BACKGROUND: Our miniaturized bloodless prime circuit for neonatal cardiopulmonary bypass (CPB) has previously been shown to elicit significantly reduced systemic inflammation. We studied the effects of this circuit on cerebral reperfusion because the pathophysiology of "no-reflow" is believed to have an inflammatory component. METHODS: Twenty neonatal piglets were randomized to CPB with miniaturized circuitry using either blood (group 1) or bloodless (group 2) prime. At 18 degrees C, piglets underwent 60 minutes of either (A) deep hypothermic circulatory arrest (DHCA) or (B) continuous low-flow bypass (DHCLF). Analysis of cerebral blood flow (CBF) was undertaken before and after CPB in addition to quantification of circulating tumor necrosis factor-alpha (TNFalpha) and intracerebral TNFalpha messenger RNA (mRNA). RESULTS: The final hematocrit in group 2 was 22% versus 28% (p < 0.05). The CBF fell in every animal in group 1A, but increased in every animal in group 2A (p < 0.001), despite no overall change in total cardiac output. The use of DHCLF was not associated with pronounced trends in either prime group. Final serum TNFalpha concentrations were significantly higher in group 1B (3166 +/- 843 pg/mL) than group 2B (439 +/- 192 pg/mL; p < 0.05). Irrespective of the CPB strategy used, the use of a blood prime generated significantly higher levels of intracerebral TNFalpha mRNA. CONCLUSIONS: We attribute the hyperemic cerebrovascular response to reduced inflammation through avoiding allogeneic whole blood. The analysis of circulating and intracerebral TNFalpha in this study suggests that DHCLF in conjunction with a bloodless prime might offer advantages through avoiding ischemia, no-reflow, and in addition, resulting in a significantly reduced cerebral inflammatory response.
BACKGROUND: Our miniaturized bloodless prime circuit for neonatal cardiopulmonary bypass (CPB) has previously been shown to elicit significantly reduced systemic inflammation. We studied the effects of this circuit on cerebral reperfusion because the pathophysiology of "no-reflow" is believed to have an inflammatory component. METHODS: Twenty neonatal piglets were randomized to CPB with miniaturized circuitry using either blood (group 1) or bloodless (group 2) prime. At 18 degrees C, piglets underwent 60 minutes of either (A) deep hypothermic circulatory arrest (DHCA) or (B) continuous low-flow bypass (DHCLF). Analysis of cerebral blood flow (CBF) was undertaken before and after CPB in addition to quantification of circulating tumor necrosis factor-alpha (TNFalpha) and intracerebral TNFalpha messenger RNA (mRNA). RESULTS: The final hematocrit in group 2 was 22% versus 28% (p < 0.05). The CBF fell in every animal in group 1A, but increased in every animal in group 2A (p < 0.001), despite no overall change in total cardiac output. The use of DHCLF was not associated with pronounced trends in either prime group. Final serum TNFalpha concentrations were significantly higher in group 1B (3166 +/- 843 pg/mL) than group 2B (439 +/- 192 pg/mL; p < 0.05). Irrespective of the CPB strategy used, the use of a blood prime generated significantly higher levels of intracerebral TNFalpha mRNA. CONCLUSIONS: We attribute the hyperemic cerebrovascular response to reduced inflammation through avoiding allogeneic whole blood. The analysis of circulating and intracerebral TNFalpha in this study suggests that DHCLF in conjunction with a bloodless prime might offer advantages through avoiding ischemia, no-reflow, and in addition, resulting in a significantly reduced cerebral inflammatory response.