Does prolonged severe hypercapnia interfere with normal cerebrovascular function in piglets?

Abstract

Background Hypercapnia causes cerebral vasodilation and increased cerebral blood flow (CBF). During prolonged hypercapnia it is unknown whether cerebral vasodilation persists and whether cerebrovascular function is preserved. We investigated the effects of prolonged severe hypercapnia on pial arteriolar diameters (PAD) and cerebrovascular reactivity to vasodilators and vasoconstrictors. Methods Piglets were anesthetized, intubated and ventilated. Closed cranial windows were implanted to measure PAD. Changes in PAD were documented during hypercapnia (PaCO2 75–80 mm Hg). Cerebrovascular reactivity was documented during normocapnia and at 30, 60 and 120 min of hypercapnia. Results Cerebral vasodilation to hypercapnia was sustained over 120 min. Cerebrovascular responses to vasodilators and vasoconstrictors were preserved during hypercapnia. During hypercapnia, vasodilatory responses to second vasodilators were similar to normocapnia, while exposure to vasoconstrictors caused significant vasoconstriction. Conclusions Prolonged severe hypercapnia causes sustained vasodilation of pial arteriolar diameters indicative of hyperperfusion. During hypercapnia, cerebral vascular responses to vasodilators and vasoconstrictors were preserved, suggesting that cerebral vascular function remained intact. Of note, cerebral vessels during hypercapnia were capable of further dilation when exposed to additional cerebral vasodilators and, significant vasoconstriction when exposed to vasoconstrictors. Extrapolating these findings to infants, we suggest that severe hypercapnia should be avoided, because it could cause/increase cerebrovascular injury.

Cerebral perfusion and metabolism with mild hypercapnia vs. normocapnia in a porcine post cardiac arrest model with and without targeted temperature management

“…Clinical studies have illustrated the close relationship between cerebral vasodilatation and increased PaCO 2 using transcranial doppler and near-infrared spectroscopy (NIRS) to show increases in middle cerebral artery velocities and cerebral oximetry with higher PaCO 2 levels. 36 , 37 , 38 Similarly, observations from laboratory studies using invasive procedures like laser doppler flow measured directly over the dura 39 and measuring changes in the pial arteriolar diameter by a video micrometer 40 support hypercapnia as a method to increase CBF. While increasing CBF after brain injury has appeal, it would only be useful in preventing secondary injuries if there is an energy imbalance where the brains oxygen supply does not meet the demand.…”

Hemodynamic and oxygen-metabolic responses of the awake mouse brain to hypercapnia revealed by multi-parametric photoacoustic microscopy

“…Our results are in good agreement with recent studies in rats and piglets under similar hypercapnic challenges. 40,41 The arterial and venous sO 2 were readily distinguishable when the mouse was under normocapnia (Figures 1 and 2). However, a noticeable elevation in the venous sO 2 was observed within 30-minute induction of mild hypercapnia (white arrows in Figure 1) making it less distinguishable from the arterial sO 2 .…”