Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 35, Issue 8, Pages 1289-1295Publisher
SAGE PUBLICATIONS INC
DOI: 10.1038/jcbfm.2015.41
Keywords
cardiac arrest; complement; mild hypothermia; neuroprotection; pig
Categories
Funding
- Liaoning Province Nature Science Foundation [2013023020]
- Training Programs of Talents in Science and Technology Grant [2013D003]
Ask authors/readers for more resources
Complement activation has been implicated in ischemia/reperfusion injury. This study aimed to determine whether mild hypothermia (HT) inhibits systemic and cerebral complement activation after resuscitation from cardiac arrest. Sixteen minipigs resuscitated from 8 minutes of untreated ventricular fibrillation were randomized into two groups: HT group (n = 8), treated with HT (33 degrees C) for 12 hours; and normothermia group (n = 8), treated similarly as HT group except for cooling. Blood samples were collected at baseline and 0.5, 6, 12, and 24 hours after return of spontaneous circulation (ROSC). The brain cortex was harvested 24 hours after ROSC. Complement and pro-inflammatory markers were detected using enzyme-linked immunosorbent assay. Neurologic deficit scores were evaluated 24 hours after ROSC. C1q, Bb, mannose-binding lectin (MBL), C3b, C3a, C5a, interleukin-6, and tumor necrosis factor-alpha levels were significantly increased under normothermia within 24 hours after ROSC. However, these increases were significantly reduced by HT. Hypothermia decreased brain C1q, MBL, C3b, and C5a contents 24 hours after ROSC. Hypothermic pigs had a better neurologic outcome than normothermic pigs. In conclusion, complement is activated through classic, alternative, and MBL pathways after ROSC. Hypothermia inhibits systemic and cerebral complement activation, which may provide an additional mechanism of cerebral protection.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available