Key result
Ascorbic acid prevents intermittent hypoxia-induced hypertension and oxidative stress in preclinical models.
Why the study?
Oxidative stress is a potential mediator of carotid body chemosensory and cardiorespiratory alterations induced by intermittent hypoxia, but its role and prevention by antioxidants needed investigation.
Does ascorbic acid prevent cardiorespiratory alterations and hypertension induced by intermittent hypoxia in male Sprague-Dawley rats?
Does ascorbic acid prevent cardiorespiratory alterations and hypertension induced by intermittent hypoxia in male Sprague-Dawley rats?
Antioxidant treatment with ascorbic acid prevents intermittent hypoxia-induced hypertension and cardiorespiratory alterations in a rat model, highlighting the role of oxidative stress in sleep apnea-related cardiovascular pathology.
Antioxidant prevented IH-induced hypertension and chemosensory changes in rats; leaves open translation to human OSA.
Intermittent hypoxia, a feature of obstructive sleep apnoea, potentiates ventilatory hypoxic responses, alters heart rate variability and produces hypertension, partially owing to an enhanced carotid body responsiveness to hypoxia. Since oxidative stress is a potential mediator of both chemosensory and cardiorespiratory alterations, we hypothesised that an antioxidant treatment may prevent these alterations. Accordingly, we studied the effects of ascorbic acid (1.25 g.L(-1) drinking water) on plasma lipid peroxidation, nitrotyrosine and inducible nitric oxide synthase (iNOS) immunoreactivity in the carotid body, ventilatory and carotid chemosensory responses to acute hypoxia, heart rate variability and arterial blood pressure in male Sprague-Dawley rats exposed to 5% O(2); 12 episodes.h(-1); 8 h.day(-1) or sham condition for 21 days. Intermittent hypoxia increased plasma lipid peroxidation, nitrotyrosine and iNOS expression in the carotid body, enhanced carotid chemosensory and ventilatory hypoxic responses, modified heart rate variability and produced hypertension. Ascorbic acid prevented the increased plasma lipid peroxidation and nitrotyrosine formation within the carotid body, and the enhanced carotid chemosensory and ventilatory responses to hypoxia, as well as heart rate variability alterations and hypertension. The present results support an essential role for oxidative stress in the generation of carotid body chemosensory potentiation and systemic cardiorespiratory alterations induced by intermittent hypoxia.
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Río et al. (2009) studied Intermittent hypoxia. Ascorbic acid vs. Sham condition was evaluated on Plasma lipid peroxidation, nitrotyrosine and iNOS immunoreactivity, ventilatory and carotid chemosensory responses, heart rate variability, and arterial blood pressure. Ascorbic acid (1.25 g/L) prevented intermittent hypoxia-induced increases in plasma lipid peroxidation, nitrotyrosine formation, enhanced chemosensory responses, and hypertension in rats.
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