Key result
Hypoxic and hyperoxic injuries cause selective morphological and functional changes in the nucleus tractus solitarii and carotid body, potentially contributing to Sudden Infant Death Syndrome.
This review highlights the anatomical and functional vulnerability of cardiorespiratory centers to hypoxia and hyperoxia, providing insights into the pathogenesis of Sudden Infant Death Syndrome.
The aim of the present paper is to briefly review the changes occurring in the nucleus tractus solitarii and carotid body in response to hypoxic and hyperoxic injuries. Selective alterations of dendrites and Fos-immunoreactivity of neurons have been observed in the subnucleus gelatinosus of the nucleus tractus solitarii of adult subjects dying after hypoxic-ischaemic injury. The selective vulnerability of this portion of the nucleus tractus solitarii may be explained mainly with reference to the vascularization of medullary tegmentum. In the carotid body, chronic hypoxia and hyperoxia cause a series of morphological, cellular and biochemical changes which may play a major role during the first postnatal period and may have implications in the pathogenesis of Sudden Infant Death Syndrome. Intermittent hypoxia may cause hypersensitivity of the carotid body, possibly increasing the risk of unstable respiration. Conversely, hyperoxia exposure has been reported to cause hyposensitivity and reduction in volume of the carotid body, possibly leading to ineffective response.
No takes yet. Share an insight, caveat, or question.
De et al. (2010) conducted a review in Hypoxic and hyperoxic injuries to cardiorespiratory regulation centers. Hypoxia and hyperoxia was evaluated. Hypoxic and hyperoxic injuries cause selective morphological and functional changes in the nucleus tractus solitarii and carotid body, potentially contributing to Sudden Infant Death Syndrome.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: