Responses of Gerbil Cerebral Unit Activity to Declining Tissue PO₂

Abstract

Within the central nervous system, microregional differences may exist in tissue oxygen tension due to the variation in such factors as blood flow, capillary density, and rates of tissue respiration. Also, cells located near the venous portion of a capillary should be exposed to a lower oxygen tension than cells at the arterial end as suggested by mathematical modeling based on the Krogh cylinder (Krogh, 1918). Such PO₂ differences within brain tissue, in fact, have been demonstrated experimentally (Silver, 1965; Metzger and Heuber, 1977). Taking these variations in tissue PO₂ into account, is there then a relative vulnerability of neurons to ischemia or hypoxia? Namely, do those cells normally existing within low PO₂ areas suffer the most in that during such an episode of low oxygen availability the PO₂ will reach zero in these regions first, or have these low PO₂ neurons undergone some adaptive process such that they better tolerate an ischemic or hypoxic insult than cells always normally exposed to a generous oxygen supply? The term “critical PO₂” has been used for that PO₂ below which cellular dysfunction occurs.