A previous study indicated that
diaspirin-crosslinked
hemoglobin (
DCLHb) decreases
cerebral ischemia after
subarachnoid hemorrhage. However, the study was limited in that
DCLHb was given to animals with an intact vasculature. As extravasated
hemoglobin has been implicated in the pathogenesis of
cerebral vasospasm,
DCLHb in the subarachnoid space might in theory have a detrimental effect on cerebral perfusion after
subarachnoid hemorrhage. In the current study, autologous blood was administered into the cistema magna of
isoflurane-anesthetized rats. After 30 minutes, the animals received one of the following in the cistema magna (n=8 for each group): The control group received mock cerebral spinal fluid, the "
blood" group received autologous blood, the "
DCLHb" group received
DCLHb, and the "Alb" group received
human serum albumin. After 20 minutes, areas of reduced cerebral blood flow (CBF, 0-20 and 21-40 ml/100 g/min) were assessed in five coronal brain sections with 14C-iodoantipyrine. The data were evaluated by analysis of variance. The areas of 0-20 ml/100 g/min CBF were greater in all five brain sections in the
Blood group than in the other three groups; were greater in four brain sections in the
DCLHb group than in the Control group; and were greater in three brain sections in the Alb group than in the Control group (p < 0.05). The areas of 21-40 ml/100 g/min CBF were greater in three sections in the
Blood group than in the other three groups; and were greater in two brain sections in the
DCLHb group than in the Alb group (p < 0.05). These data support a hypothesis that subarachnoid blood induces cerebral hypoperfusion, and that although molecular
hemoglobin decreases CBF, the potential adverse effects are less than those produced by blood.