PubMed Health⌕ Search

Biomedical subjects

T Tulassay

Publications and source records attributed to T Tulassay.

At least 109 records · Page 6Linked to original sources
PubMed1989

Intra- and extrarenal factors of oedema formation in the nephrotic syndrome.

The role of intra- and extrarenal factors in oedema formation in children with nephrotic syndrome is reviewed. Oedema reflects an abnormal accumulation of fluid within the interstitial tissue. At the capillary level oedema develops when increased lymph flow is no longer effective for the removal of interstitial fluid and the maintenance of intravascular volume. Alterations of intrarenal haemodynamics and tubular sodium reabsorption contribute to sodium retention. Recent studies suggest that during oedema formation reduced effective circulatory volume triggers changes in various hormonal systems, such as renin-angiotensin-aldosterone, noradrenaline, dopamine, vasopressin, prostaglandins and natriuretic factors, which contribute to sodium and water retention. It appears that the release of atrial natriuretic peptide following central volume expansion is responsible for the increased urine flow and natriuresis after intravenous administration of albumin.

Child↗
PubMed1989

Change of serum inorganic phosphate complexes in diabetic ketoacidosis.

The concentrations of serum inorganic phosphate complexes (HPO4(2-), H2PO4-, NaHPO4-, KHPO4-, CaHPO4 and MgHPO4) were studied during diabetic ketoacidosis. On admission to hospital the H2PO4- concentration was significantly increased, in comparison with well-controlled diabetics. After 12-24 h the concentration of all phosphate complexes decreased. At 72 h only the MgHPO4 concentration was decreased. These changes are related to acidosis, insulin therapy and tubular dysfunction.

Adolescent↗
PubMed1988

Effect of low-dose dopamine infusion on urinary prostaglandin E2 excretion in sick, preterm infants.

In pharmacological doses dopamine (DA) will interact with several endocrine systems and both inhibit (prolactin, thyrotropin) and enhance (renin, angiotensin) hormonal release. In this study we have examined whether DA given to preterm neonates will influence prostaglandin (PG) production. The question is of importance since vasodilator PGs play a role in postnatal adaptation. We determined the effect of low dose DA infusion on the 24 h urinary PGE2 excretion rate (an index of renal PGE2 synthesis) in preterm infants. Six preterm neonates, with a 24-h requirement of 2 micrograms/kg per min DA treatment for oedema, moderate oliguria, poor peripheral perfusion and/or mild systemic hypotension were studied on days 2 (Day 1), 3 (Day 2, the day of DA infusion), and 4 (Day 3, DA discontinued) of life. Six preterm infants (control group) that did not require DA infusion were also studied to monitor possible spontaneous changes in the renal PGE2 production on days 2, 3 and 4 of life. In the control group urine output (Uv) and PGE2 excretion rate remained unchanged during the study. In the study group DA administration resulted in nearly two-fold increases in both the Uv (194%) and PGE2 excretion (182%). Urinary PGE2 excretion was, however, closely related to urine flow in both the control infants (Day 1-3) and the study group infants (Day 1-2). Since increased diuresis stimulates renal PGE2 production, our data suggest that the increased PGE2 excretion on Day 2 in the study group was not due to a direct effect of DA on PGE2 synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Dinoprostone↗
PubMed1988

Excretion of primary prostanoids and their metabolites during acute volume expansion.

