Abstract
BackgroundNewborn mammals suffering from moderate hypoxia during or after birth are able to compensate a transitory lack of oxygen by adapting their vital functions. Exposure to hypoxia leads to an increase in the sympathetic tone causing cardio-respiratory response, peripheral vasoconstriction and vasodilatation in privileged organs like the heart and brain. However, there is only limited information available about the time and intensity changes of the underlying complex processes controlled by the autonomic nervous system.MethodsIn this study an animal model involving seven piglets was used to examine an induced state of circulatory redistribution caused by moderate oxygen deficit. In addition to the main focus on the complex dynamics occurring during sustained normocapnic hypoxia, the development of autonomic regulation after induced reoxygenation had been analysed. For this purpose, we first introduced a new algorithm to prove stationary conditions in short-term time series. Then we investigated a multitude of indices from heart rate and blood pressure variability and from bivariate interactions, also analysing respiration signals, to quantify the complexity of vegetative oscillations influenced by hypoxia.ResultsThe results demonstrated that normocapnic hypoxia causes an initial increase in cardiovascular complexity and variability, which decreases during moderate hypoxia lasting one hour (p < 0.004). After reoxygenation, cardiovascular complexity parameters returned to pre-hypoxic values (p < 0.003), however not respiratory-related complexity parameters.ConclusionsIn conclusion, indices from linear and nonlinear dynamics reflect considerable temporal changes of complexity in autonomous cardio-respiratory regulation due to normocapnic hypoxia shortly after birth. These findings might be suitable for non-invasive clinical monitoring of hypoxia-induced changes of autonomic regulation in newborn humans.
Highlights
Newborn mammals suffering from moderate hypoxia during or after birth are able to compensate a transitory lack of oxygen by adapting their vital functions
The results demonstrated that hypoxic conditions lead to an increase in sympathetic activity which decreases during the hypoxia process
Ongoing normocapnic hypoxia leads to a gradual decrease in cardiovascular variability and complexity
Summary
Newborn mammals suffering from moderate hypoxia during or after birth are able to compensate a transitory lack of oxygen by adapting their vital functions. The majority of newly born humans establish normal respiratory and circulatory function, 1-2% may run into difficulties due to a disturbance to the normal adaptive processes required for a smooth transition from intrauterine to extrauterine life [1] Under such circumstances, sustained systemic hypoxia (for review see [2]) is a common consequence and may lead to fatality or severe lifelong disabilities in case of a progressive lack of oxygen. Moderate systemic hypoxia of a lower degree is compensated by the neonate during a prolonged time period [3] This is due to a well-established and coordinated neuroendocrine response to systemic hypoxia which functions at birth and is controlled mainly by complex autonomic processing. In these studies mainly linear measures from time- and frequency domains [3,6,7,8,9] were applied
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
