Studies such as the Boston Circulatory Arrest Study (see Part V) have demonstrated that deep hypothermic circulatory arrest alone does not provide complete cerebral protection, particularly when the arrest period is extended beyond 30 to 45 minutes. However, this is not adequate time to undertake complex reconstructive procedures for some congenital heart anomalies in children, nor is it adequate for complete replacement of the aortic arch for degenerative disease in adults. For this reason a number of investigators have studied the possibility of adjunctive methods of cerebral protection including the use of cerebral perfusion with cerebroplegia. 1 , 2 In the previous chapter, Dr. Swain described studies of a cerebroplegia solution which is essentially the same as many cardioplegia solutions. This cold oxygenated crystalloid solution was delivered into the cerebral circulation through the carotid arteries. While control animals demonstrated a complete loss of cerebral ATP, as measured by magnetic resonance spectroscopy after 30 minutes of circulatory arrest (as we have also found in similar studies [see Chapter 20]), the animals that received cerebroplegia had measurable amounts of ATP at the end of the arrest period, showed less intracellular acidosis, and had an earlier return of EEG. In a follow-up survival study, Dr. Swain found that sheep receiving crystalloid cerebroplegia antegrade through the carotid arteries had a greater neurological score than control animals or animals receiving cerebroplegia retrograde through the superior vena cava. Interestingly the animals that had their heads packed in ice during the arrest period did as well as those receiving antegrade cerebroplegia.