Simultaneous determination of urinary excretion rates of primary unmetabolized prostanoids and their enzymatic metabolites were performed by gas chromatography-mass spectrometry (GC/MS) or tandem mass spectrometry (GC/MS/MS). Changes in kidney function were induced by acute (4 h) volume expansion. Despite marked changes in urine flow, GFR, urinary pH, osmolality, sodium and potassium excretion, only a insignificant or transient rise in the enzymatic prostanoid metabolites (2,3-dinor-6-keto-PGF1 alpha, PGE-M, 2,3-dinor-TxB2 and 11-dehydro-TxB2) was observed. The excretion rates of the primary prostanoids were elevated in parallel with the rise in urine flow: PGE2 rose (p less than 0.05) from 14.2 +/- 4.0 to 86.2 +/- 20.7, PGF2 alpha from 60.0 +/- 4.9 to 119.8 +/- 24.0, 6-keto-PGF2 alpha from 7.2 +/- 1.3 to 51.5 +/- 17.0, and TxB2 from 11.2 +/- 3.3 to 13.6 +/- 3.6 ng/h/1.73 m2 (means +/- SEM) at the maximal urine flow. Except for 6-keto-PGF1 alpha and TxB2, this rise in urinary prostanoid levels was only transient despite a sustained fourfold elevated urine flow. We conclude that urine flow rate acutely affect urine prostanoid excretion rates, however, over a prolonged period of time these effects are not maintained. The present data support the concept that urinary levels of primary prostanoids mainly reflect renal concentrations whereas those of enzymatic metabolites reflect systemic prostanoid activity. From the excretion pattern of TxB2 one can assume that this prostanoid represents renal as well as systemic TxA2 activity.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Atrial natriuretic peptide in volume expansion-induced natriuresis in man.

The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.

Adult↗
PubMed1988

[Clinical relevance of the determination of plasma atrial natriuretic peptide in children with chronic renal failure].

To investigate whether plasma atrial natriuretic peptide (ANP) is a valuable index to detect fluid expansion in children with endstage renal disease, we studied 34 children and adolescents on regular intermittent hemodialysis or on continuous ambulatory peritoneal dialysis (CAPD). In 22 pediatric patients, plasma ANP was markedly elevated prior to hemodialysis and fell to near normal levels after dialysis (109.9 +/- 80.0 to 39.0 +/- 23.1 fmol/ml, means +/- SD). During removal of fluid excess by 1-h sequential ultrafiltration without dialysis in eight adolescents, plasma ANP fell from 123.8 +/- 97.0 to 45.3 +/- 24.6 fmol/ml. Ultrafiltration was followed by 3 h hemodialysis with fluid removal and ANP decreased further to 29.6 +/- 12.1 fmol/ml. In 12 patients on CAPD, plasma ANP was similar to that in 96 healthy control children (29.3 +/- 28.9 vs 23.9 +/- 11.9 fmol/ml) and did not differ from that in 12 children with advanced chronic renal failure (32.6 +/- 20.1 fmol/ml) and seven successfully transplanted children (32.4 +/- 8.5 fmol/ml). Four patients on hemodialysis (post dialysis), one on patients on hemodialysis (post dialysis), one on CAPD and two with advanced chronic renal failure had definitely elevated ANP levels (greater than 56 fmol/ml = greater than 3 SD mean of controls) indicating fluid volume overload. It is concluded that plasma ANP is elevated in children with chronic renal failure due to volume expansion and that measurement of plasma ANP is a sensitive marker to detect fluid overload in these children.

Adolescent↗
PubMed1988

Alterations of vasoconstrictor and sodium-regulating hormone systems in vascularly decompensated liver cirrhosis.

Plasma levels of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP), and the plasma renin activity (PRA) were examined in 15 vascularly decompensated patients suffering from liver cirrhosis, before and after administration of albumin and after a subsequent administration of furosemide. The initial ANP level was lower in 9 patients (group "A") and higher in 6 patients (group "B") than in healthy controls (Group "A": 19.5 +/- 3.0 fmol/ml; group "B": 36.7 +/- 3.9 fmol/ml; control: 25.8 +/- 2.4 fmol/ml). The initial PRA (4.4 +/- 1.0 ng AngI/ml/h) and AVP (8.5 +/- 1.5 pg/ml) activity in group "A" increased significantly compared to group "B" (PRA: 0.44 +/- 0.09; AVP: 4.1 +/- 0.5), indicating an intravascular volume depletion in group "A". Albumin infusion raised the urine and sodium excretion and the plasma concentration of ANP in group "A" but lowered in plasma levels of renin and vasopressin. The same parameters were not changed by albumin in group "B". Furosemide equally raised the urine flow rate and sodium excretion in both groups. Plasma ANP level depends on the intravascular volume, and the secondary change in its plasma concentration plays a considerable role in the retention of fluid and electrolytes in patients with cirrhosis. The increased intravascular volume in these patients depletes the fluid and electrolyte retention via the increase in ANP level.

Adult↗