Impact of Norepinephrine and Fluid on Cerebral Oxygenation in Experimental Hemorrhagic Shock

Few data exist regarding resuscitation of hypovolemic shock in infants, and alternative strategies such as vasopressor therapy merit further evaluation. However, the effects of norepinephrine on cerebral perfusion and oxygenation during hemorrhagic shock in the pediatric population are still unclear. Eight anesthetized piglets were subjected to hypotension by blood withdrawal of 25 mL/kg. Norepinephrine was titrated to achieve baseline mean arterial blood pressure (MAP), and cerebral oxygenation was determined by brain tissue Po2(Ptio2) and near-infrared spectroscopy-derived tissue oxygen index (TOI). Then, norepinephrine was stopped, MAP was allowed to decrease again below 30 mm Hg, and shed blood was retransfused. During hemorrhage, TOI dropped from 69 ± 3 to 59 ± 3%, and Ptio2from 29 ± 6 to 13 ± 1 mm Hg (mean ± SEM; p< 0.001). Following norepinephrine, cerebral perfusion pressure (CPP) could be restored immediately, whereas TOI and Ptio2did not increase significantly. In contrast, following retransfusion, TOI and Ptio2increased to 68 ± 3% and 27 ± 7 mm Hg reaching baseline values, respectively. In conclusion, while norepinephrine increased CPP immediately, cerebral oxygenation as reflected by TOI and Ptio2could not be improved by norepinephrine, but only by retransfusion.