Abstract：
AIMS:The cerebellum is among the brain regions most vulnerable to damage caused by cardiac arrest, and cerebellar Purkinje cell loss may contribute to neurologic dysfunction, including post-hypoxic myoclonus. However, it remains unknown whether cerebellar Purkinje cells are protected by post-cardiac arrest therapeutic hypothermia (TH). Therefore, we examined the effect of post-cardiac arrest TH onset and duration on cerebellar Purkinje cell loss. METHODS:Samples from a previously published study of post-cardiac arrest TH were utilized for the present analysis. Adult male rats subjected to asphyxial cardiac arrest and cardiopulmonary resuscitation were block randomized to normothermia (37.0°C) or TH (33.0°C) initiated 0, 1, 4, or 8h after return of spontaneous circulation (ROSC) and maintained for 24 or 48 h. Cerebella from rats surviving 7 days after ROSC were processed for histology and immunohistochemistry. Purkinje cell density was quantified in Nissl-stained sections of the primary fissure of the cerebellar vermis. RESULTS:With post-cardiac arrest normothermia, Purkinje cell density in the primary fissure was severely reduced compared to sham-injured controls (3.8 ± 1.8 cells mm(-1) vs. 35.9 ± 2.4 cells mm(-1), p<0.001). TH moderately improved Purkinje cell survival in all groups combined (14.0 ± 5.6 cells mm(-1), p<0.001 compared to normothermia). There was no statistical difference in Purkinje cell protection based on TH onset time or duration. CONCLUSION:These results indicate that post-cardiac arrest TH protects selectively vulnerable cerebellar Purkinje cells within a broad therapeutic window. The potential clinical implications for improving Purkinje cell survival require further investigation.
journal_name
Resuscitationjournal_title
Resuscitationauthors
Paine MG,Che D,Li L,Neumar RWdoi
10.1016/j.resuscitation.2012.05.022subject
Has Abstractpub_date
2012-12-01 00:00:00pages
1511-6issue
12eissn
0300-9572issn
1873-1570pii
S0300-9572(12)00274-2journal_volume
83pub_type
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