Abstract
The effect of respiration on the cerebrovascular response to elevated intracranial pressure (ICP) was studied in anesthetized dogs. Total and regional cerebral blood flows were measured using labelled microspheres. In spontaneously breathing dogs total and regional cerebral blood flows increased when cerebral perfusion pressure was reduced to 20 mm Hg. The increase in regional flows was greater in the infratentorial areas than in the supratentorial areas. The increase in cerebral flow in spontaneously breathing dogs was associated with the development of hypoxemia and respiratory acidosis secondary to depression of ventilation. Elevation in ICP while regulating PO2, PCO2, and pH by controlled ventilation resulted in decrease in the total and regional cerebral blood flows. The decrease in regional flows was greater in the supratentorial areas. Induction of respiratory acidosis during elevated ICP in the controlled ventilated dogs with a 5% CO2 in air gas mixture, reversed the decrease in cerebral flows. The results suggest that the increase in cerebral blood flow during elevated ICP in spontaneously breathing dogs is secondary to the development of hypoxemia and respiratory acidosis since cerebral vessels retain responsiveness to increased PaCO2 when the vessels are dilated due to elevated ICP. The results also indicate that the regional cerebrovascular response to elevated ICP is non-uniform.
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