PubMed Health⌕ Search

Biomedical subjects

F Escrivá

Publications and source records attributed to F Escrivá.

26 records · Page 2Linked to original sources
PubMed1984

Evidence that hepatic mitochondrial mass decreases during the first sixteen hours following birth in starved newborn rats.

Fatty acid oxidation increases in newborn rats between 0 and 16 h after birth. We have tested the hypothesis that such a rise might be due to an increase in hepatic mitochondrial mass. The ratio total activity/specific activity for cytochrome c oxidase and citrate synthase was used as an index that reflected the changes in mitochondrial mass. This ratio was decreased by about 25% 16 h after delivery, indicating that hepatic mitochondrial mass was lower 16 h after birth than at birth in starved rats. We conclude that changes in the mitochondrial mass are not responsible for the increase in liver capacity to oxidize fatty acids.

Animals↗
PubMed1983

Effects of L-thyroxine treatment on pituitary GH content of adult rats with neonatal thyrotoxicosis.

Rats receiving large doses of thyroxine (30 micrograms/5 doses) during their first days of life develop an apparently permanent alteration of the hypothalamus-pituitary-thyroid complex. This neonatal thyrotoxicosis has been called neo-T4 syndrome. A state of permanent but not very severe hypothyroidism seems to be induced, accompanied by a decrease in pituitary GH content at least until day 22. In this work, growth hormone content has been measured by a specific radioimmunoassay in the anterior pituitary of 45 and 78 day old neo-T4 and control (saline-injected) rats. GH content of the adult neo-T4 treated animals was significantly lower than that of the adult controls. Administration of different doses of T4 (1.7 micrograms/100 g body weight/3 doses or 2.5 micrograms/100 g body weight/8 doses, to 70 day old rats, and 5 micrograms/100 g body weight/3 doses to 42 day old rats) to adult neo-T4 rats did not alter these decreased pituitary GH levels. This differs from hypothyroid rats, in which T4 administration has been shown to increase pituitary GH content. A third approach was to thyroidectomize neo-T4 and control rats and administer 5 micrograms T4/100 g body weight, which produced the same increase in pituitary GH in both groups of animals. These results seem to indicate that changes in pituitary GH content of neo-T4 rats are not due to hypothyroidism. Thus, it would appear that treatment with large T4 doses during the early perinatal period not only deranges the hypothalamic-pituitary-thyroid axis but other pituitary functions as well.

Animals↗
PubMed1983

Circulating glucose, insulin and ketone bodies and enzymes of ketone body utilization in brain mitochondria from suckling rats treated with high L-thyroxine doses.

The neo-T4 syndrome was induced by subcutaneous administration of a total dose of (150 micrograms) L-thyroxine (T4) to rats from their first day of live. Neo-T4 animals and their controls were sacrificed at 2, 4, 8, 11, 14, 22 and 25 days of age. A decrease in body weight was observed from the second day of life, and a decrease in brain weight from the eighth day of life in the neo-T4 animals. Blood glucose and plasma insulin levels were decreased from 2nd day through 22nd day of life. Total plasma ketone bodies and beta-OH butyrate levels increased in the neo-T4 animals with respect to controls. until 8th day, although acetoacetate increased only until 4th day. The activity of key enzymes in the ketone bodies utilization pathway (3-hydroxybutyrate dehydrogenase, 3-oxoacid CoA-transferase and acetoacetyl-CoA thiolase) were also measured in the animals brain. We found an activation of 3-hydroxybutyrate dehydrogenase until 11th day and 3-oxoacid CoA-transferase until 14th day, but no change in acetoacetyl CoA-thiolase was observed. Ketone bodies play a key role as energy substrates and precursors of brain lipids during the period of intense growth and myelination of the CNS. Considering the alterations described in this paper it seems that neo-T4 syndrome could be an interesting model for studying metabolism of those substances in brain.

Acetyl-CoA C-Acetyltransferase↗
PubMed1982

[Liver glycogen, blood glucose, somatotropic hormone, and hypophyseal thyrotropin in neonatal rats treated with cortisol and in malnourished ones].

