Abstract
Exposure to hypercapnic hypoxia (asphyxia), but not hyperoxic hypercapnia, results in increased sympathetic activity that persists after exposure. To determine the contribution of CO2 to the post-hypoxia sympathoexcitation, we exposed 12 normal volunteers to hypocapnic and hypercapnic hypoxia (SaO2 ∼ 85%) for 20 min each on different days. We measured plethysmographic forearm blood flow, muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate. MSNA increased during both exposures but remained elevated for 15 min only after asphyxia. Following asphyxia, MAP returned to pre-exposure values, but after hypocapnic hypoxia MAP decreased below baseline for 15 min. There were sustained decreases in heart rate after hypocapnic, but not hypercapnic hypoxia. Forearm vascular resistance (FVR) decreased below baseline during both exposures, reached its highest value above baseline after asphyxia and then declined. After hypocapnic hypoxia FVR rose to baseline after exposure. Hemodynamics are differently altered by hypercapnic relative to hypocapnic 20 min hypoxia, while only hypercapnic hypoxia produces sustained elevation of MSNA during recovery.
