Regional dependence of cerebral reperfusion after circulatory arrest in rats

The severity of neurologic dysfunction after circulatory arrest depends on cerebral reperfusion during and after resuscitation. The objective of cur-r ent study was to investigate the temporal and spatial patterns of the cereb ral perfusion immediately after resuscitation. Precise control of circulato ry arrest was achieved in rats by combination of asphyxia and transient blo ckage of cardiac-specific P-adrenergic receptors with esmolol, an ultra-sho rt-acting P-blocker. Animals were randomized into 3 groups with resuscitati on starting 0.5 (sham group, no asphyxia, n = 5), 4 (Group 2, n = 5), or 12 minutes (Group 3, n = 8) later by retrograde intraarterial infusion of don or blood along with a resuscitation mixture. Cerebral perfusion was measure d by magnetic resonance imaging (MRI) using arterial spin labeling. The ave rage perfusion before arrest was 163 +/- 27 mL 100 g(-1) min(-1) under isof lurane anesthesia. Resuscitation led to transient perfusion increase, which started from thalamus and hypothalamus and later shifted to the cortex. Se vere hypoperfusion to as low as 6% to 20% of the normal level developed in the first 10 to 20 minutes of reperfusion and lasted for at least 2 hours, On the fifth day after circulatory arrest, all animals showed a normal leve l of perfusion (159 +/- 57 mL 100 g(-1) min(-1)) and minimal neurologic def icit. Nevertheless, histologic examination revealed extensive changes in th e CAI region of the hippocampus consistent with global ischemia and reperfu sion damage. The combination of an improved circulatory arrest model and no ninvasive MRI cerebral perfusion measurements provides a powerful tool for investigations of circulatory arrest and resuscitation, allowing for evalua tion of therapies aimed at modulating cerebral reperfusion.