Cerebral O₂ and CO₂ transport in isovolumic haemodilution: Compensation of cerebral delivery of O₂ and maintenance of cerebrovascular reactivity to CO₂

Abstract

This study investigated the influence of acute reductions in arterial O2 content (CaO2) via isovolumic haemodilution on global cerebral blood flow (gCBF) and cerebrovascular CO2 reactivity (CVR) in 11 healthy males (age; 28 ± 7 years: body mass index; 23 ± 2 kg/m2). Radial artery and internal jugular vein catheters provided measurement of blood pressure and gases, quantification of cerebral metabolism, cerebral CO2 washout, and trans-cerebral nitrite exchange (ozone based chemiluminescence). Prior to and following haemodilution, the partial pressure of arterial CO2 (PaCO2) was elevated with dynamic end-tidal forcing while gCBF was measured with duplex ultrasound. CVR was determined as the slope of the gCBF response and PaCO2. Replacement of ∼20% of blood volume with an equal volume of 5% human serum albumin (Alburex® 5%) reduced haemoglobin (13.8 ± 0.8 vs. 11.3 ± 0.6 g/dL; P < 0.001) and CaO2 (18.9 ± 1.0 vs 15.0 ± 0.8 mL/dL P < 0.001), elevated gCBF (+18 ± 11%; P = 0.002), preserved cerebral oxygen delivery (P = 0.49), and elevated CO2 washout (+11%; P = 0.01). The net cerebral uptake of nitrite (11.6 ± 14.0 nmol/min; P = 0.027) at baseline was abolished following haemodilution (−3.6 ± 17.9 nmol/min; P = 0.54), perhaps underpinning the conservation of CVR (61.7 ± 19.0 vs. 69.0 ± 19.2 mL/min/mmHg; P = 0.23). These findings demonstrate that the cerebrovascular responses to acute anaemia in healthy humans are sufficient to support the maintenance of CVR.

The jugular venous‐to‐arterial PCO2${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$ difference during rebreathing and end‐tidal forcing: Relationship with cerebral perfusion

“…We assessed nine young healthy participants (eight males and one female; age: 29 ± 8 years; body mass index: 24.9 ± 3.8 kg m –2 ) during a modified rebreathing protocol (hyperoxic and hypercapnic with prior hyperventilation). We also conducted retrospective analyses of two previously published data sets that included arterial and jugular bulb blood sampling during hypercapnia using ETF (Carr et al., 2023; Hoiland et al., 2022).…”

“…During rebreathing and ETF, participants rested in the supine position and were instrumented with internal jugular vein and radial artery catheters as previously described (Carr et al., 2023; Hoiland et al., 2022). Following catheterization, the remainder of participant instrumentation was completed and participants rested for 20 min.…”

“…Data from two previously published ETF protocols were used (Carr et al., 2023; Hoiland et al., 2022). We controlled $${P_{{\mathrm{ET}}{{\mathrm{O}}_{\mathrm{2}}}}}$$ and $${P_{{\mathrm{ETC}}{{\mathrm{O}}_{\mathrm{2}}}}}$$ with a portable dynamic ETF system.…”

“…Data from two previously published ETF protocols were used (Carr et al, 2023;Hoiland et al, 2022). We controlled P ETO 2 and P ETCO 2 with a portable dynamic ETF system.…”

“…An adjunct to this assumption is that rebreathing precludes any influence of cerebral blood flow (CBF) on the P bt‐a CO 2 gradient, and, therefore, the measured ventilatory response to increases in $${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$$. Outside the context of rebreathing, increases in $${P_{{\mathrm{aC}}{{\mathrm{O}}_{\mathrm{2}}}}}$$ mediate elevations in CBF, which offsets the minimization of the P bt‐a CO 2 gradient that would otherwise occur (Neubauer & Santiago, 1985), therefore offsetting the elevation of P bt CO 2 , via CO 2 washout (Carr et al., 2023). The magnitude of change in CBF for a given CO 2 stimulus, termed cerebrovascular CO 2 reactivity (CVR) (Hoiland et al., 2019), is therefore a contributing determinant of the $${P_{{\mathrm{C}}{{\mathrm{O}}_{\mathrm{2}}}}}$$stimulus for central ventilatory chemoreceptors (Ainslie & Duffin, 2009; Carr, Caldwell, Ainslie, 2021), as well as the subsequent ventilatory response (Xie et al., 2006).…”