Abstract
In the present study, the relationships among electroencephalographic (EEG) amplitude shifts, cerebral blood flow (CBF), and cerebral oxygen uptake (CMRO2) have been characterized in halothane-anesthetized rabbits. CBF was measured by timed collection of venous effluent from the superior sagittal sinus. CMRO2 was calculated as the product of CBF and the arteriovenous difference in oxygen content. The depth of anesthesia in the first series of experiments was maintained at a constant level that was characterized by spontaneous EEG shifts from high- to low-voltage states (HV-LV shifts). These shifts were associated with transient decreases in mean arterial pressure (MAP), which averaged 23 ± 2 mm Hg (n = 17). Ninety seconds after spontaneous HV-LV shifts, MAP had returned to its original value, CBF had increased by 26 ± 7% (n = 8), and CMRO2 had increased 22 ± 4% (n = 7). In a second series of experiments, HV-LV shifts were induced by a 90-s application of a standardized nociceptive stimulus (n = 13). Following these stimulation-induced HV-LV shifts, CBF increased 28 ± 5% and CMRO2 increased 27 ± 4%. Under scopolamine (0.35 mg/kg, i.v., n = 8), no change in CBF was observed following HV-LV shifts induced by 90-s of stimulation, although CMRO2 increased significantly by 14 ± 3%. After 300 s of post-scopolamine stimulation, however, both CBF and CMRO2 had significantly increased by 12 ± 3 and 15 ± 3% (n = 8) of control, respectively. These results demonstrate that HV-LV shifts, whether spontaneous or stimulation-induced, are associated with significant increases in both CBF and CMRO2. Because the early (90-s) increases in CBF but not those in CMRO2 could be blocked by scopolamine, we suggest that the cerebral vasodilatation that occurs during the early phase of HV-LV shifts involves cholinergic mechanisms. Because scopolamine could not block the increase in CBF observed after 300 s of stimulation, we suggest that the final value of CBF obtained after an HV-LV shift is determined by a combination of both cholinergic and noncholinergic factors.