Abstract
Cerebral vasomotor reactivity (CVMR; the relationship of cerebral blood flow responses to changes in arterial carbon dioxide (PCO2)) is used to assess cerebral vascular function. CVMR is generally assessed during either steady-state or transient breathe-by-breathe changes in PCO2. In the transient method, a brief period of hyperventilation hypocapnia is often followed by hypercapnic rebreathing to induce a wide range of change in PCO2 to assess the capacity of CVMR. Assessment of CVMR during transient changes in PCO2 has been reported to be about 30% lower than that under steady-state conditions. One possibility for this discrepancy is that cerebral vasoconstriction during hyperventilation immediately before rebreathing may attenuate cerebral vasodilation and thus, CBF responses during the subsequent hypercapnic rebreathing. PURPOSE: To test the hypothesis that CVMR during rebreathing hypercapnia would be blunted when the rebreathing is preceded by a period of hyperventilation. METHODS: End-tidal carbon dioxide (PETCO2), middle cerebral artery blood velocity (CBFV), cerebral vascular conductance (CVCI; CBFV/mean arterial pressure) and CVMR (slope of the linear regression between changes in CBFV and CVCI vs. PETCO2) were assessed in 8 healthy individuals. CVMR was assessed twice, once immediately following a brief period of hyperventilation (hyperventilation for 1 min + rebreathe 4 min) and once during rebreathing only (rebreathe). The trials were counterbalanced and randomized with a minimum of 15 min elapsing between the protocols. RESULTS: The slope of the linear regression for CBFV vs. PETCO2 was reduced during hyperventilation + rebreathe relative to rebreathe only (hyperventilation + rebreathe: 3.16 ± 0.97 % / Torr, R = 0.93 ± 0.05; rebreathe: 5.03 ± 1.11 % / Torr, R = 0.83 ± 0.25; P<0.01). Likewise, the slope of the linear regression for CVCI vs. PETCO2 was reduced during hyperventilation + rebreathe (hyperventilation + rebreathe: 2.58 ± 0.89 % / Torr, R = 0.88 ± 0.09; rebreathe: 4.34 ± 1.07 % / Torr, R = 0.89 ± 0.08; P<0.01). CONCLUSION: These results indicate that hyperventilation induced hypocapnia attenuates the cerebral vasodilatory responses during a subsequent period of rebreathing induced hypercapnia.
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