Abstract 1233 Neonatal Disease Oriented Research: Molecular Events and Brain Injury Poster Symposium, Tuesday, 5/4

Preterm infants often receive volume 'boluses' after birth to increase or maintain mean blood pressure (MAP), but the cerebrovascular effects of this therapeutic strategy are unknown. We tested the hypothesis that acute volume expansion increases cerebral venous pressure (saggital sinus, SSP), but not MAP, and consequently decreases cerebral perfusion pressure (CPP). We gave 7 near-term (126-132 days gestation) chronically catheterized fetal sheep 2 IV boluses of 20 mL/kg of Dextran 70 each over 15 minutes separated by 30 minutes and measured cerebral blood flow (CBF - microspheres), blood volume (technetium-labeled RBCs), and arterial (CaO2) and venous (CvO2) oxygen content at baseline and 15 minutes after completion of each bolus. We calculated cerebrovascular resistance (CVR) as MAP/CBF, cerebral O2 delivery (OD) as CaO2×CBF, and cerebral O2 consumption (CMRO2) as (CaO2-CvO2)×CBF. Results: (mean±SD, * p<0.05 vs. baseline, π p<0.05 vs. Bolus #1) (Table)

Table 1 No caption
Full size table

Conclusions: A single volume bolus which expanded blood volume by 26% caused an increase in MAP and SSP, and consequently no change in CPP. Due to the dilutional decrease in hematocrit, CaO2 fell, but surprisingly there was no significant increase in CBF. A second volume bolus with a further 18% increase in blood volume resulted in a further decrease in CaO2. While CPP was still maintained, CBF remained unchanged so that OD and CMRO2 decreased. Acute volume expansion does not alter CPP in developing brain. More importantly, the expected dilutional decrease in CaO2 was not accompanied by a compensatory increase in CBF to maintain cerebral oxygen delivery. This response could be detrimental, particularly during hypoxemia or ischemia.