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. 2014 Jun 27;2(6):e12059.
doi: 10.14814/phy2.12059. Print 2014 Jun 1.

The effect of hypercapnia on static cerebral autoregulation

Affiliations

The effect of hypercapnia on static cerebral autoregulation

Blake G Perry et al. Physiol Rep. .

Abstract

Hypercapnia impairs cerebrovascular control during rapid changes in blood pressure (BP); however, data concerning the effect of hypercapnia on steady state, nonpharmacological increases in BP is scarce. We recruited fifteen healthy volunteers (mean ± SD: age, 28 ± 6 years; body mass, 77 ± 12 kg) to assess the effect of hypercapnia on cerebrovascular control during steady-state elevations in mean arterial BP (MAP), induced via lower body positive pressure (LBPP). Following 20 min of supine rest, participants completed 5 min of eucapnic 20 and 40 mm Hg LBPP (order randomized) followed by 5 min of hypercapnia (5% CO2 in air) with and without LBPP (order randomized), and each stage was separated by ≥5 min to allow for recovery. Middle cerebral artery blood velocity (MCAv), BP, partial pressure of end-tidal carbon dioxide (PETCO2) and heart rate were recorded and presented as the change from the preceding baseline. No difference in MCAv was apparent between eupcapnic baseline and LBPPs (grouped mean 65 ± 11 cm·s(-1), all P > 0.05), despite the increased MAP with LBPP (Δ6 ± 5 and Δ8 ± 3 mm Hg for 20 and 40 mm Hg, respectively, both P < 0.001 vs. baseline). Conversely, MCAv during the hypercapnic +40 mm Hg stage (Δ31 ± 13 cm·s(-1)) was greater than hypercapnia alone (Δ25 ± 11 cm·s(-1), P = 0.026), due to an increased MAP (Δ14 ± 7 mm Hg, P < 0.001 vs. hypercapnia alone and P = 0.026 vs. hypercapnia +20 mm Hg). As cardiac output and PETCO2 were similar across all hypercapnic stages (all P > 0.05), our findings indicate that hypercapnia impairs static autoregulation, such that higher blood pressures are translated into the cerebral circulation.

Keywords: Cerebral blood flow; hypercapnia; lower body positive pressure; static cerebral autoregulation.

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Figures

Figure 1.
Figure 1.
Experimental protocol. All experiments were conducted in the above order, however, the lower body positive pressure stages were randomized. Baseline and washout periods lasted until all variables had returned to initial baseline levels.
Figure 2.
Figure 2.
Absolute changes from baseline for mean middle cerebral artery blood flow velocity (MCAvmean, A), mean arterial blood pressure (MAP, B) and cerebrovascular conductance (CVC, C). The 0 reference on the y‐axis represents the eucapnic baseline values for each variable. The letters a, b, and c represent the lower body positive pressure levels baseline (no pressure), 20 and 40 mm Hg, respectively. Bolded and underlined letters represent differences between these pressure stages within each CO2 trial (P <0.05). Significant main effect of pressure, P 0.05; *significant main effect of CO2, P 0.05; pressure‐by‐CO2 interaction, P 0.05, §trend to be different from baseline P =0.06. Values are means ± SE.
Figure 3.
Figure 3.
Individual mean middle cerebral artery blood flow velocity (MCAvmean, A) and mean arterial blood pressure (MAP, B) responses to 5% CO2 (5%) alone and in combination with 20 and 40 mm Hg of lower body positive pressure. The 0 reference on the y‐axis represents the eucapnic baseline values. Individuals are represented by the same symbol in both graphs.

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