A population of rats treated with a single dose of cortisol on their first day of life and a population of rats underfed since day sixteen of gestation until sacrificed have been studied. Body, brain and liver glycogen content have been measured at eight, twelve and twenty-two days of life and compared to controls of the same age. Pituitary growth hormone and thyrotrophin content have also been measured in the same population of animals and at the same stages of life. Results are compared to those found in "neo-T4" rats -- which receive 30 micrograms T4 in 5 doses during the first days of life -- at the same ages.

Animals↗
PubMed1981

Decrease of blood glucose, liver glycogen, and insulin and changes in glucose tolerance in suckling rats treated neonatally with high L-thyroxine doses.

The neo-T4 syndrome was induced by sc administration of high doses (30 microgram) of L-T4 (T4) during 5 consecutive days in the early postnatal period. Rats were injected starting on the 3rd or 6th day of life. Blood glucose and insulin levels as well as liver glycogen levels were determined between the 5th and 20th days of life. This covers the critical period for brain development (the 7th to 12th day) during which most myelination takes place. Blood glucose and insulin and liver glycogen started to decrease after the second injection of T4 and remained quite low until 2 days after the last injection. Glucose tolerance testing was performed on 8- and 12-day-old neo-T4 rats; treatment was started at 3 days of age. After 70 min of fasting, 200 mg glucose/100 g BW were injected ip. Low plasma insulin levels were found after a glucose load. Plasma ketone bodies were higher in neo-T4 rats than in controls after 4 or 5 days of treatment. The rats appeared to be in a severe catabolic state and were using up their reserves. These alterations in carbohydrate metabolism in suckling rats should be considered when interpreting the brain damage produced by large doses of T4 during the early neonatal period.

Animals↗
PubMed1979

[Long term renal function following acute failure in the newborn (author's transl)].

A long-term follow-up study of 27 survivors of acute renal failure in newborns was performed. A study of the evolution of renal function was possible in 20 cases, with follow-up periods ranging from 15 to 62 months (mean follow-up: 38 months). Renal function was determined by assessing glomerular filtration rate, free-water reabsorption, tubular reabsorption of phosphate and acidification ability. Results show a marked difference, according to the etiology of the acuete renal failure, between the two groups studied: 1) Most of those displaying renal failure following neonatal hipoxia, maintained persistent nephrological sequels. II) Parameters of renal function normalized between 6 and 12 months of age in those in which renal failure was related to hypovolemic shock, caused by hypertonic dehydration. Of the six patients with acute renal failure caused by neonatal hypoxia and shock (group 1), only one displayed normal renal function after 17 months. In the remaining fire patients, glomerular filtration rate continued to decrease even after three years. Three of them displayed urinary acidification disorders. An alteration in free-water reabsorption was found in the majority of the patients in both groups during the first year. This alteration persisted after three years in only four patients of group 1, although in relation to decreased glomerular filtration rate.

Acute Kidney Injury↗
PubMed1975

[Variations in hyperbilirrubinemia in low birth weight newborns under phototherapy and continous or discontinous agar oral administration (author's transl)].

Therapeutic attitude in hyperbilirrubinemia is always worth because other infrequent complications but not for this, less important. Phototherapy innocuousness, largely demonstrated, fosters its profilactic use at beginning and not only for those babies with serum bilirrubin over 10 mg % in the first day of life. Previously we have reported positive results with agar oral administration without collateral effects. On this grounds we have planned the following experience in a homogenous group of L.B.W.: one group was fed with agar previously to each formula administration; other group received the same amount of agar but divided in only three administrations in 24 hours; the last group received continuous phototherapy for 96 hours with a white cold fluorescent light from a source of 8-Vita-lite lamp of 40 watts with a intensity of 500 foot candle and 30 lumens. All of these babies weighed less than 2.500 g. and were between 10 and 90 percentil of Lubschenko diagram. They were fed with the same formula and same time table with no infusions, rejecting all that presented any type of pathology. Obstetric conditions were basically identical. This population was randomly divided in four groups. 1) Control group with no profilaxis, but with identical bilirrubin andhematocrit determinations. 2) Group with continuous agar oral administration, 125 mg. before each of the seven formula feeding. 3) Group with discontinuous agar administration, 250 mg. before three of the seven formula feeding. 4) Group with continuous phototherapy for 96 hours. These is initial identification of the groups with statistic signification, and after that a quantitative and sequential evolution of bilirrubin is analized in each group.

Administration, Oral↗