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Biomedical subjects

I Varga

Publications and source records attributed to I Varga.

159 records · Page 9Linked to original sources
PubMedDate not supplied

Analysis of maternal circulation and renal function in physiologic pregnancies; parallel examinations of the changes in the cardiac output and the glomerular filtration rate.

OBJECTIVE: The aim of the study was to examine the temporal relations between the parameters of the maternal hemodynamics and homeostasis in different phases of pregnancy and the postpartum period. METHODS: Eleven healthy pregnant women were involved in the study. The value of the peripheric vasodilatation was measured by the ratio I/A of the maternal sphygmogram (I: incisure point, A: amplitude of the carotid pressure curve). The change of the cardiac output was determined by the ejection angle composed from maternal carotid sphygmogram and its first electrical derivate (dP/dT). The glomerular filtration rate (GFR) was measured with the in vitro radiofluorescent method. RESULTS: The primary peripheral vasodilatation and GFR increase occur early in the first trimester of a normal pregnancy, start to decrease at the end of the third trimester, and return to the normal value in the postpartum period. The increase of GFR precedes the increase of cardiac output. The cardiac output increases progressively from the first trimester and starts to decrease in the third trimester of a normal pregnancy. The extracellular volume increases at the beginning of first trimester progressively until the end of pregnancy and returns to the normal value in the postpartum period. DISCUSSION: The increase of GFR and the cardiac output during pregnancy are contributed to volume-establishment and to the cessation of the special "underfilled" condition of the maternal circulation in the normal pregnancy. We suppose that the maximal increase of GFR precedes the maximal increase of the cardiac output because the GFR increase is caused by maximal renal vasodilatation. The increase of cardiac output is caused in the first trimester by the shunt effect of the enhanced renal blood flow of maternal kidneys, and in the second and third trimester by the shunt effect of the feto-placental unit and the shunt effect of the maternal kidneys.

Adolescent↗
PubMedDate not supplied

The predictive value of dermatoglyphic anomalies in the diagnosis of fra(X)-positive Martin-Bell syndrome (MBS)

In a representative group of 160 institutionalized mentally retarded males without Down syndrome, prospective dermatoglyphic-cytogenetic studies were performed in order to assess the utility of the dermatoglyphic index system of Rodewald [1986] for an efficient ascertainment of patients with Martin-Bell syndrome (MBS). A negative (abnormal) score was found in 32 men (20 +/- 3%), 14 of whom (predictive value: 44 +/- 9%) were fra(X)-positive. This prevalence of 14/160 = 9 +/- 2% patients with fra(X)-positive MBS indicates that in our study most, if not all, MBS patients have been detected by the simple pre-screening of dermatoglyphics. In the MBS patients, there was no correlation between the dermatoglyphic scores and percentage of fra(X)-positive cells.

Adult↗
PubMedDate not supplied

Leptin inhibits cortisol and corticosterone secretion in pathologic human adrenocortical cells.

Regulation of adrenal corticosteroid secretion by leptin may involve interactions at multiple levels of the hypothalamic-pituitary-adrenal axis. To investigate the possible direct effects of leptin on corticosteroid secretion of human adrenocortical adenomas, cells from adrenocortical adenomas causing primary aldosteronism (n = 1) and Cushing's syndrome (n = 1), as well as cells from nonhyperfunctioning adrenocortical adenomas (n = 5) were isolated and incubated for 2 h with human recombinant leptin (1-1000 ng/ml) in the presence and absence of adrenocorticotrop hormone (ACTH), then cortisol, corticosterone and aldosterone concentrations in incubating media were determined using radioimmunoassays. It was found that leptin effectively and dose-dependently inhibited basal and ACTH-stimulated cortisol and corticosterone secretion in the three types of human adrenocortical adenoma cells. The inhibiting effect of basal corticosterone secretion was detectable in the presence of leptin concentration as low as 1 ng/ml, with decreases of corticosterone secretion to 34+/-4%, 57+/-11% and 79+/-9% in Cushing's syndrome, primary aldosteronism, and nonhyperfunctioning adrenocortical adenoma cells, respectively. The inhibition of basal cortisol secretion in the presence of low concentration of leptin was less prominent, but 10 ng/ml leptin significantly diminished basal cortisol secretion to 81+/-9% in adrenocortical adenoma cells from Cushing's syndrome, to 68+/-6% in adenoma cells from primary aldosteronism, and to 83+/-8% in cells from nonhyperfunctioning adenomas. The inhibition of ACTH-stimulated cortisol and corticosterone secretion by leptin was similar to those found in cells without ACTH stimulation. By contrast, leptin even at 1000 ng/ml concentration exerted no clear effect on basal and ACTH-stimulated aldosterone secretion in cells from primary aldosteronism and in those nonhyperfunctioning adenoma cells in which aldosterone secretion was detectable. These results indicate that leptin is a potent inhibitor of cortisol and corticosterone secretion in human adenomatous adrenocortical cells. The inhibition of these corticosteroids by leptin may represent a potentially important interaction that exists between leptin and the hypothalamic-pituitary-adrenal axis.

Adenoma↗
PubMedDate not supplied

Influence of the dopamine agonist alpha-dihydroergocryptine on the pharmacokinetics of levodopa in patients with Parkinson's disease.

This study investigated whether chronic coadministration of alpha-dihydroergocryptine (DHEC) altered the plasma pharmacokinetics of individualized treatments with levodopa in 12 patients with Parkinson's disease. Steady-state pharmacokinetics of plasma levodopa (L-Dopa) under combined treatment were compared with those under treatment with L-Dopa alone. There was no evidence of increased exposure to L-Dopa caused by concomitant treatment with DHEC. In contrast, additional treatment with DHEC reduced the overall exposure to L-Dopa (17.5% reduction in area under the curve; 95% CI: 23%-6%). This effect was small but statistically significant for the area under the plasma concentration-time curve, whereas tmax (time of maximum plasma concentration) and peak-to-trough fluctuation were not affected. Cmax (maximum plasma concentration), on average, was reduced to a similar extent (-14.5%; 95% CI: 38% to -17%), albeit not significantly. The magnitude of the interaction does not suggest changing the current clinical practice of up-titrating DHEC and subsequently adapting L-Dopa to the individual needs of patients.

Adult↗