THE CEREBRAL FUNCTIONAL, METABOLIC, AND HEMODYNAMIC-EFFECTS OF DESFLURANE IN DOGS

The effects of 0.5-2.0 MAC (3.6-15%) desflurane on cerebral function, metabolism, and hemodynamics and on systemic metabolism and hemodynamics were examined in dogs. Desflurane produced a significant dose-related decrease in cerebral vascular resistance from 1.53 ± 0.21 mmHg · ml-1 · min · 100 g at 0.5 MAC to 0.50 ± 0.03 mmHg · ml-1 · min · 100 g at 2.0 MAC desflurane. This was accompanied by an increase in cerebral blood flow (CBF) from 61 ± 7 ml · min-1 · 100 g-1 at 0.5 MAC to 78 ± 3 ml · min-1 · 100 g-1 at 1.5 MAC desflurane. At 2.0 MAC desflurane CBF was 52 ± 2 ml · min-1 · 100 g-1 but was associated with a decrease in mean arterial pressure (MAP) to 43 ± 2 mmHg. When MAP was increased to 73 ± 3 mmHg with phenylephrine, CBF increased to 87 ± 3 ml · min-1 · 100 g-1 at this concentration. At 0.5 MAC desflurane, intracranial pressure (ICP) was 15 ± 5 mmHg, higher than normal, but did not change significantly with increasing concentrations of desflurane. Increasing concentrations of desflurane initially produced on the EEG the common pattern sequence of increasing depth of anesthesia with decreasing frequency and increasing amplitude progressing to burst suppression and then at 2.0 MAC desflurane to regular attenuation with interruption by periodic polyspiking, a pattern similar to that seen with isoflurane. At both 1.5 and 2.0 MAC the EEG pattern initially observed at that concentration changed to one with faster background activity with time. In parallel with changes observed on EEG desflurane produced a significant decrease in the cerebral metabolic rate for oxygen to 2.52 ± 0.1 ml · min-1 · 100 g-1 at 2.0 MAC, which is comparable to that produced by other anesthetics. Cerebral metabolites measures at the end of the study were within normal limits. Desflurane produced a dose-related decrease in mean arterial pressure from 114 ± 5 mmHg at 0.5 MAC to 43 ± 2 mmHg at 2.0 MAC due primarily to a significant decrease in systemic vascular resistance. Only at 2.0 MAC was there a significant decrease in cardiac index, which may have also have contributed to the decreased MAP at this concentration. Increasing doses of desflurane had no effect on heart rate or whole body oxygen consumption. It is concluded that desflurane is a cerebral vasodilator similar to that of the other volatile anesthetics and a cerebral metabolic suppressant similar to isoflurane. It differs from the other anesthetics in that the effect of higher concentrations of desflurane on EEG activity may be limited with time.