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Biomedical subjects

F Varga

Publications and source records attributed to F Varga.

At least 73 records · Page 4Linked to original sources

Hormonal control of sodium content in human milk.

The possible role of prolactin (PRL) and aldosterone (Aldo) in regulation of Na content of human milk was investigated. Simultaneous determinations of Na and K in milk, PRL and Aldo in maternal plasma and milk were performed on postpartum days 2, 4 and 6, in samples from 15 mothers giving birth at term and from 8 mothers giving preterm birth. Na concentration and Na/K ratio in milk, Aldo concentration in milk and maternal plasma decreased significantly with advancing lactation. In preterm plasma and milk PRL concentration remained unchanged, whereas in term plasma PRL decreased, milk PRL increased significantly by the 6th day post partum. After preterm delivery milk Na and K levels were significantly higher, maternal plasma and milk Aldo slightly lower than after delivery at term. Daily Aldo and PRL excretion into the milk markedly increased during lactation irrespective of the length of gestation and showed a significant negative correlation with milk Na level and Na/K ratio. It is suggested that the increasing rate of Aldo and PRL excretion into the milk may be of importance in the regulation of Na concentration in human milk.

Adolescent↗

Effect of bile acids on the biliary excretion of amaranth and the respiration of liver mitochondria.

The effects of lithocholic acid (LCA), chenodeoxycholic acid (CDCA), deoxycholic acid (DOCA), cholic acid (CA) and dehydrocholic acid (DHCA) on the biliary excretion of amaranth (AM) in rats and on the respiration of isolated liver mitochondria were investigated. Bile acids diminished the biliary excretion of AM, and in vitro they enhanced the state 4 mitochondrial respiration and inhibited DNP- and ADP-stimulated oxygen consumption. The ID50 values (mumol/kg i.v.) and I50 concentrations (X 10(-5) M) of the bile acids for inhibiting AM excretion and ADP-stimulated mitochondrial respiration, respectively, were as follows: for LCA 16 and 3.3, for CDCA 160 and 24, for DOCA 230 and 31, for CA 680 and 105, and for DHCA 700 and 260. LCA, CDCA and DOCA inhibited the biliary excretion of AM uncompetitively. It is concluded that the toxic effect of LCA, CDCA and DOCA on mitochondria might play a role in their inhibitory action on the biliary transport of AM.

Amaranth Dye↗

Activity of the renin-angiotensin-aldosterone system in full-term newborn infants during the first week of life.

A study was performed in 7 healthy full-term newborn infants with mean birth weight of 3130 g (range, 2650-2850 g) and a mean gestational age of 38.8 weeks (range, 37-41 weeks) to investigate the postnatal changes of plasma renin activity (PRA), plasma aldosterone concentration (PA) and urinary aldosterone excretion (UAE) in relation to electrolyte balance. PRA, PA and UAE fell significantly from their initially high values of 28.36 +/- 3.6 ng/ml/hr 1.5 +/- 3 ng/ml and 7.1 +/- 1.9 microgram/day on the first day to 6.84 +/- 2.9 ng/ml/hr (p less than 0.01), 0.71 +/- 0.1 ng/ml (p less than 0.01) and 5.5 +/- 1.6 microgram/day (p less than 0.05), respectively, on the 5th day. No significant correlation was found between either PRA and PA or PA and UAE. PRA and UAE showed a significant negative correlation with dietary sodium intake, the other parameters of sodium and potassium homeostasis, however, had no apparent influence on the activity of RAAS. The initial high level and the rapid postnatal decline in RAAS activity has been attributed to perinatal stress imposed by labour and delivery and not to the changes in sodium or potassium balance in the early days of life.

Aldosterone↗

The influence of bile acids on biliary excretion of indocyanine green in rats of different ages.

In rats of different ages bile flow and biliary excretion of indocyanine green (ICG) were estimated in dependence on bile acid excretion. In 20, 30, 60 and 180 day old rats bile acid excretion was diminished to a quarter of the control by pretreatment with cholestyramine (1.5 g/kg b.wt.). To enhance bile acid excretion, taurocholate sodium (TC, 50 mg/kg b.wt.) was given together with the dye. Bile acid depletion diminished the bile flow to a greater extent in young rats, which were found to have a higher bile acid dependent fraction of canalicular bile flow (60%) compared to 60 (35%) and 180 day old rats (20%). After bile acid depletion the decrease in ICG excretion was more pronounced in 30 and 60 day old rats which exhibit highest dye excretion rates. TC was able to enhance the bile flow in all age groups investigated, however, the ICG excretion was enhanced only in adult animals. Our results indicate that the bile acid dependence of the hepatobiliary transport of ICG is influenced by age.

Age Factors↗

Effect of insulin on the biliary excretion of some organic anions in rats.

In rats insulin enhanced the biliary excretion of rose bengal (50 mg/kg) and bromcresol green (25 mg/kg), and raised the depressed bile flow caused by these organic anions. There was, however, no parallelism between the choleretic effect of insulin and the increase in biliary transport of the two dyes.

