Human ventilatory response to 8 h of euoxic hypercapnia.

Ventilation (VE) rises throughout 40 min of constant elevated end-tidal PCO2 without reaching steady state (S. Khamnei and P. A. Robbins. Respir. Physiol. 81: 117-134, 1990). The present study investigates 8 h of euoxic hypercapnia to determine whether VE reaches steady state within this time. Two protocols were employed: 1) 8-h euoxic hypercapnia (end-tidal PCO2 = 6.5 Torr above prestudy value, end-tidal PO2 = 100 Torr) followed by 8-h poikilocapnic euoxia; and 2) control, where the inspired gas was air. VE was measured over a 5-min period before the experiment and then hourly over a 16-h period. In the hypercapnia protocol, VE had not reached a steady state by the first hour (P < 0.001, analysis of variance), but there were no further significant differences in VE over hours 2-8 (analysis of variance). VE fell promptly on return to eucapnic conditions. We conclude that, whereas there is a component of the VE response to hypercapnia that is slow, there is no progressive rise in VE throughout the 8-h period

Effects of 8h of eucapnic and poikilocapnic hypoxia on middle cerebral artery velocity and heart rate in humans.

This study examines the effects of prolonged hypoxia, with and without control of end-tidal CO2 partial pressure (PET,CO2), on the intensity-weighted mean velocity of blood flow in the middle cerebral artery (VIWM) and on heart rate (HR). Specifically, the time course of the responses, their reversibility with brief periods of hyperoxia and the recovery phase following prolonged hypoxia were all investigated. Twelve subjects were studied, of whom nine provided satisfactory data. A purpose-built chamber was used for the prolonged control of the end-tidal gases, and an end-tidal forcing system was used for generating the brief variations in end-tidal gases. Three 16 h protocols were employed: (1) 8 h eucapnic (average PET,CO2 = 39 mmHg) hypoxia (end-tidal O2 partial pressure, PET,O2 = 55 mmHg) followed by 8 h eucapnic euoxia (PET,O2 = 100 mmHg); (2) 8 h poikilocapnic (average PET,CO2 4 mmHg below eucapnia) hypoxia (PET,O2 = 55 mmHg) followed by 8 h poikilocapnic euoxia (PET,O2 = 100 mmHg); and (3) control (air inspired throughout). VIWM (using Doppler ultrasound) and HR were measured during brief exposures to hypoxic/euoxic and hyperoxic conditions with PET,CO2 held 1-2 mmHg above eucapnia, at 0, 20, 240 and 480 min in the first 8 h, and at the same times in the second 8 h. There were no significant trends in VIWM under hypoxic conditions for either hypoxic protocol (ANOVA) and no significant differences between the three protocols for VIWM in hyperoxia (ANOVA). In contrast to VIWM, there was a significant increase in HR over time during both hypoxic exposures (P &lt; 0.01, ANOVA). HR increased to a similar extent for the two types of hypoxia, and there was some suggestion that HR remained elevated after the relief of hypoxia. The results suggest that, with the level of hypoxia employed, progressive changes in HR occur, but that this level and duration of hypoxia has little sustained effect on VIWM

Time course of the human pulmonary vascular response to 8 hours of isocapnic hypoxia.

To examine the hypothesis that the human pulmonary vascular response to hypoxia has a component with a slow time course, we measured pulmonary vascular resistance (PVR) in six healthy adult males during 8 h of isocapnic hypoxia. A balloon-tipped pulmonary artery catheter with thermistor was introduced via a forearm vein and used to derive PVR. The subjects were seated in a chamber in which the oxygen and carbon dioxide concentrations were adjusted to maintain an end-tidal Po2 of 50 Torr and an end-tidal Pco2 equal to the subject's normal prehypoxic value. PVR was measured before and at 0.5-h intervals during 8 h of hypoxia, the following 3 h of isocapnic euoxia (end-tidal Po2 100 Torr), and a subsequent 1-h reexposure to hypoxia. PVR rose from 1.23 +/- 0.26 (SE) Torr-min.1(-1) under euoxia [time (t) = 0] to 1.77 +/- 0.21 Torr.min.1(-1) at t = 0.5 h, reached a maximum at 2 h (2.91 +/- 0.33 Torr.min.1(-1)), and remained fairly constant between 2 and 8 h. Restoration of euoxia at 8 h led to a reduction in PVR with a slow component. Reexposure to hypoxia at 11 h resulted in a greater increase in PVR than at 1 h. Systemic vascular resistance had a similar slow component to its response, falling from 18.6 +/- 1.3 Torr.min.1(-1) at t = 0 to 17.3 +/- 1.4 Torr.min.1(-1) at t = 0.5 h, 14.4 +/- 0.6 Torr.min.1(-1) at t = 4 h, and 13.8 +/- 0.8 Torr.min.1(-1) at t = 8 h. The human pulmonary and systemic vascular responses to hypoxia extend over at least several hours