Hypoxic control of the development of the surfactant system in the chicken: evidence for physiological heterokairy.

Am J Physiol Regul Integr Comp Physiol

Environmental Biology, School of Earth and Environmental Sciences, University of Adelaide, Adelaide, South Australia 5005, Australia.

Published: August 2004

AI Article Synopsis

  • The surfactant system, essential for lung function and the first breath after birth, consists of lipids and proteins that manage surface tension.
  • Hypoxia, or low oxygen levels, can alter the timing and speed of surfactant development in embryos, allowing them to survive if they hatch early; this phenomenon is known as heterokairy.
  • Experimental results show that hypoxia and glucocorticoid treatment accelerate surfactant lipid maturation, indicating the body's ability to adapt developmentally in response to environmental changes.

Article Abstract

The surfactant system, a complex mixture of lipids and proteins, controls surface tension in the lung and is crucial for the first breath at birth, and thereafter. Heterokairy is defined as plasticity of a developmental process within an individual. Here, we provide experimental evidence for the concept of heterokairy, as hypoxia induces a change in the onset and rate of development of surfactant, probably via endogenous glucocorticoids, to produce individuals capable of surviving early hatching. Chicken eggs were incubated under normoxic (21% O(2)) conditions throughout or under hypoxic (17% O(2)) conditions from day 10 of incubation. Embryos were sampled at days 16, 18, and 20 and also 24 h after hatching. In a second experiment, dexamethasone (Dex), tri-iodothyronine (T(3)), or a combination (Dex + T(3)) was administered 24 and 48 h before each time point. Both hypoxia and Dex accelerated maturation of the surfactant lipids by increasing total phospholipid (PL), disaturated phospholipid (DSP), and cholesterol (Chol) in lavage at days 16 and 18. Maturation of surfactant lipid composition was accelerated, with day 16 %DSP/PL, Chol/DSP, and Chol/PL resembling the ratios of day 20 control animals. The effect of Dex + T(3) was similar to that of Dex alone. Hypoxia increased plasma corticosterone levels at day 16, while plasma T(3) levels were not affected. Hence, exposure to hypoxia during critical developmental windows accelerates surfactant maturation, probably by increasing corticosterone production. This internal modulation of the developmental response to an external stimulus is a demonstration of physiological heterokairy.

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http://dx.doi.org/10.1152/ajpregu.00399.2003DOI Listing

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