Enhancement of brain tissue oxygenation during high dose isoflurane anesthesia in the dog.

Abstract

It is reported that high dose desflurane can increase brain tissue oxygen pressure (PtO2) in patients during cerebral aneurysm surgery. The purpose of this study was to determine whether high dose isoflurane anesthesia can produce a similar effect in dogs and the importance of cerebral perfusion pressure in mediating this effect. Six dogs were anesthetized, and ventilated with isoflurane inspired oxygen concentration of 40%. Following a craniotomy, a catheter was inserted into the sagittal sinus for cerebral venous blood samples and a Neurotrend probe was inserted into cortex brain tissue to measure PtO2, carbon dioxide pressure (PtCO2), and pH (pHt). Brain tissue and arterial and sagittal sinus blood gas tensions and pH were measured under the following conditions: 1 = baseline 1.5% isoflurane, 2 = 1.5% isoflurane + increase mean arterial pressure (MAP) by 50 mm Hg, 3 = 3% isoflurane anesthesia, 4 = 3% isoflurane anesthesia + increase MAP 55 mm Hg, 5 = 1.5% isoflurane anesthesia, 6 = 1.5% isoflurane anesthesia + increase MAP 35 mm Hg. In the first and second trial with 1.5% end-tidal isoflurane, PtO2 increased 15% during an increase in MAP without a change in sagittal sinus oxygenation. At 3% isoflurane, PtO2 increased 90% and sagittal sinus PO2 increased 38% during an increase in MAP. These results show that the cerebral metabolic depression and cerebrovasodilatory effects of high dose isoflurane can enhance brain tissue oxygenation. Normal brain vascular regulation that limits hyperperfusion and hyperoxygenation of brain tissue is antagonized by high dose isoflurane.