We analyzed the effect of a new volatile anesthetic, sevoflurane (2%-5% in oxygen) on the electroencephalogram (EEG) of the neocortex, amygdala, and hippocampus, cortical somatosensory evoked potential (SEP), and brainstem reticular multiunit activity (R-MUA) in cats. Sevoflurane suppressed the background activity of the neocortex more than the amygdala and hippocampus. With increasing concentration of sevoflurane, the cortical EEG progressed from high-amplitude slow waves to a suppression-burst pattern, which was followed by an isoelectric pattern and then spikes with isoelectricity. The amplitude of the SEP was augmented and the R-MUA was suppressed by sevoflurane in a dose-related manner. Repetitive peripheral electrical stimulation induced generalized seizures at 5% sevoflurane in 2 of 13 cats. These results suggest that sevoflurane suppresses the background central nervous system electrical activities in a dose-related manner, leaving the reactive capabilities facilitated at deep anesthesia.

Using cats with chronically implanted brain electrodes, we have compared the effects of propofol on CNS electrical activities with those of thiopentone. Ten cats were allocated to receive either propofol (n = 5) or thiopentone (n = 5). Cats were anaesthetized initially with 4% halothane in oxygen. The trachea was intubated and the lungs ventilated mechanically. A femoral artery and a vein in a forepaw were cannulated for arterial pressure monitoring and fluid infusion. After the inspired concentration of halothane was maintained at 0.5%, EEG in the cortex, the amygdala and the hippocampus, somatosensory evoked potential (SEP) and reticular multi-unit activity (R-MUA) were recorded. Incremental doses of propofol or thiopentone were administered i.v. at 5-min intervals during 0.5% halothane anaesthesia. The cumulative doses of propofol and thiopentone were 2, 5, 10 and 20 mg kg-1, and 4, 10, 20 and 40 mg kg-1, respectively. Arterial pressure was maintained in excess of 100 mm Hg systolic by infusion of phenylephrine. All cats in the propofol group survived, but two in the thiopentone group died after the administration of thiopentone 40 mg kg-1. Changes observed in CNS activity were dose-related in all cases. The EEG changed with the increments of doses of propofol or thiopentone, from fast, small amplitude to complexes of fast and slow, large amplitude activities, burst suppression and flat EEG. SEP latency was prolonged by both agents: the peak latency of N1 changed from 15 (SD 2) ms to 20 (5) ms with propofol 20 mg kg-1, and from 14 (1) ms to 27 (2) ms with thiopentone 40 mg kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of halothane, isoflurane, and enflurane on background neuronal activity and reactive capability in the central

To plan the optimal BNCT using BSH for glioblastoma patients, the 10B concentration in tumor and blood was investigated in 11 newly diagnosed glioblastoma patients. All patients received 20 mg BSH/kg body weight 2.5-16 hrs prior to tumor removal. The quantitative distribution of 10B was determined by prompt gamma ray spectrometry and/or alpha-track autoradiography. 10B distribution in tumors was heterogeneous, +/- 25% of scattering at the microscopic level, and the distribution was also heterogeneous at the tissue level. 10B concentration in blood decreased in bi-exponential decay as a function of the time after the end of the administration. The T/B ratio showed non-exponential increase with large variation. The maximum T/B ratio would be around 1. The tumor/normal brain (T/N) ratio of 10B concentration was 11.0 +/- 3.2. The 10B content in normal brain is originated in vascular 10B in parenchyma, since the 10B content in normal brain to blood (N/B ratio) being compatible with the blood content in parenchyma. These values allow for BNCT, using thermal neutrons, on brain tumors located less than approximately 3.3 cm in depth from the brain surface of neutron incidence, providing that the dose on the normal endothelium is controlled to less than the tolerance limit. In our preliminary study of BNCT, a 31% 3-year survival was achieved over all for 16 glioblastoma patients and a 50% 2-year survival was achieved on 8 glioblastoma patients in our recent dose escalation study based on these data.

The effects of two kinds of induction speed of sevoflurane anesthesia on the EEG pattern were compared in the same individual using medical student volunteers: a first exposure of 4% was given, followed after full recovery, by incremental doses of 1, 2 and 4% successively, each being administered for 10 min. The arterial blood level of the anesthetic was measured using gaschromatograph. The changes of EEG pattern during fast induction with 4% were not represented by the abbreviation of those observed during the slow induction with the incremental doses. The administration of 4% induced a sudden appearance of high voltage, rhythmic slow waves of 2-3 Hz at 1-3 min when the arterial blood anesthetic level increased maximally, which was then followed by a pattern of faster activities of 10-14 Hz mixed with 5-8 Hz slow waves. In contrast, the administration of incremental doses induced an increase in frequency and amplitude of EEG activities in the light plane, followed by their decreases in deeper planes. The final EEG patterns were identical for both these methods of induction. These findings confirmed our previous hypothesis that not only the arterial blood level of anesthetics but the rate of its increase are important factors determining the EEG pattern of anesthesia