CO2 responsiveness of the cerebral circulation has been measured in baboons before, during, and after halothane-induced hypotension. At a systolic blood pressure (BP) of 60 mmHg, C02 responsiveness was abolished, but was maintained at higher levels of BP. After hypotension, CO2 responsiveness returned to control values. Autoregulation to BP increases induced by intravenous noradrenaline was impaired when cerebral perfusion pressure during the hypotensive period had been below 30-40 mmHg. It is concluded that at levels of halothane-induced hypotension commonly employed clinically, CO2 responsiveness of the cerebral circulation may be absent. The return of CO2 responsiveness in the post-hypotensive phase argues in favour of controlled hyperventilation after neurosurgery which has involved induced hypotension.
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