Summary Advances in technology have made available a variety of approaches and instruments to monitor target indicators of brain oxygenation. These have already contributed significantly to the study of brain metabolic physiology and should become increasingly useful in clinical medicine. Improvements in positron emission tomography (PET), magnetic resonance spectroscopy (MRS), optical and electrode techniques will undoubtedly occur that will increase their sensitivity and allow them to become more quantitative. At present, each offers useful information and each has advantages and limitations that must be considered when application decisions are being made. The present review offered three themes. The first was that target indicators can be categorized between those that are continuously sensitive and those that are threshold-sensitive to brain oxygenation. We have considered the former to be predominately trend monitors while conceding to the latter the capability to evaluate metabolic status quantitatively. The monitoring of trend indicators, particularly by optical techniques, offers good temporal resolution with relative simplicity and low instrumentation cost. The monitoring of metabolic status by MRS and PET procedures offers quantitative information, such as on the severity of brain metabolic insults for emergencies or when chronic monitoring is not possible. But these procedures have disadvantages of expense, portability and temporal resolution. While PET may offer trend as well as status indications of metabolism, parameters monitored by MRS appear limited by their threshold sensitivity. There is every likelihood that future research will enhance many of the target-indicating approaches beyond present limits. At least for clinical purposes, for example, optical and polarographic techniques must yet be considered as trend indicators since absolute calibration is difficult. For tP O 2 , such calibration requires the recording of an oxygen profile which is more invasive and decreases temporal resolution. For the monitoring of mitochondrial redox ratios, a usual procedure is to compare the ‘base-line' status in terms of maximal oxidation (produced by inspiration of hyperoxic gas mixtures) and maximal reduction (produced by replacement of oxygen with nitrogen in the inspired gas mixture) (Sylvia and Rosenthal, 1978). Such extreme manipulations are not compatible with proper patient management. However, experiments are ongoing to enhance optical monitoring as a status indicator of brain oxygenation. These are based on reports that NAD or cytochrome a,a 3 respond to neuronal activation with shifts toward oxidation in normoxic brain but with shifts toward reduction when brain oxygenation decreases below a threshold level (LaManna et al, 1984; Milito et al, 1988). Preliminary data suggests that this ‘transition' from oxidation to reduction occurs at Pa O 2 levels at which phosphocreatine:P i decline is first resolvable (Smith et al, 1986). A second theme is that interpretation of the target signals must be made in terms of brain metabolic physiology, especially if these signals are to provide a useful ‘warning' for clinical intervention during cardiopulmonary insults. For example, hypoxaemia of moderate intensity may provoke large decreases in haemoglobin saturation and significant reduction of mitochondrial electron transport carriers without noticeable effect on synaptic transmission or metabolite levels. However, as oxygenation declines to levels beyond threshold for declines in phosphocreatine:P i (and toward possible brain damage), optical and polarographic signals may change relatively little because they have already undergone large shifts. While MRS may not be sensitive at moderate insults, this approach exhibits greatest sensitivity at critical levels of insult. A third theme is that interpretation of each target of brain oxygenation is best accomplished in terms of other complementary target indicators and that information derived from the monitoring of only one indicator should be considered with caution. Glucose consumption may increase during hypoxia or increased brain activity, for example, but definition between these can be made with polarographic technique ( tP O 2 will markedly decrease during hypoxia and will be relatively unchanged by changes in brain activity) or with optical procedures (mitochondria will be reduced in hypoxia, oxidized with increased activity) or by reference to electrophysiological function. A combination of techniques, and in particular the simultaneous interpretation of metabolism and brain activity, should be the goal of experimental and clinical approaches to brain oxygenation. The monitoring of brain oxygenation and metabolism in the clinical management of diseases or anaesthesia will provide no cure in itself and, at least in the context of normal patient care, will offer little insight into physiological or biochemical mechanisms. However, the use of safe, sensitive and effective monitoring technology can lead to better patient management by contributing to decision-making processes and by increasing the rapidity that compensatory measures can be undertaken when circumstances alter tissue function and threaten survival. Biomedical science has developed and is improving many approaches to such goals. Implementation of these approaches will be a primary objective of many clinician-scientists in the next several years.