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Infrared transmission spectroscopy was used to detect changes in cerebral oxy- and deoxyhemoglobin attenuation of infrared light in a patient undergoing circulatory arrest at 15 degrees C. Wavelength specific attenuation was used to determine hemoglobin oxygen saturation in the cerebral vasculature using a previously described paradigm. The fate of the residual oxygenated hemoglobin in the cerebrovascular compartment was followed during 15 min of circulatory arrest at 15 degrees C, and cerebral oxygen metabolism was identified as the progressive desaturation of this hemoglobin. The aggregate arterial and venous saturation fell from a normal value of 70% to an abnormally low value of 50%. Reperfusion resulted in near normalization of cerebrovascular oxygen saturation over 5 min, but evidence of persistent mild desaturation below prearrest baseline followed reperfusion. This case demonstrates both continued cerebral oxygen metabolism under hypothermic, circulatory arrest conditions and a cerebral oxygen delivery-consumption mismatch during reperfusion.

✓ Cerebral oxygen metabolism was studied in the dog at brain temperatures ranging from 37° to 8°C. As brain temperature decreased, the cerebral oxygen metabolism (CMRO2) decreased following the Arrhenius equation. The natural logarithm of the CMRO2 was a linear function of the reciprocal of the absolute (K) brain temperature. Oxygen metabolism, although much decreased, continued at very low brain temperatures. The CSF composition was unchanged after 1 hour at brain temperatures down to 10°C. Circulatory arrest for tolerable periods and longer caused changes only in the CSF potassium concentration. The interval between the onset of circulatory arrest and the beginning of the CSF K concentration increased with decreasing temperature and the rate of CSF K increase was increasingly slower at lower temperatures. At all temperatures the rate of CSF K changed gradually increased with time. The interval before the CSF K started to increase was dependent upon the amount of O2 available in the brain and the length of this interval was inversely proportional to the CMRO2. The amount of CSF K concentration was not clearly related to the tolerable periods of circulatory arrest, but at normal temperatures an obviously increased CSF K following a period of acute cerebral anoxia without CSF hemorrhage may indicate brain damage.

Effects of hypocapnia on cerebral oxygen consumption (CMRO2) and blood flow (CBF) in cerebral ischemia were studied in 19 patients. The CMRO2 did not change significantly during hypocapnia within the whole group of patients, because 10 out of 19 cases showed a decrease (p less than 0.001) and other 9 showed an increase (p less than 0.01) of CMRO2 during hypocapnia. The first 10 showed higher resting CMRO2 (p less than 0.001) and arteriovenous differences of oxygen content (AVDO2; p less than 0.02) than the other 9. However, the resting CBF and CO2 reactivity to hypocapnia were not different between them, and clinical situations were also similar. A dissociation between flow and metabolism was suggested in the first 10 with rather preserved CMRO2, while reduced metabolic demands were suggested in the other 9. Different responses of CMRO2 to hypocapnia are expected in cerebral ischemia, i.e. in cases with rather preserved CMRO2 it decreases despite an AVDO2 increase, suggesting a capability of CMRO2 to respond to CBF reduction, while it increases in cases with more decreased CMRO2, as the AVDO2 increase exceeds the CBF reduction to maintain the decreased CMRO2 for a further CBF reduction. The vascular CO2 reactivity, therefore, might be maintained to be constant between these patients.

Cerebral oxygen metabolism (CMRO2) and fractional extraction (OEF) regional values obtained using the 15O steady-state method and positron-emission tomography (PET) were corrected for the activity remaining in blood vessels (a source of overestimation of the OEF neglected in the simple steady-state model) using an additional scan during continuous inhalation of nontoxic amounts of carbon monoxide labeled with 15O (C15O). The method was applied to ten serial PET studies. In normal tissue, OEF overestimation was 11% +/- 2.6% and 9% +/- 2.0% in gray and white matter, respectively. In pathological tissue, the OEF overestimation was, on average, higher than in normal tissue (28% +/- 17% in the core of lesions), but more variable. In both normal and abnormal tissue, however, it was found that (1) the lower the real OEF, the larger the correction applied, and (2) the correction appears to be particularly necessary in situations of abnormally low OEF. The use of C15O continuous inhalation is a simple, direct, and accurate method for blood-activity correction when the 15O steady-state technique is employed to study pathophysiology.

One of the major factors leading to secondary brain damage in raised ICP is probably disturbed cerebral blood flow, metabolism and oxygenation secondary to raised ICP. Our hypothesis was that apart from measuring pressure it could be worthwhile to monitor cerebral oxygenation. The pO2 in CSF can be regarded as a parameter that reflects the oxygen supply to the brain, the cerebral blood flow and the rate of cerebral oxygen metabolism. The aim of this study was to evaluate the possibility and clinical relevance of continuous CSF pO2 monitoring.

Oxygen-15 labeled compounds in blood have been used successfully for cerebral circulation and cerebral oxygen metabolism measurements. The present paper describes a system for the rapid sequential production of 15OHgB, C15OHgb and H215O in blood under sterile and pyrogen-free conditions. A tonometer has been adopted for labeling blood without hemolysis and foam production.

To clarify the pathophysiology of normal pressure hydrocephalus (NPH) after subarachnoid hemorrhage, the authors measured cerebral blood flow (CBF), cerebral oxygen metabolic rates (CMRO2), the cerebral oxygen extraction fraction (OEF), and cerebral blood volume (CBV) in eight normal volunteers, six SAH patients with NPH, and seven patients without NPH by 150-labeled gas and positron emission tomography (PET). In the NPH group, PET revealed a decrease in CBF in the lower regions of the cerebral cortex and a diffuse decrease in CMRO2. The decrease in CBF in the lower frontal, temporal, and occipital cortices was significantly greater in the NPH than in the non-NPH group. Reduction of CMRO2 was also more extensive in the NPH group, and both CBF and CMRO2 were more markedly decreased in the lower frontal region. OEF was increased in all areas in both of the patient groups, but the increase was not significant in most areas. CBF, CMRO2 and OEF did not significantly differ between the non-NPH group and the normal volunteers. There was no significant difference in CBV among the three groups. These results indicate that NPH involves impairment of cerebral oxygen metabolism in the lower regions of the cerebral cortex, particularly in the lower frontal region. (Neurol Med Chir (Tokyo) 29:382–388, 1989)

BabyLux project is driven by the end-users working with academia and industry to develop a hybrid near-infrared diffuse correlation spectroscopy (DCS)/ time resolved spectroscopy (TRS) system to address the challenge of a user-friendly, medical grade device for neonatology.