Animals↗

Effects of barbiturates on the hepatic cytochrome P-450 dependent enzyme system and biliary excretion of exogenous organic anions in rats.

Effect of pretreatment (150 mumol/kg i.p. twice daily for 5 days) wtih six barbiturates (barbital, butobarbital, pentobarbital, amobarbital, phenobarbital and thiopental) on the hepatic microsomal drug methabolizing enzyme system and biliary excretion of bromcresol green and bromsulphthalein-glutathione conjugate has been investigated in rats. All six barburates produced microsomal induction. Phenobarbital, thiopental, barbital and butobarbital increased liver weight, biliary flow and biliary excretion of bromcresol green and bromsulphthalein-glutathione conjugate, however, pentobarbital and amobarbital were ineffective in these parameters. Our results seem to indicate that the enhanced biliary excretion of exogenous anions produced by barbiturates is independent of microsomal enzyme induction.

Animals↗

On the mechanisms of renal sodium handling in newborn infants.

In an attempt to delineate the specific tubular defect in sodium reabsorption in low-birth-weight neonates, fractional sodium excretion (CNa/CCr), distal tubular sodium delivery (CNa+CH2O), and tubular sodium reabsorption [(CH2O/CH2O+CNa) X 100] were determined in 8 healthy premature and 10 full-term newborn infants. The mean birth weight was 1,701 g (range: 1,240--2,120 g) and the mean gestational age was 32.6 weeks (range: 28--35 weeks) for premature; and 3,199 g (range: 2,670--3,670 g) and 38.9 weeks (range: 38--41 weeks) for full-term neonates. It was demonstrated that the significantly higher fractional sodium excretion in premature infants (1.44 +/- 0.33 SE versus 0.36 +/- 0.09%), p less than 0.01) resulted from significantly decreased proximal (CNa+CH2O : 0.674 +/- 0.105 versus 0.360 +/- 0.069 ml/min/1.73m2, p less than 0.05) and distal [(CH2O/CH2O+CNa) X 100:69.9 +/- 3.3 versus 85.8 +/- 3.4%, p less than 0.01] tubular sodium reabsorption.

Blood↗

Postnatal changes in urinary prostaglandin E excretion in premature infants.

Urinary PGE excretion was measured by radioimmunoassay in a group of 11 healthy premature infants with a mean birth weight of 1,502 g (range 1,050--1,950 g) and a mean gestational age of 31.6 weeks (range 29--33 weeks), respectively. Measurements were made on the 7th day of life and at weekly intervals thereafter until the 5th week of life. It was demonstrated that urinary PGE excretion significantly increased from the very low level of 6.23 +/- 0.70 ng/24 h (mean +/- SE) on the 7th day to a value of 17.99 +/- 3.53 ng/24 h by the end of the 3rd week (p less than 0.005). Later on it remained practically unchanged. It is suggested that its rapid increase during the first 3 weeks of life may be the result of the highly elevated activity of the renin-angiotensin-aldosterone system and it may play a role in controlling renal blood flow.

Aging↗

Furosemide-induced alterations in the electrolyte status, the function of renin-angiotensin-aldosterone system, and the urinary excretion of prostaglandins in newborn infants.

To assess the responsiveness of the renin-angiotensin-aldosterone system of the neonate to acute furosemide stimulation and the role of renal prostaglandins in mediating the response of the renin-angiotensin-aldosterone system, this study was carried out to determine simultaneously plasma renin activity, plasma aldosterone concentration, urinary aldosterone, prostaglandin E, and prostaglandin F2 alpha excretion along with determination of plasma electrolyte concentration and urinary electrolyte excretion. Measurements were made on 19 newborn infants with mean birth weight and gestational age of 3009 g (range, 2700 to 4150 g) and 38.7 wk (range, 36 to 41 wk) at the age of 4 to 7 days before and after IM administration of furosemide in a dose of 1 mg/kg. It was demonstrated that in response to furosemide, urine volume (P less than 0.001), urinary sodium (P less than 0.001), potassium (P less than 0.05), and chloride (P less than 0.001) excretion increased significantly. Furosemide administration also resulted in a significant increase from 4.41 +/- 2.00 to 9.70 +/- 2.32 ng/ml/hr (P less than 0.02) in plasma renin activity, from 1.17 +/- 0.22 to 1.68 +/- 0.36 ng/ml (P less than 0.025) in plasma aldosterone, from 0.93 +/- 0.16 to 1.53 +/- 0.35 microgram/12 hr (P less than 0.025) in urinary aldosterone, from 17.53 +/- 3.37 to 23.73 +/- 3.16 ng/12 hr (P less than 0.025) in prostaglandin E, and from 16.48 +/- 4.12 to 26.27 +/- 4.12 ng/12 hr (P less than 0.05) in prostaglandin F2 alpha. It is concluded that the renin-angiotensin-aldosterone system of the neonate responds to acute furosemide challenge in spite of its high baseline activity, and its response may be mediated by increased renal prostaglandin production.

