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1 Department of Anaesthesiology, University of Toronto, St. Michael's Hospital, Toronto, ON, Canada
2 Biotechnology Centre for Applied Research and Training, Seneca College, Toronto, ON, Canada
3 Transplant Research Division, Toronto General Hospital, Toronto, ON, Canada
4 Department of Public Health, University of Toronto, St. Michael's Hospital, Toronto, ON, Canada
* To whom correspondence should be addressed. E-mail: hareg{at}smh.toronto.on.ca.
Severe hemodilutional anemia may reduce cerebral oxygen delivery resulting in cerebral tissue hypoxia. Increased nitric oxide synthase (NOS) expression has been identified following cerebral hypoxia and may contribute to the compensatory increase in cerebral blood flow (CBF) observed following hypoxia and anemia. However, changes in cerebral NOS gene expression have not been reported following acute anemia. This study tests the hypothesis that acute hemodilutional anemia causes cerebral tissue hypoxia triggering changes in cerebral NOS gene expression. Anesthetized rats underwent hemodilution by exchanging 30 ml.kg-1 of blood with pentastarch, to a final hemoglobin concentration of 51.0 ± 1.2 g.L-1 (n=7). Caudate tissue oxygen tension (PBrO2) decreased transiently from 17.3 ± 4.1 to 14.4 ± 4.1 mmHg (p< 0.05), before returning to baseline after about 20 minutes. An increase in CBF may have contributed to restoring PBrO2 by improving cerebral tissue oxygen delivery. An increase in nNOS mRNA was detected by RT-PCR in the cerebral cortex of anemic rats, after 3 hours (P<0.05, n=5). A similar response was observed after exposure to hypoxia. By contrast, no increases in mRNA for eNOS or IL-1
were observed following anemia or hypoxia. Hemodilutional anemia caused an acute reduction in caudate tissue oxygen tension and an increase in cerebral cortical nNOS mRNA, supporting a role for nNOS in the physiological response to acute anemia.
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