RESPONSE OF THE CEREBRAL-CIRCULATION TO HYPOCAPNIA IN POSTASPHYXIA NEWBORN LAMBS

Respiratory alkalosis is used in the treatment of newborn infants with persistent pulmonary hypertension. Many of these infants have suffered a prior asphyxial insult. Previous studies in a newborn lamb postasphyxia model have demonstrated abnormalities in the response of the cerebral circulation to hypoxia and to changes in blood pressure. Although vasodilation in response to these stimuli was impaired, the ability of the brain to extract oxygen was not. Therefore, because the principal response of the cerebral circulation to lowering arterial carbon dioxide tension is vasoconstriction with a compensatory increase in oxygen extraction, it was hypothesized that the postasphyxia response of the cerebral circulation to decreases in carbon dioxide tension would be intact. Ten newborn lambs were subjected to an asphyxial insult. Postasphyxia whole brain and regional blood flows were measured at three to four different levels of arterial carbon dioxide tension using the radiolabeled microsphere technique. In addition, arterial and venous oxygen content and blood gases were measured in the brachiocephalic artery and the sagittal sinus. The response of whole brain cerebral blood flow (CBF) to changes in arterial carbon dioxide tension (PaCO2) is described by In CBF = 0.031 PaCO2 + 3.15 (r = 0.83, p < 0.001). Responses of individual brain regions did not differ from whole brain flow. Cerebral oxygen consumption remained stable, and fractional O2 extraction (E) increased according to the relationship In (1 - E) = -0.023 PaCO2 - 1.35 (r = 0.89, p < 0.001). No significant differences in responses of cerebral hemodynamics to hypocarbia were found in comparison of data from this study with previous work in nonasphyxiated lambs. Thus, the response of the cerebral circulation to hypocarbia is not affected by a prior asphyxial insult in the newborn lamb.