MILD HYPOTHERMIA AFTER CARDIAC-ARREST IN DOGS DOES NOT AFFECT POSTARREST MULTIFOCAL CEREBRAL HYPOPERFUSION

Background and Purpose: Although mild resuscitative hypothermia (34-de grees-C) immediately after cardiac arrest improves neurological outcom e in dogs, its effects on cerebral blood flow and metabolism are unkno wn. Methods: We used stable xenon-enhanced computed tomography to stud y local, regional, and global cerebral blood flow patterns up to 4 hou rs after cardiac arrest in dogs. We compared a normothermic (37.5-degr ees-C) control group (group I, n=5) with a postarrest mild hypothermic group (group II, n=5). After ventricular fibrillation of 12.5 minutes and reperfusion with brief cardiopulmonary bypass, the ventilation, n ormotension, normoxia, and mild hypocapnia were controlled to 4 hours after cardiac arrest. Group II received (minimal) head cooling during cardiac arrest, followed by systemic bypass cooling (to 34-degrees-C) during the first hour of reperfusion after cardiac arrest. Results: Th e postarrest homogeneous transient hyperemia was followed by global hy poperfusion from 1 to 4 hours after arrest, with increased ''no-flow'' and ''trickle-flow'' voxels (compared with baseline), without group d ifferences. At 1 to 4 hours, mean global cerebral blood flow in comput ed tomographic slices was 55% of baseline in group I and 64% in group II (NS). No flow (local cerebral blood flow <5 mL/100 cm3 per minute) occurred in 5 +/- 2% of the voxels in group I versus 9 +/- 5% in group II (NS). Trickle flow (5 to 10 mL/100 cm3 per minute) occurred in 10 +/- 3% voxels in group I versus 16 +/- 4% in group II (NS). Cerebral b lood flow values in eight brain regions followed the same hyperemia-hy poperfusion sequence as global cerebral blood flow, with no significan t difference in regional values between groups. The global cerebral me tabolic rate of oxygen, which ranged between 2.7 and 4.5 mL/100 cm3 pe r minute before arrest in both groups, was at 1 hour after arrest 1.8 +/- 0.3 mL in normothermic group I (n=3) and 1.9 +/- 0.4 mL in still-h ypothermic group II (n=5); at 2 and 4 hours after arrest, it ranged be tween 1.2 and 4.2 mL in group I and between 1.2 and 2.6 mL in group II . Conclusions: After cardiac arrest, mild resuscitative hypothermia la sting I hour does not significantly affect patterns of cerebral blood flow and oxygen uptake. This suggests that different mechanisms may ex plain its mitigating effect on brain damage.