Fetal head compression during labor may increase intracranial pressure (ICP) and decrease cerebral perfusion pressure (CPP). An increase in mean arterial pressure (MAP) associated with the Cushing response normally acts to mitigate an ischemic insult when the increase in ICP approaches MAP. However, the premature fetus may be limited in its ability to increase MAP. We compared the efficacy of the pressor response in sustaining CPP, cerebral blood flow (CBF), and cerebral O2 consumption (CMRO2) in chronically catheterized fetal sheep at 0.6 gestation (92 d; n = 7) and 0.9 gestation (133 d; n = 7). When fetal ICP was increased to baseline MAP (41 ± 3 mm Hg; ±SEM) in 92-d fetuses, MAP increased by 7 ± 2 mm Hg and remained stable during 30 min of constant ICP elevation; CBF decreased by 72% and CMRO2 decreased by 46%. In 133-d fetuses, MAP increased from 53 ± 2 to 65 ± 4 mm Hg at 3 min of elevated ICP; CBF decreased by 62% and CMRO2 decreased 30%. However, MAP continued to increase after 3 min and reached a stable level of 75 ± 3 mmHg at 30 min in 133-d fetuses. The additional increase in MAP restored CBF and CMRO2 to baseline values. Plasma epinephrine and vasopressin concentrations increased between 6 and 33 min of elevated ICP to levels, exceeding those in 92-d fetuses. We conclude that the arterial pressure response to intracranial hypertension is present at 0.6 gestation but is less well developed than at 0.9 gestation in fetal sheep, possibly due to immaturity of the sympathoadrenal and vasopressin systems. Consequently, CBF and CMRO2 are not as well defended at mid-gestation against elevated ICP as might occur during difficult labor.
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health