Hypoxic-ischemic encephalopathy: cerebrovascular carbon dioxide reactivity in neonates.
Using noninvasive measurement of cranial blood flow, we previously demonstrated that full-term asphyxiated neonates have decreased cerebral perfusion that can persist up to 5 days of age. In an attempt to test their postischemic cerebrovascular CO2 reactivity, we measured cranial blood flow in ten asphyxiated term (39 +/- 0.8 weeks and 3078 K 400 gm) infants with and without inhaled carbon dioxide (3 percent). The end tidal CO2 (PaCO2) increased significantly, from 28.8 +/- 1.0 mm Hg to 32.3 +/- 2.0 mm Hg after CO2 inhalation (p less than 0.01), whereas the cranial blood flow showed no significant change (38.5 +/- 5.0 ml/min/100 gm brain weight to 37.6 +/- 6.0 ml/min/100 gm brain weight). We conclude that term infants with hypoxic-ischemic encephalopathy have low cranial blood flow at 3 days of age. Their cerebrovascular response to inhaled CO2 is variable and suggests some impairment.
D001238:Asphyxia Neonatorum / Q000503:physiopathology*; D002545:Brain Ischemia / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000502:physiology; D002531:Cerebellum / Q000098:blood supply; D002560:Cerebrovascular Circulation; D006801:Humans; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007231:Infant, Newborn; D012039:Regional Blood Flow
D002245:Carbon Dioxide