Anesthetic modulation of cerebral hemodynamic and evoked responses to transient middle cerebral artery occlusion in cats

We measured cerebral blood flow and somatosensory evoked potentials during transient focal cerebral ischemia in cats to compare the effects of four commonly used anesthetic regimens: ketamine/fentanyl/N₂O (fentanyl), pentobarbital, ketamine/α-chloralose (a-chloralose), and ketamine/halothane/N₂O (halothane). Six cats in each group were subjected to 60 minutes of left middle cerebral artery occlusion followed by 120 minutes of reperfusion. Although the amplitude of the initial somatosensory evoked potential wave complex was highest in the tt-chloralose group (58.6±16.5 µV)and smallest in the halothane group (27.5±5.7 µV), amplitude fell by 75% in all groups upon occlusion. Baseline cerebral blood flow varied substantially between groups (e.g., in the right intersylvian gyrus: fentanyl, 96±12; pentobarbital, 30±5; α-chloralose, 24±3; and halothane, 76±11 ml/min/100 g). Occlusion decreased cerebral blood flow to subcortical (e.g., left caudate) structures in all groups (fentanyl, 29 ±11%; pentobabital, 45±12%; α-chloralose, 27±13%; and halothane, 18±5% of baseline). Postisch-emic hyperemia occurred in the cortical regions of cats anesthetized with pentobarbital or «-chloralose that had reduced cerebral blood flows during occlusion but not in cats anesthetized with fentanyl (cerebral blood flow during occlusion not different from that of cats anesthetized with pentobarbital or <α-chloralose) or halothane. After 120 minutes of reperfu-sion, cerebral blood flow had returned to baseline values in all groups. Recovery of cerebral blood flow and somatosensory evoked potential amplitude at that time did not differ among groups. We conclude that anesthetics alter baseline cerebral blood flow and baseline somatosensory evoked potentials as well as the cerebral blood flow pattern during reperfusion after middle cerebral artery occlusion independent of insult severity.