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In order to explore the sensitivity of spatially resolved 1H and 31P NMR spectroscopy on a whole-body NMR instrument, cerebral metabolic changes in human volunteers were measured during hyperventilation provocation. During hyperventilation the flow velocity in the middle cerebral artery decreased significantly and the EEG showed a marked increase in slow activity. 1H NMR spectra revealed an increase in cerebral lactate concentration. 31P NMR spectra showed no changes in ATP or PCr peak heights, but a shift toward tissue alkalosis was derived from changes in Pi chemical shift. During subsequent recovery, lactate concentration decreased and a slight intracellular acidosis was detected. In three experiments broadening of the lactate resonance peak resulted in separation into two components at 1.32 and 1.48 ppm, in which the latter signal possibly arose from alanine.

SununaryA standardized hyperventitation (HV) procedure has been developed in which the end-tidal pCO 2 was decreased to 2 kpa. In 24 young male subjects blood flow velocity and qEEG were studied before, during and after HV. This standardized hyperventilation procedure gave rise to a decrease in blood flow velocity to 40% of baseline value and highly significant qEEG changes in 3 derivations. Both relative and absolute band power estimates showed an increase in slow activity and a decrease in alpha and beta activity. The use of subtraction spectra led to a more precise and detailed presentation of these changes than the use of classical qEEG parameters. These changes were reproducible after 1 week. The effects found in the presented model of HV-induced ischaemia appeared to be twice as large as those found in a model of hypobaric hypoxia. The present model might be used to test the efficacy of anti-ischaemic drugs in young human subjects. Key words: qEEG; Transient ischaemia model; Normal subjectsOf all physical activation methods in use for the provocation of EEG changes, hyperventilation (HV) is perhaps the most commonly used. HV gives rise to a decrease in arterial pCO2, leading to vasoconstriction of the arteriolar channels and as a consequence a decrease in cerebral blood flow (CBF) (Kety and Schmidt 1948;Yamaguchi 1979). Recently a reduction in blood flow velocity (BFV) in the large cerebral vessels has been demonstrated using the transcranial Doppler (TCD) technique (Markwalder et al. 1984). Despite ample administration of oxygen, the HV-induced flow reduction may lead to cerebral tissue hypoxia (Clark et al. 1958;Sugioka and Davis 1960;Kennealy et al. 1980) and to cerebral tissue lactic acidosis (Plum and Posner 1967; Kogure et al.Correspondence to: V. Kraaier, Dept. of Clinical Neurophysiology, University Hospital Utrecht, Utrecht (The Netherlands).1975; Luyten et al. 1987). Thus, HV may be considered as an experimental method of inducing transient ischaemic hypoxia. The fact that similar EEG changes are observed in normal subjects during HV and in patients with cerebral ischaemia gives further support to this conception.Aim of this study was to establish a model of reversible HV-induced ischaemic hypoxia. This was achieved by standardizing the HV procedure by means of capnographic monitoring, which resuited in reproducible changes in BFV and quantitative EEG (qEEG). In this model several qEEG parameters were studied in 3 derivations for both relative and absolute power densities. Furthermore, a comparison was made between spectral changes in this HV model and in the earlier described hypobaric hypoxia model (Kraaier et al. 1988).Since the effect of HV in the EEG decreases with age (Yamaguchi et al. 1979), only young subjects (age 20-25 years) were studied.0013-4649/88/$03.50