Changes of cortical oxidative metabolism and cortical oxygen tension in hypoxia, anoxia and ischaemia.

The changes of oxidative metabolism in mitochondria with hypoxia, anoxia and ischaemia were studied by a compensated fluorometer/reflectometer in rabbits. The NADH redox state exponentially increased with the decrease of cortical oxygen tension (CoPO2) which was recorded simultaneously under systemic hypoxia or anoxia. This correlation was statistically significant (p less than 0.001). It is suggested that oxidative metabolism in mitochondria can be improved by rather small increases of CoPO2 in a severely ischaemic area. Focal cerebral ischaemia was induced by occlusion of the middle cerebral artery (MCA-O) through a transorbital approach. The NADH promptly increased with MCA-O and reached a maximal level (29.9% from the control level on average) at 20-110 s of MCA-O. Then, it partially improved to 21.2% from the control level after 5 min of MCA-O, which was statistically less than the maximal reduction level. After 5 min of MCA-O, it was shown to be stable for up to 30 min of MCA-O. It appears that the partial recovery of the NADH redox state in the acute phase of arterial occlusion occurs because of the improvement of the collateral circulation demonstrated previously. This suggests one pathophysiological mechanism for transient ischaemic attacks.