Vascular reactivity in the primate brain after acute cryogenic injury.
The effects of an acute cryogenic injury on cerebral flow (CBF) and cerebral vascular reactivity were studied in 12 anaesthetised, ventilated baboons. Autoregulation, defined in this study as intact with a greater than 20% change in cerebrovascular resistance in response to a change in cerebral perfusion pressure, was tested before the lesion by arterial hypotension. Intact autoregulation was found in half the animals, but all animals showed an increase in CBF with hypercarbia. The cryogenic lesion was followed by a marked rise in intracranial pressure, and a fall in CBF which was only partly related to the status of autoregulation beforehand. After injury, arterial hypertension caused an increase in cerebrovascular resistance of more than 20% in half the animals. This response was not related to the presence of autoregulation before the lesion, and was accompanied by a greater impairment of the cerebrovascular response to carbon dioxide, more severe brain oedema, and lower cerebral oxygen consumption, than in the remaining baboons which had a pressure passive response to arterial hypertension. This study confirms that the failure of CBF to increase with arterial hypertension may indicate severe brain damage rather than intact physiological autoregulation.
D000818:Animals; D001794:Blood Pressure; D001812:Blood-Brain Barrier; D001923:Brain Chemistry; D001930:Brain Injuries / Q000378:metabolism / Q000503:physiopathology*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation; D003080:Cold Temperature / Q000009:adverse effects*; D000882:Haplorhini; D006706:Homeostasis; D010215:Papio; D012964:Sodium / Q000032:analysis; D014655:Vascular Resistance; D014867:Water / Q000032:analysis
D014867:Water; D002245:Carbon Dioxide; D012964:Sodium