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1 Anesthesia, Cara Phelan Centre for Trauma Research, Keenan Research Centre in The Li Ka Shing Knowledge Institute and Physiology, University of Toronto, St. Michael's Hospital, Toronto, Canada
2 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, Canada
3 Interdepartmental Division of Critical Care Medicine and Paediatrics and the Neuroscience and Mental Health Program, University of Toronto, The Hospital for Sick Children, Toronto, Canada
4 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, Canada
5 Critical Care Medicine and Paediatrics and the Neuroscience and Mental Health Program, Hospital for Sick Children, Toronto, Canada
6 Critical Care Medicine and Paediatrics and the Neuroscience and Mental Health Program, University of Toronto, The Hospital for Sick Children, Toronto, Canada
7 Division of Neuropathology, Department of Laboratory Medicine, University of Toronto, The Hospital for Sick Children, Toronto, Canada
* To whom correspondence should be addressed. E-mail: hareg{at}smh.toronto.on.ca.
Anemia may worsen neurological outcomes following traumatic brain injury (TBI) by undefined mechanisms. We hypothesized that anemia accentuates hypoxic cerebral injury following TBI. Anesthetized rats underwent TBI or sham injury (n
7). Target hemoglobin concentrations between 50 and 70 g.L-1 were achieved by exchanging 40-50% of the blood volume (1:1) with pentastarch. The effect of TBI, Anemia and TBI-Anemia were assessed by measuring brain tissue oxygen tension (PBrO2), regional cerebral blood flow (rCBF), jugular venous oxygen saturation (SjvO2), cerebral contusion area and nuclear staining for cell death. Baseline post-injury PBrO2 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 PBrO2 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 SjvO2 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 cell death were increased following TBI and 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 PBrO2 and oxygen extraction and increased cell death following TBI. These results support our hypothesis that anemia accentuated hypoxic cerebral injury after neurotrauma.
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