Regulation of cerebral blood flow after asphyxia in neonatal lambs

Abstract

In a postasphyxia neonatal lamb model, the responses of the cerebral circulation to hypoxic hypoxia and changes in systemic arterial blood pressure were examined. Ventilated newborn lambs (n = 14) were subjected to a gradual asphyxial insult, resuscitated, and returned to control ventilator settings. During the tune 2-5 hours after asphyxia, the responses of cerebral blood flow (CBF), cerebral oxygen delivery (OD), cerebral oxygen consumption (CMRO2), and cerebral fractional oxygen extraction (E) to changes in either arterial oxygen content (CaO2) or mean arterial blood pressure (MAP) were assessed. These data were compared with measurements from nonasphyxiated lambs (n = 7). With hypoxia (n = 7), cerebral blood flow increased (CBF=646/CaO2 +44) compared with nonasphyxiated lambs (CBF = 1121/CaO2 +11). In asphyxiated lambs, cerebral oxygen delivery decreased (OD = 0.41 CaO2 + 6.87), but cerebral oxygen consumption remained stable due to a proportional increase in cerebral fractional oxygen extraction (E= —0.014 CaO2 + 0.65). In nonasphyxiated lambs, cerebral oxygen delivery, consumption, and fractional extraction were unchanged with hypoxia. In response to alterations in blood pressure, both cerebral blood flow (CBF = 0.84 MAP+6.62) and oxygen delivery (OD = 0.13 MAP + 0.77) were pressure-passive. With hypotension, cerebral fractional oxygen extraction increased (E = -0.003 MAP + 0.69) but not enough to prevent a decrease in cerebral oxygen consumption (CMRO2 = 0.042 MAP+1.79). In nonasphyxiated lambs, cerebral blood flow, oxygen delivery, consumption, and fractional extraction did not vary with blood pressure. My data demonstrate unpaired cerebral vasodilation in response to hypoxia and hypotension after an asphyxic insult. In a second study (n = 10), the role of cerebral edema in postasphyxia abnormalities of cerebral blood flow regulation was assessed. The impairment of postasphyxia cerebral vasodilation could not be attributed to the evolution of gross cerebral edema. © 1988 American Heart Association, Inc.