ABSTRACT
The rationale for conducting research in the newborn dog relates to the well established observation that acute brain damage secondary to systemic hypoxia, hypotension, or cardiac arrest is prevented, or at least reduced, by prior or concurrent hypothermia. To ascertain alterations in cerebral metabolism that occur during hypothermic circulatory arrest, additional experiments were conducted in anesthetized, paralyzed, and artificially ventilated newborn dogs that were surface-cooled to 20°C followed by cardiac arrest with KCl for up to 1.75 hours. The findings suggest that maintenance of adequate systemic blood pressure and hence cerebral perfusion in the early postoperative period are important to prevent or minimize ischemic brain damage in newborn infants subjected to hypothermic circulatory arrest. The systemic physiologic and regional cerebral blood flow and metabolic responses to hypothermia alone, as well as during and following hypothermic circulatory arrest, have been well characterized.
