STUDIES OF TISSUE PO2 IN NORMAL AND PATHOLOGICAL HUMAN BRAIN CORTEX

Brain cortex PO2 was measured after craniotomy and opening of the dura mater in 26 patients. We determined the brain tissue PO2 under standa rd narcotic conditions and after changing arterial PO2 and PCO2. Patie nts were divided into two groups (normal and pathological), depending on the aspect of their cortex on Ct/MRI and intraoperative appearance of the cortex. No statistical significantly difference was seen betwee n tissue PO2 of the normal and the pathological group. A significant d ifference was seen only between the normal group and a subgroup with b rain swelling (p = 0.0344). In the normal group no correlation was see n between tissue PO2 and arterial PO2 (r = 0.1541, p = 0.3076), wherea s in the pathological group and especially in the oedema subgroup ther e was a highly significant correlation between tissue PO2 and PaO2 (r = 0.754, p = 0.0015 and r = 0.888, p = 0.0007). Breathing 100% oxygen changed tissue PO2 to 137.8 or 352 mmHg in the normal or the pathologi cal group, respectively. Again, there was no correlation between tissu e PO2 and PaO2 in the normal group (r = 0.1071, p = 0.392), whereas th is correlation was significant in the pathological and the oedema subg roup (r = 0.629 1, p = 0.0473 and r = 0. 8385, p = 0.0185). This is ev idence for regulatory mechanisms of tissue PO2. During hyperventilatio n no significant difference in tissue PO2 between the normal and the p athological group was seen. Low tissue PO2 values, however, indicate a risk for inducing ischaemia.