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Biomedical subjects

T Ertl

Publications and source records attributed to T Ertl.

At least 55 records · Page 3Linked to original sources
PubMed1984

Noradrenaline content of cerebrospinal fluid in preterm and term infants recovering from perinatal asphyxia.

Noradrenaline content was measured in the cerebrospinal fluid of 17 full-term and 16 premature newborns with or without perinatal asphyxia. Upon the effect of asphyxia the noradrenaline content of cerebrospinal fluid exhibited a more than three-fold increase (from 2.61 +/- 1.45 microgram/l to 10.86 +/- 4.02 micrograms/l) in mature newborns, but it decreased to about half of the control value in premature babies (from 2.39 +/- 0.72 microgram/l to 1.25 +/- 0.70 microgram/l). The observations emphasize the role of central noradrenergic structures in the organization of asphyxia-induced stress-response and in the regulation of adaptation to extrauterine life.

Asphyxia Neonatorum↗
PubMed1983

Postnatal development of plasma prolactin level in premature infants with and without NaCl supplementation.

The role of prolactin in the adaptation of premature infants to the alterations of sodium balance was investigated by measuring plasma prolactin levels serially in 7 low birth weight, premature infants with (group I) and without (group II) NaCl supplementation. The study was performed on the 7th day and weekly thereafter until the 5th week of life. NaCl supplementation was given in a dose of 3-5 mEq/kg/day and 1.5-2.5 mEq/kg/day for 8-21 days and 22-35 days, respectively. It was demonstrated that before NaCl supplementation plasma prolactin concentration was similarly elevated in the two groups (6,490 +/- 1,291 mU/l in group I versus 7,661 +/- 1,094 mU/l in group II), and without supplementation it remained at about the same level throughout the study. When supplemental sodium was given, the plasma prolactin level declined with age at a steady rate to the mean value of 3,516 +/- 502 mU/l by the end of 5th week. In the 3rd-5th weeks it proved to be significantly higher in group II than in group I. It is concluded that physiological sodium depletion may account for the prolonged hyperprolactinemia and prolactin might have some importance in the control of sodium homeostasis in low birth weight, premature infants.

Age Factors↗
PubMed1983

Thyrotropin and prolactin response to thyrotropin-releasing hormone in healthy and asphyxiated full-term neonates.

To evaluate the effect of perinatal asphyxia on the pituitary response to thyrotropin-releasing hormone (TRH) in full-term newborn infants, serum thyrotropin (TSH) and prolactin (PRL) levels were measured before and 30 and 180 min after i.v. administration of 40 micrograms TRH. Birth weight, gestational and postnatal age were similar in the healthy (group NA) and in the asphyxiated (group A) babies. Hormone levels were determined by radioimmunoassay using commercial kits. It was demonstrated that the basal TSH level was slightly higher and the basal PRL level significantly (p less than 0.05) higher in group A than in group NA. In response to TRH administration in group A a marked increase in PRL occurred from 6781 +/- 887 to 11 072 +/- 1318 and 9636 +/- 1024 mU/l at 0, 30 and 180 min, respectively. A similar response was seen in group NA; the values, however, remained significantly lower during the TRH-test. The respective PRL values at 0, 30 and 180 min were 4672 +/- 411, 7945 +/- 343 (p less than 0.05) and 5963 +/- 372 mU/l (p less than 0.05). TRH administration also resulted in a significant elevation of the serum TSH level from 6.20 +/- 1.30 to 49.02 +/- 7.25 (p less than 0.01) and 18.72 +/- 6.35 mU/l (p less than 0.05) in group A, and from 3.90 +/- 0.57 to 24.01 +/- 3.81 (p less than 0.01) mU/l in group NA, but in group NA the 180 min TSH value of 6.07 +/- 1.25 mU/l did not differ statistically from the basal level (p greater than 0.1). It is concluded that the pituitary PRL and TSH reserves are maintained in full-term newborn infants recovering from perinatal asphyxia whose biochemical findings are indicative of subclinical hypothyroidism.

Asphyxia Neonatorum↗
PubMed1982

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1979

Postnatal development of renin-angiotensin-aldosterone system, RAAS, in relation to electrolyte balance in premature infants.

In an attempt to provide information about the role of RAAS in development of late hyponatremia in low-birthweight neonates, simultaneous measurement of plasma renin activity, (PRA), plasma aldosterone concentration (PA), and urinary aldosterone excretion (UAE) was made using RIA methods along with determination of Na and K balance weekly up to the 6th week of life. Seven healthy male infants with mean birthweight of 1580 g, range: 1160-1850 g, and mean gestational age of 31 weeks, range: 30-32 weeks, were selected for the study. Due to the increased urinary Na loss, negative Na balance developed in the first 2 weeks followed positive balance thereafter. PRA, PA, and UAE increased tremendously from the initially high values of 18.2 +/- 4.1 ng/ml/hr, 1.7 +/- 0.5 ng/ml, and 2.6 +/- 0.4 microgram/day, mean and SEM, to their maximum of 78.6 +/- 18.1 ng/ml/hr, p less than 0.01, 6.8 +/- 3.7 ng/ml, p less than 0.05, and 26.4 +/- 2.9 microgram/dayp less than 0.01, in the 3rd week, respectively. Later on, gradual declines occurred, however, PRA, PA, and UAE remained highly elevated even at the 6th week with values of 45.5 +/- 15 ng/ml/hr, 1.6 +/- 0.5 ng/ml, and 14.5 +/- 1.4 microgram/day, respectively. It is suggested that late hyponatremia of premature infants is due to tubular unresponsiveness to aldosterone and not to inadequate response of RAAS to stimulation.

Aldosterone↗
PubMed1979

Urinary excretion of prostaglandin E and F 2 alpha in healthy newborn infants and in infants with hyaline membrane disease.

Urinary PGE and PGF 2 alpha excretion was estimated in 11 healthy full-term (mean birth weight, 3327 g; mean gestational age, 39.2 weeks). 15 healthy preterm (mean birth weight, 1722 g; mean gestational age, 32.1 weeks) and in 9 preterm infants suffering from hyaline membrane disease (HMD) (mean birth weight: 1454 g, mean gestational age: 31 weeks). Measurements were carried out on the 1st, 3rd and 5th days of life by radioimmunoassay, using Clinical Assays Inc. RIA kits. Urinary PGE excretion on the first day of life was 3.76 +/- 0.41 ng/day, 2.43 +/- 0.65 ng/day and 1.19 +/- 0.27 ng/day for healthy full-term, healthy premature and premature infants with HMD, respectively. The differences were significant at the level of p less than 0.05. With advancing postnatal age urinary PGE excretion markedly increased in each group (p less than 0.05). Urinary PGF 2 alpha excretion on the first day was 10.8 +/- 2.0 ng/day in full-term, 6.6 +/- 2.2 ng/day in healthy premature and 4.35 +/- 1.9 ng/day in premature infants with HMD. Then an inconsistent rise could be observed without statistically significant difference between the individual groups of various postnatal age and between the different groups of the same postnatal age. The decreased renal PGE production is suggested to be involved in the pathomechanism of HMD.

Humans↗