Electrocerebral silence by intracarotid anesthetics does not affect early hyperemia after transient cerebral ischemia in rabbits.

UNLABELLED: Evidence suggests that early postischemic hyperemia is mediated by both neurological and vascular mechanisms. We hypothesized that if neuronal activity were primarily responsible for reperfusion hyperemia, then electrocerebral silence induced by intracarotid anesthetics (propofol and pentothal) would attenuate the hyperemic response. New Zealand white rabbits were subjected to 10 min of cerebral ischemia using bilateral carotid occlusion and systemic hypotension. Subsequently, carotid occlusion was released, and the mean arterial blood pressure was increased to baseline values. In the control group, intracarotid saline was periodically injected during reperfusion. In the treatment groups, intracarotid propofol or thiopental was administered to maintain electrocerebral silence for 10 min. Physiological data were measured at baseline, during ischemia, and at reperfusion. Satisfactory data were available for 16 of 19 rabbits. Mean arterial blood pressure, end-tidal CO(2), and cerebral blood flows decreased significantly in both groups during carotid occlusion. During early reperfusion, a similar percent increase in cerebral blood flow from baseline values was observed in all 3 groups (192% +/- 76%, 218% +/- 84%, and 185% +/- 101% for saline, propofol, and pentothal, respectively). These results suggest that suppression of neuronal activity during reperfusion does not affect early hyperemia after transient cerebral ischemia. IMPLICATIONS: Intracarotid injection of anesthetic drugs in doses that are sufficient to produce electrocerebral silence do not obtund early cerebral hyperemia after transient cerebral ischemia. This suggests that vascular, not neuronal mechanisms, are primarily responsible for early postischemic cerebral hyperperfusion.