Extracranial hypothermia during cardiac arrest and cardiopulmonary resuscitation is neuroprotective in vivo

Michael P. Hutchens, Tetsuhiro Fujiyoshi, Ines P. Koerner, Paco S. Herson

研究成果: ジャーナルへの寄稿記事

5 引用 (Scopus)

抄録

There is increasing evidence that ischemic brain injury is modulated by peripheral signaling. Peripheral organ ischemia can induce brain inflammation and injury. We therefore hypothesized that brain injury sustained after cardiac arrest (CA) is influenced by peripheral organ ischemia and that peripheral organ protection can reduce brain injury after CA and cardiopulmonary resuscitation (CPR). Male C57Bl/6 mice were subjected to CA/CPR. Brain temperature was maintained at 37.5°C ± 0.0°C in all animals. Body temperature was maintained at 35.1°C ± 0.1°C (normothermia) or 28.8°C ± 1.5°C (extracranial hypothermia [ExHy]) during CA. Body temperature after resuscitation was maintained at 35°C in all animals. Behavioral testing was performed at 1, 3, 5, and 7 days after CA/CPR. Either 3 or 7 days after CA/CPR, blood was analyzed for serum urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase, and interleukin-1β; mice were euthanized; and brains were sectioned. CA/CPR caused peripheral organ and brain injury. ExHy animals experienced transient reduction in brain temperature after resuscitation (2.1°C ± 0.5°C for 4 minutes). Surprisingly, ExHy did not change peripheral organ damage. In contrast, hippocampal injury was reduced at 3 days after CA/CPR in ExHy animals (22.4% ± 6.2% vs. 45.7% ± 9.1%, p=0.04, n=15/group). This study has two main findings. Hypothermia limited to CA does not reduce peripheral organ injury. This unexpected finding suggests that after brief ischemia, such as during CA/CPR, signaling or events after reperfusion may be more injurious than those during the ischemic period. Second, peripheral organ hypothermia during CA reduces hippocampal injury independent of peripheral organ protection. While it is possible that this protection is due to subtle differences in brain temperature during early reperfusion, we speculate that additional mechanisms may be involved. Our findings add to the growing understanding of brain-body cross-talk by suggesting that peripheral interventions can protect the brain even if peripheral organ injury is not altered.

元の言語英語
ページ(範囲)79-87
ページ数9
ジャーナルTherapeutic hypothermia and temperature management
4
発行部数2
DOI
出版物ステータス出版済み - 6 1 2014
外部発表Yes

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Cardiopulmonary Resuscitation
Heart Arrest
Hypothermia
Brain Injuries
Brain
Ischemia
Wounds and Injuries
Body Temperature
Resuscitation
Temperature
Reperfusion
Encephalitis
Aspartate Aminotransferases
Alanine Transaminase
Interleukin-1
Urea
Creatinine
Nitrogen

All Science Journal Classification (ASJC) codes

  • Critical Care and Intensive Care Medicine
  • Anesthesiology and Pain Medicine

これを引用

Extracranial hypothermia during cardiac arrest and cardiopulmonary resuscitation is neuroprotective in vivo. / Hutchens, Michael P.; Fujiyoshi, Tetsuhiro; Koerner, Ines P.; Herson, Paco S.

:: Therapeutic hypothermia and temperature management, 巻 4, 番号 2, 01.06.2014, p. 79-87.

研究成果: ジャーナルへの寄稿記事

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abstract = "There is increasing evidence that ischemic brain injury is modulated by peripheral signaling. Peripheral organ ischemia can induce brain inflammation and injury. We therefore hypothesized that brain injury sustained after cardiac arrest (CA) is influenced by peripheral organ ischemia and that peripheral organ protection can reduce brain injury after CA and cardiopulmonary resuscitation (CPR). Male C57Bl/6 mice were subjected to CA/CPR. Brain temperature was maintained at 37.5°C ± 0.0°C in all animals. Body temperature was maintained at 35.1°C ± 0.1°C (normothermia) or 28.8°C ± 1.5°C (extracranial hypothermia [ExHy]) during CA. Body temperature after resuscitation was maintained at 35°C in all animals. Behavioral testing was performed at 1, 3, 5, and 7 days after CA/CPR. Either 3 or 7 days after CA/CPR, blood was analyzed for serum urea nitrogen, creatinine, alanine aminotransferase, aspartate aminotransferase, and interleukin-1β; mice were euthanized; and brains were sectioned. CA/CPR caused peripheral organ and brain injury. ExHy animals experienced transient reduction in brain temperature after resuscitation (2.1°C ± 0.5°C for 4 minutes). Surprisingly, ExHy did not change peripheral organ damage. In contrast, hippocampal injury was reduced at 3 days after CA/CPR in ExHy animals (22.4{\%} ± 6.2{\%} vs. 45.7{\%} ± 9.1{\%}, p=0.04, n=15/group). This study has two main findings. Hypothermia limited to CA does not reduce peripheral organ injury. This unexpected finding suggests that after brief ischemia, such as during CA/CPR, signaling or events after reperfusion may be more injurious than those during the ischemic period. Second, peripheral organ hypothermia during CA reduces hippocampal injury independent of peripheral organ protection. While it is possible that this protection is due to subtle differences in brain temperature during early reperfusion, we speculate that additional mechanisms may be involved. Our findings add to the growing understanding of brain-body cross-talk by suggesting that peripheral interventions can protect the brain even if peripheral organ injury is not altered.",
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