Document Detail


On the pulmonary toxicity of oxygen. 4. The thyroid arena.
MedLine Citation:
PMID:  22138105     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Normally developed thyroid function is critical to the transition from fetal to neonatal life with the onset of independent thermoregulation, the most conspicuous of the many ways in which thyroid secretions act throughout the body. A role for thyroid secretions in growth and maturation of the lungs as part of the preparation for the onset of breathing has been recognized for some time but how this contributes to tissue and cell processes and defenses under the duress of respiratory distress has not been well examined. Extensive archival autopsy material was searched for thyroid and adrenal weights, first by gestational age, and then for changes during the first hours after birth as ratios to body weight. After a gestational age of 22weeks the fetal thyroid and adrenal glands at autopsy in those with hyaline membrane disease are persistently half the size of those in "normal" infants dying with other disorders. When the thyroid is examined shortly after birth it reveals a post natal loss of mass per body weight of similar orders of magnitude which does not occur in the control group. A clinical sample of premature infants with (12) and without (14) hyaline membrane disease was tested for T(4), TSH, TBG, and total serum protein. The results also demonstrate a special subset with lower birth weights at the same gestational age, and lower serum T(4) and total serum protein. Ventilatory distress in newborn rabbits was induced by bilateral cervical vagotomy at 24h post natal following earlier injection of thyroxine (T(4)) or thyroid stimulating hormone (TSH) and comparisons were made with untreated animals and by dose. Early life thyroidectomy was performed followed by exposure to either air or 100% oxygen. A final experiment in air was vagotomy after thyroidectomy. Composite analysis of these methods indicates that thyroid factors are both operative and important in the newborn animal with ventilatory distress. This work and the archival data indicate those infants destined to develop hyaline membrane disease through respiratory distress are a distinct developmental and clinical subset with the point of departure from otherwise normal development and maturation in the second or early third trimester. This interval is known to be a period of marked variation in the overview indicators of fetal progress through gestational time. The initiating factor or circumstance which then separates this special subset from normal future development is placed by these observations firmly into the period when human fetal TSH dramatically rises 7-fold (17.5-25.5weeks) followed by a lesser 3 to 4-fold increase in T(4) which is extended into the early third trimester. The earlier part of this interval is characterized by the thyrotrophic action of chorionic gonadotropin (hCG). The possibility that abnormalities in the intrauterine environment secondary to maternal infection play a role within this time frame is indicated by the demonstration that interleukin-2 (IL-2) induces an anterior pituitary release of TSH. Since IL-2 has this property and is not an acute phase cytokine, some form of chronic infection or an immunopathic process seems more likely as a possible active factor in pathogenesis.
Authors:
D Radford Shanklin
Related Documents :
10102245 - Statistical considerations in infant nutrition trials.
8410515 - Infant feeding and idiopathic intussusception.
11787715 - From bioactive substances to research on breast-feeding promotion.
3684395 - Commercial discharge packs and breast-feeding counseling: effects on infant-feeding pra...
6795325 - Skin-surface co2 measurement in sick preterm and term infants.
10785345 - Hormonal correlates of paternal responsiveness in new and expectant fathers.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-11-25
Journal Detail:
Title:  Experimental and molecular pathology     Volume:  -     ISSN:  1096-0945     ISO Abbreviation:  -     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-12-5     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370711     Medline TA:  Exp Mol Pathol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier Inc.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  RXR? deletion and E6E7 oncogene expression are sufficient to induce cervical malignant lesions in vi...
Next Document:  Effects of a peripheral cholinesterase inhibitor on cytokine production and autonomic nervous activi...