Carbon Dioxide Reactivity of the Cerebral Circulation in Extremely Premature Infants: Effects of Postnatal Age and Indomethacin

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Abstract
Little is known about the vasoactivity of cerebral arterioles in extremely premature infants. We have assessed the effects of a small rise in PaCO2 of 1 kPa (7.5 mm Hg) on cerebral blood flow velocity measured by duplex Doppler ultrasound. Nineteen mechanically ventilated infants of 33 wk gestational age or less in whom direct arterial blood pressure monitoring was available, were studied on 45 occasions. There was a close relationship between increasing PaCO2 and increasing cerebral blood flow velocity (p < 0.005) but on seven of 45 occasions the cerebral blood flow velocity fell with rising PaCO2. There was a 44% (median value) rise in cerebral blood flow velocity per 1 kPa rise in PaCO2 (5.9%/l mm Hg) in 21 infants tested within 24 h of birth and this increased to a 53% (median value) rise (7%/l mm Hg) in 20 infants tested after 24 h (p < 0.001). Eleven infants had paired studies, the first within 24 h and a second at a median age of 48 h. There was a statistically significant increase in percentage reactivity when the later group was compared to those tested within 24 h (p < 0.001). Carbon dioxide reactivity was also assessed before and after indomethacin infusion (0.2 mg/kg) on four occasions and there was a reduction in reactivity from a median value of 144 to 49.5%, 10 min after indomethacin. The extremely immature, ill infant is less sensitive to a small change in PaCO2 within 24 h of birth and after indomethacin infusion. We speculate that this may be related to a state of relative arteriolar vasoconstriction compared with infants 24 h or more after birth and those not influenced by the vasoconstrictor properties of indomethacin.