We investigated blood-brain barrier permeability in 2-3-week-old anesthetized pigs during and after cardiopulmonary resuscitation. We assessed permeability by tissue uptake of radiolabeled aminoisobutyric acid, after correcting for plasma counts in tissue with radiolabeled inulin. Among 14 regions examined, the transfer coefficient of aminoisobutyric acid in nonischemic control animals ranged from 0.0018 ±0.0001 ml/g/min in diencephalon to 0.0049±0.0003 ml/g/min in cervical spinal cord. After 8 minutes of cardiac arrest followed by either 10 or 40 minutes of continuous sternal compression, there was no increase in the transfer coefficient Likewise, during the immediate period after ventricular defibrillation, there was no increase in transfer coefficient despite the brief, transient hypertension. However, after 8 minutes of arrest, 6 minutes of cardiopulmonary resuscitation, and 4 hours of spontaneous circulation, the transfer coefficient was significantly increased by 59-107% in 10 of 11 regions rostral to the pons. Plasma volume in tissue measured by inulin was not elevated, suggesting that the increased transfer coefficient was not due to increased surface area. Thus, after an 8-minute period of complete ischemia, the blood-brain barrier remains intact during and immediately after resuscitation despite large vascular pressure fluctuations. However, in contrast to previous work on adult dogs, immature pigs are prone to a delayed increase in permeability, thereby allowing circulating substances greater access to the brain. {Stroke 1991^2:477-483) B lood-brain barrier function after cardiac arrest is important in limiting access to the brain of endogenously released humoral substances and exogenously administered drugs that could affect cerebral metabolism or vascular smooth muscle. We have reported previously that external cardiopulmonary resuscitation (CPR) does not result in disruption of the blood-brain barrier as assessed by the transfer coefficient of the small molecule a-aminoisobutyric acid (AIB).1 This finding was unexpected because cyclic chest compression produces large pulse pressures in the range of 60-100 mm Hg in the aorta and 30-40 mm Hg in the cerebral venous sinuses.2 -3 Large pulse pressures in a postischemic,