CEREBRAL BLOOD-FLOW DURING HYPOXIC HYPOXIA WITH PLASMA-BASED HEMOGLOBIN AT REDUCED HEMATOCRIT

We determined whether cerebral blood flow (CBF) remained related to ar terial O-2 content (Ca-O2) during hypoxic hypoxia when hematocrit and hemoglobin concentration were independently varied with cell-free, tet ramerically stabilized hemoglobin transfusion. Three groups of pentoba rbital sodium-anesthetized cats were studied with graded reductions in arterial O-2 saturation to 50%: 1) a control group with a hematocrit of 31 +/- 1% (mean +/- SE; n = 7); 2) an anemia group with a hematocri t of 21 +/- 1% that underwent an isovolumic exchange transfusion with an albumin solution (n = 8); and 3) a group transfused with an intramo lecularly cross-linked hemoglobin solution to decrease hematocrit to 2 1 +/- 1% (n = 10). Total arterial hemoglobin concentration (g/dl) afte r hemoglobin transfusion (8.8 +/- 0.2) was intermediate between that o f the control (10.3 +/- 0.3) and albumin (7.2 +/- 0.4) groups. Forebra in CBF increased after albumin and hemoglobin transfusion at normoxic O-2 tensions to levels attained at equivalent reductions in Ca-O2 in t he control group during graded hypoxia. Over a wide range of arterial O-2 saturation and sagittal sinus PO2, CBF remained greater in the alb umin group. When CBF was plotted against Ca-O2 for all three groups, a single relationship was formed. Cerebral O-2 transport, O-2 consumpti on, and fractional O-2 extraction were constant during hypoxia and equ ivalent among groups. We conclude that CBF remains related to Ca-O2 du ring hypoxemia when hematocrit is reduced with and without proportiona l reductions in O-2-carrying capacity. Thus O-2 transport to the brain is well regulated at a constant level independently of alterations in hematocrit, hemoglobin concentration, and O-2 saturation.