An NO-dependent basal vasodilator tone in the rat saphenous vein responsible for 10.9 +/- 0.3% of the total vessel diameter was found. After ST administration the venous diameter reduction was similar to that measured after deendothelization or L-NNA. We conclude that ST in situ induces NO release from endothelial cells of rat saphenous artery causing vasodilation, whereas, in contrast, it inhibits the basal NO-dependent vasodilator tone of the saphenous vein inducing vasoconstriction.

Animals↗

Regional differences in nitric oxide-dependent vascular responses to somatostatin.

The mechanisms of the vascular effects of somatostatin (ST) are not well known. This study compares the direct effect of ST in different vascular regions and species. Isolated perfused segments of the cat superior mesenteric artery in vitro did not exhibit a vascular response in the resting state, however, ST-induced vasodilatation was observed with norepinephrine preconstriction. In contrast, ST only slightly dilated superior mesenteric vein segments. In the artery, NG-nitro-L-arginine inhibited both ST and endothelium-dependent nitric oxide (NO) mediated response. No regular dose-response curves were found when ST was applied on the large mesenteric artery in the cat, but rings of small mesenteric artery from both cats and dogs exhibited dose-dependent relaxations. These effects were also NO-dependent. Local application of ST on the rat saphenous artery in situ elicited NO-mediated dose-dependent vasodilatation. However, ST constricted rat saphenous veins in the case of either adventitial or intraluminal application. It is concluded that ST exerts different actions on the arterial and the venous vessel wall. The major response in arteries is endothelium-mediated vasodilatation seen in various species and vascular beds. Large and small arteries respond differently to ST but these differences require further elucidation.

Acetylcholine↗

[Somatostatin plasma level in patients with liver cirrhosis].

The significance of changes in plasma somatostatin level at patients with vascularly decompensated liver cirrhosis was investigated. The plasma level of somatostatin, glucagon, gastrin and blood glucose concentration were determined under basal condition and after testmeal in patients with vasculary decompensated cirrhosis, in cirrhotic-patients without ascites formation and in control subjects. The basaline levels and the postprandial increases of plasma somatostatin concentrations were significantly lower in cirrhotic patients with ascites, compared to the other two groups. The glucagon concentrations--both the basaline and the postprandial--were significantly higher in the cirrhotic patients-groups, compared to the controls. The gastrin and blood glucose levels were not different in the three groups. The decrease in plasma somatostatin concentration present in cirrhosis associated with ascites represents a secondary phenomena, and suggest that endogen somatostatin plays a role in maintaining body fluid homeostasis.

Adult↗