HYPERBARIC-OXYGEN TOLERANCE IN NEWBORN MAMMALS HYPOTHESIS ON MECHANISMS AND OUTCOME

Citation
D. Torbati et al., HYPERBARIC-OXYGEN TOLERANCE IN NEWBORN MAMMALS HYPOTHESIS ON MECHANISMS AND OUTCOME, Free radical biology & medicine, 14(6), 1993, pp. 695-703
Citations number
76
Categorie Soggetti
Biology
ISSN journal
08915849
Volume
14
Issue
6
Year of publication
1993
Pages
695 - 703
Database
ISI
SICI code
0891-5849(1993)14:6<695:HTINMH>2.0.ZU;2-V
Abstract
Newborn mammals, compared to adults, are extremely resistant to the CN S effects of hyperbaric oxygenation (HBO) induced by excessive generat ion of reactive oxygen species. This tolerance to HBO may be related t o either physiological responses or the chemical characteristics of th e immature brain, including a low cerebral blood flow and energy metab olism, and a low concentration of polyunsaturated fatty acids. In adul t mammals the main protective mechanism against CNS oxygen toxicity, b esides endogenous antioxidants, is a transient HBO-induced cerebral va soconstriction. How cerebral vasculature reacts to HBO in the immature brain is not known. We present indirect evidence suggesting that HBO in newborn rats induces a persistent cerebral vasoconstriction concurr ently with a severe and maintained reduction in ventilation. It is spe culated that the outcome of these physiologic responses to hyperoxic e xposures may be: (a) extension of tolerance to both CNS and pulmonary oxygen poisoning; (b) creation of a profound hypoxic-ischemic conditio n in vulnerable neural structures; and (c) impairment of the circulato ry and ventilatory responses to hypoxic stimuli on return to air with consequent development of a secondary hypoxic-ischemic condition. Thes e hypothetical pre- and post-HBO events may set the stage for the deve lopment of some delayed neurological disorders, including the retinopa thy of prematurity and the retardation of brain development in fetuses or prematurely-born infants subjected to oxygen therapy.