Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2013
Treatment with a highly selective β₁ antagonist causes dose-dependent impairment of cerebral perfusion after hemodilution in rats.
Acute β-blockade has been associated with a dose-dependent increase in adverse outcomes, including stroke and mortality. Acute blood loss contributes to the incidence of these adverse events. In an attempt to link the risks of acute blood loss and β-blockade, animal studies have demonstrated that acute β-blockade impairs cerebral perfusion after hemodilution. We expanded on these findings by testing the hypothesis that acute β-blockade with a highly β(1)-specific antagonist (nebivolol) causes dose-dependent cerebral hypoxia during hemodilution. ⋯ Our data demonstrate that nebivolol resulted in a dose-dependent decrease in cerebral oxygen delivery after hemodilution as reflected by a decrease in brain tissue Po(2) and an increase in hypoxic protein responses (HIF-1α and nNOS). Low-dose nebivolol treatment did not result in worsened tissue hypoxia after hemodilution, despite comparable effects on HR and CO. These data support the hypothesis that acute β-blockade with a highly β(1)-specific antagonist causes a dose-dependent impairment in cerebral perfusion during hemodilution.