Aldosterone↗

Choleric potencies of some bile acids and their effect on biliary excretion of eosin in the rat.

The effect of bile acids on bile flow and biliary excretion of eosine (80 mg/kg i.v.) has been investigated in anaesthetized (urethane 1.2 g/kg i.p.), bile duct-cannulated female Sprague-Dawley rats weighing 180--220 g. The biliary flow was significantly enhanced by cholic acid, glycocholic acid, taurocholic acid, deoxycholic acid, chenodeoxycholic acid and dehydrocholic acid (each in a dose of 100 mg/kg i.v.). However, it was definitely decreased by lithocholic acid (10o mg/kg i.v.). The biliary excretion of eosine was increased by cholic acid and dehydrocholic acid, whereas it was decreased by chenodeoxycholic acid and lithocholic acid. Deoxycholic acid, glycocholic acid and taurocholic acid had no effect on the biliary excretion rate of eosine. These results suggest that no parallelism exists between the choleretic effect of bile acids and their influence on the biliary excretion of eosin.

Animals↗

Function of the renin-angiotensin-aldosterone system in relation to electrolyte balance in the small-for-date neonate.

To assess the influences of intrauterine growth retardation on the electrolyte status and the activity of renin-angiotensin-aldosterone system of newborn infants, sodium and potassium balance, as well as plasma renin activity, plasma aldosterone concentration and urinary aldosterone excretion were determined simultaneously in a group of healthy growth retarded and healthy normally grown neonates. It was observed that intake, urinary excretion and retention rate of sodium and potassium as well as the plasma sodium and potassium levels were essentially the same in the two groups. Similarly, no significant difference was found in plasma renin activity, plasma aldosterone level and urinary aldosterone excretion between the neonates whose birth weight was small or appropriate for gestational age. It is concluded that intrauterine growth retardation has no significant influence on the electrolyte status and the activity of the renin--angiotensin--aldosterone system, suggesting that in the regulation of these functions gestational factors are mainly involved.

Aldosterone↗

Effect of cholestyramine-induced bile acid depletion on the hepatobiliary transport of cholephilic organic anions in rats.

Four hours after oral administration of cholestyramine (1.0 g/kg) the biliary output of bile acids decreased to 21 per cent of the control value. The biliary excretion of indocyanine green (ICG; 15--60 mumol/kg i.v.), rose bengal (RB; 15--60 mumol/kg i.v.), bromsulphthalein (BSP; 15--60 mumol/kg i.v.), bromcresol green (BCG;15--60 mumol/kg i.v.) and eosine (EO; 30--120 mumol/kg i.v.) was considerably depressed by cholestyramine pretreatment. The extent and duration of the reduction in the biliary excretion of organic anions in response to bile acid depletion were found to increase with their doses. In contrast, the biliary excretion rates of bromsulphthalein-glutathione conjugate (BSP-GSH; 60--240 mumol/kg i.v.) and amaranth (AM; 60--240 mumol/kg i.v.) remained unchanged following bile acid depletion. The hepatic uptake of the cholephilic agents investigated was not affected by bile acid depletion. It is concluded that the biliary excretion rates of ICG, RB, BSP, BCG and EO are dependent on the excretion rates of endogenous bile acids. The hepatic transport rates of BSP-GSH and AM, however, seem to be relatively insensitive to the biliary output of endogenous bile salts.

Animals↗

Comparison of the effects of cholestyramine and aluminium hydroxide on the biliary bile acid excretion in rats. An experimental model for the depletion of bile acids in bile.

Bile flow and biliary excretion of dihydroxy- and trihydroxy-bile acids have been determined in control, cholestyramine (250--2000 mg/kg p.os)- and aluminium hydroxide (250--2000 mg/kg p.os)-pretreated rats. Cholestyramine proved to be a more potent bile acid depleting agent than aluminium hydroxide. The depressing effect of cholestyramine on bile flow was also more significant than that of aluminium hydroxide. Cholestyramine-pretreatment seemed to be a suitable experimental model for the depletion of bile acids in rat bile.

Aluminum Hydroxide↗

Sodium, potassium and aldosterone content of human milk during the first postnatal week.

In an attempt to obtain information about the hormonal control of the sodium content of human milk, simultaneous determinations were performed of the Na, K and aldosterone concentrations in milk samples collected from 6 mothers on the 2nd, 4th and 6th days after delivery. Na concentration (p less than 0.01), Na/K ratio (p less than 0.01) and aldosterone concentration (p less than 0.01) decreased significantly with advancing lactation. The rate of daily aldosterone excretion, however, rose considerably from 4.8 +/- 0.9 ng/day (mean +/- SE) on the 2nd to 12.2 +/- 1.6 ng/day on the 6th day post partum (p less than 0.01). A significant negative correlation was found between daily aldosterone excretion and Na concentration (p less than 0.05), as well as between aldosterone excretion and Na/K ratio (p less than 0.05) in human milk during the first week after delivery. It is suggested that the rate of aldosterone excretion may be of importance in the regulation of the Na concentration in human milk.

Aldosterone↗