CEREBROVASODILATION ELICITED BY FASTIGIAL STIMULATION IS PRESERVED UNDER DEEP HALOTHANE ANESTHESIA

We studied the effect of halothane anesthesia on the increases in cerebral blood flow (CBF) and arterial pressure (AP) elicited by electrical stimulation of the cerebellar fastigial nucleus (FN). Rats were anesthetized (0.75-2% halothane), instrumented for continuous recording of AP, and ventilated. The FN was stimulated through stereotaxically implanted microelectrodes. In CBF experiments the elevations in AP resulting from FN stimulation were eliminated by spinal cord transection at C1. After cord transection AP was maintained by intravenous phenylephrine. CBF or cerebral glucose utilization (CGU) was measured by laser-Doppler flowmetry or the 2-deoxyglucose method, respectively. FN stimulation produced increases in CBF that were graded with the intensity (10-150 muA) or frequency (10-150 Hz) of stimulation. At 1% halothane, FN stimulation (100 muA; 75 Hz; n = 8) increased CBF by 123 +/- 16%. The elevations in CBF were attenuated by increasing levels of halothane anesthesia in a dose-dependent manner. At halothane concentrations of 1.5 and 2% the CBF response to FN stimulation (100 muA; 75 Hz) was reduced by 58 +/- 6 and 77 +/- 4%, respectively (P < 0.05 from 0.75% halothane; analysis of variance and Tukey's test). In contrast, the increases in CBF elicited by hypercapnia were not attenuated (P > 0.05 from 0.75% halothane). At 1% halothane, FN stimulation did not change CGU in neocortex (frontal cortex: unstimulated 48 +/- 6, mumol.100 g-1.min-1, FN stimulation: 47 +/- 11; P > 0.05; n = 5/group). In the group of rats in which the pressor response was studied (n = 7), halothane produced a dose-dependent attenuation of the elevations in AP. The degree of attenuation of the AP response was comparable to that of the CBF response (P > 0.05). Thus the increase in CBF elicited by FN stimulation is well preserved under surgical levels of halothane anesthesia and, in neocortex, is independent of local metabolic activity. The results demonstrate that the cerebrovascular effects of FN stimulation are not secondary to arousal in lightly anesthetized preparations and support the hypothesis that there are intrinsic neural networks that influence neocortical blood flow independently of local metabolic activity.