The jugular venous-to-arterial P_CO2 difference during rebreathing and end-tidal forcing: Relationship with cerebral perfusion

We examined two assumptions of the modified rebreathing technique for the assessment of the ventilatory central chemoreflex (CCR) and cerebrovascular CO2 reactivity (CVR), hypothesizing: (1) that rebreathing abolishes the gradient between the partial pressures of arterialand brain tissue CO2 [measured via the surrogate jugular venous PCO2 and arterial PCO2 difference (Pjv-aCO2)] and (2) rebreathing eliminates the capacity of CVR to influence the Pjv-aCO2 difference, and thus affect CCR sensitivity. We also evaluated these variables during two separate dynamic end-tidal forcing (ETF) protocols (termed: ETF-1 and ETF-2), another method of assessing CCR sensitivity and CVR. Healthy participants were included in the rebreathing (n = 9), ETF-1 (n = 11) and ETF-2 (n = 10) protocols and underwent radial artery and internal jugular vein (advanced to jugular bulb) catheterization to collect blood samples. Transcranial Doppler ultrasound was used to measure middle cerebral artery blood velocity (MCAv). The Pjv-aCO2 difference was not abolished during rebreathing (6.2 +/- 2.6 mmHg; P < 0.001), ETF-1 (9.3 +/- 1.5 mmHg; P < 0.001) or ETF-2 (8.6 +/- 1.4 mmHg; P < 0.001). The Pjv-aCO2 difference did not change during the rebreathing protocol (-0.1 +/- 1.2 mmHg; P = 0.83), but was reduced during the ETF-1 (-3.9 +/- 1.1 mmHg; P < 0.001) and ETF-2 (-3.4 +/- 1.2 mmHg; P = 0.001) protocols. Overall, increases in MCAv were associated with reductions in the Pjv-aCO2 difference during ETF (-0.095 +/- 0.089mmHg cm(-1) s(-1); P = 0.001) but not during rebreathing (-0.028 +/- 0.045 mmHg center dot cm(-1) center dot s(-1); P = 0.067). These findings suggest that, although the Pjv-aCO2 is not abolished during any chemoreflex assessment technique, hyperoxic hypercapnic rebreathing is probablymore appropriate to assess CCR sensitivity independent of cerebrovascular reactivity to CO2.