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Severe hemodilutional anemia increases cerebral tissue injury following acute neurotrauma

¹Department of Anesthesia, Cara Phelan Centre for Trauma Research, Keenan Research Centre in the Li Ka Shing Knowledge Institute, University of Toronto, St. Michael's Hospital, Toronto; ²Department of Physiology, University of Toronto, Toronto; ³Departments of Critical Care Medicine and Paediatrics and the Neuroscience and Mental Health Program, The Hospital for Sick Children, Toronto; ⁴Interdepartmental Division of Critical Care, Faculty of Medicine, University of Toronto, Toronto; and ⁵Division of Neuropathology, Department of Laboratory Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada

Submitted 20 November 2006 ; accepted in final form 4 June 2007

Anemia may worsen neurological outcomes following traumatic brain injury (TBI) by undefined mechanisms. We hypothesized that hemodilutional anemia accentuates hypoxic cerebral injury following TBI. Anesthetized rats underwent unilateral TBI or sham injury (n 7). Target hemoglobin concentrations between 50 and 70 g/l were achieved by exchanging 40–50% of the blood volume (1:1) with pentastarch. The effect of TBI, anemia, and TBI-anemia was assessed by measuring brain tissue oxygen tension (Pbr_O2), regional cerebral blood flow (rCBF), jugular venous oxygen saturation (Sjv_O2), cerebral contusion area, and nuclear staining for programmed cell death. Baseline postinjury Pbr_O2 values in the TBI and TBI-anemia groups (9.3 ± 1.3 and 11.3 ± 4.1 Torr, respectively) were lower than the uninjured controls (18.2 ± 5.2 Torr, P < 0.05 for both). Hemodilution caused a further reduction in Pbr_O2 in the TBI-anemia group relative to the TBI group without anemia (7.8 ± 2.7 vs. 14.8 ± 3.9 Torr, P < 0.05). The rCBF remained stable after TBI and increased comparably after hemodilution in both anemia and TBI-anemia groups. The Sjv_O2 was elevated after TBI (87.4 ± 8.9%, P < 0.05) and increased further following hemodilution (95.0 ± 1.6%, P < 0.05). Cerebral contusion area and nuclear counts for programmed cell death were increased following TBI-anemia (4.1 ± 3.0 mm² and 686 ± 192, respectively) relative to TBI alone (1.3 ± 0.3 mm² and 404 ± 133, respectively, P < 0.05 for both). Hemodilutional anemia reduced cerebral Pbr_O2 and oxygen extraction and increased cell death following TBI. These results support our hypothesis that acute anemia accentuated hypoxic cerebral injury after neurotrauma.

hemodilution; brain tissue oxygen tension

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