Background <p>Cerebrovascular autoregulation (CA) is the ability to maintain adequate cerebral blood flow (CBF) over a wide range of arterial blood pressures (ABPs). Carbon dioxide (CO<sub>2</sub>) is a potent vasodilator, but its precise influence on CA remains incompletely understood.</p> Methods <p>A porcine cranial window model, in which CBF can be measured directly in the pial arterioles while ABP is mechanically manipulated, is used to investigate the effect of partial pressure of CO<sub>2</sub> in arterial blood (PaCO<sub>2</sub>) on CA capacity. Hypercapnia and hypocapnia were induced in 12 male piglets each by adjusting the respiratory rate. Once stable PaCO<sub>2</sub> levels of 60 and 25&#xa0;mm&#xa0;Hg, respectively, were achieved, ABP was gradually increased in half of the animals or decreased in the other half beyond limits of CA by inflating a balloon in the aorta or inferior vena cava.</p> Results <p>Before ABP manipulation, hypercapnia already induced significant vasodilation (+ 33.9%) and an increase in CBF (+ 20.5%), whereas hypocapnia did not alter diameter or CBF. Both hypercapnia and hypocapnia significantly reduced the ability to adjust arteriolar diameters in response to changes in ABP.</p> Conclusions <p>During hypocapnia as well as hypercapnia, narrowing of the CA range with a shorter plateau between the upper and lower limit of autoregulation was observed, compared to normocapnia.</p>

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The Influence of Different Arterial Carbon Dioxide Levels on the Cerebrovascular Autoregulation Curve in a Porcine Cranial Window Model

  • Sofie Dietvorst,
  • Bavo Kempen,
  • Veerle De Sloovere,
  • Nikky Corthout,
  • Geert Meyfroidt,
  • Bart Depreitere

摘要

Background

Cerebrovascular autoregulation (CA) is the ability to maintain adequate cerebral blood flow (CBF) over a wide range of arterial blood pressures (ABPs). Carbon dioxide (CO2) is a potent vasodilator, but its precise influence on CA remains incompletely understood.

Methods

A porcine cranial window model, in which CBF can be measured directly in the pial arterioles while ABP is mechanically manipulated, is used to investigate the effect of partial pressure of CO2 in arterial blood (PaCO2) on CA capacity. Hypercapnia and hypocapnia were induced in 12 male piglets each by adjusting the respiratory rate. Once stable PaCO2 levels of 60 and 25 mm Hg, respectively, were achieved, ABP was gradually increased in half of the animals or decreased in the other half beyond limits of CA by inflating a balloon in the aorta or inferior vena cava.

Results

Before ABP manipulation, hypercapnia already induced significant vasodilation (+ 33.9%) and an increase in CBF (+ 20.5%), whereas hypocapnia did not alter diameter or CBF. Both hypercapnia and hypocapnia significantly reduced the ability to adjust arteriolar diameters in response to changes in ABP.

Conclusions

During hypocapnia as well as hypercapnia, narrowing of the CA range with a shorter plateau between the upper and lower limit of autoregulation was observed, compared to normocapnia.