CO2 Responses of the Cerebral Circulation during Drug-Induced Hypotension in the Cat

Abstract

Concern has often been expressed that hypocapnia produced by controlled hyperventilation might further reduce cerebral perfusion during drug-induced hypotension. In the present studies, hypotension was induced in cats with either practolol/trimetaphan (five experiments) or practolol/nitroprusside (five experiments) together with controlled haemorrhage. Arterial Pco2 was altered between 17 and 51 mm Hg by varying inspired CO2 during constant-volume ventilation, first during control conditions of light halothane/nitrous oxide anaesthesia and then during hypotension to mean blood pressure of 36–37 mm Hg. Cerebral cortical perfusion was measured by the krypton clearance technique and pial artery diameter by the image-splitting method. Cerebral cortical blood flow did not alter with Paco2 changes during trimetaphan hypotension, but some responsiveness to CO2 persisted during nitroprusside hypotension, though at less than half control levels. No changes in pial artery diameter were seen with CO2 during hypotension under either technique. It is postulated that CO2 responsiveness persisted with nitroprusside because cerebral blood flow (CBF) values were higher when hypotension was produced with this drug, as compared with trimetaphan. It would appear that hypocapnia does not further reduce CBF during trimetaphan hypotension but does do so with nitroprusside. However, the combination of hypocapnia and nitroprusside hypotension did not in any instance lower CBF below the values found during trimetaphan hypotension.