• Junyuan Wu, Zhiwei Li, Wei Yuan, Yongzhen Zhao, Jie Li, Zhenhua Li, Jiebin Li, and Chunsheng Li.
• Department of Emergency Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China.
• Neurocrit Care. 2020 Aug 1; 33 (1): 73-81.

BackgroundOur previous study found that mild hypothermia (MH) after resuscitation reduced cerebral microcirculation, but the mechanism was not elucidated. The aim of this study was to clarify changes of endothelin-1 (ET-1) and nitric oxide (NO) systems in brain tissue during hypothermia after resuscitation.MethodsTwenty-six domestic male Beijing Landrace pigs were used in this study. MH was intravascularly induced 1 h after resuscitation from 8-min ventricular fibrillation. Core temperature was reduced to 33 °C and maintained until 8 h after resuscitation, and then animals were euthanized. ET-1 and NO levels in brain tissue and peripheral plasma were measured. Expression of endothelin-converting enzyme-1 (ECE-1), endothelin A receptor (ET-AR), endothelin-B receptor, and nitric oxide synthase (NOS) in brain tissue was determined by Western blot analysis.ResultsCompared with non-hypothermia (NH) treatment, MH after resuscitation significantly increased the level of endothelin-1 and reduced the level of NO in peripheral blood and brain tissue. Cerebral expression of ECE-1 and ET-AR was significantly increased during MH after resuscitation. Moreover, MH significantly decreased inducible NOS expression compared with the NH group.ConclusionsThe ET-1 system is activated, while inducible NOS is inhibited in brain tissue during MH after resuscitation.

5 keywords...

hide…