Spontaneous Hypothermia Ameliorated Inflammation and Neurologic Deficit in Rat Cardiac Arrest Models Following Resuscitation

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作者：Zhou, M., Wang, P., Yang, Z., Wu, H. & Huan, Z.
期刊：Molecular medicine reports 17, 2127-2136 (2018)
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Cardiac arrest (CA) is a leading cause of mortality worldwide. The majority of the associated mortalities are caused by post?CA syndrome, which includes symptoms, such as neurologic damage, myocardial dysfunction and systemic inflammation. Following CA, return of spontaneous circulation (ROSC) leads to a brain reperfusion injury, which subsequently causes adverse neurologic outcomes or mortality. Therefore, investigating the underlying mechanisms of ROSC?induced neurologic deficits and establishing potential treatments is critical to prevent and treat post?CA syndrome. In the current study, CA rat models were established by asphyxia. Following ROSC, the temperature was controlled to achieve hypothermia. The general neurologic status was assessed using the neurologic deficit scale. Changes in the concentrations of interleukin (IL)?18 and IL?1β were measured with ELISA and the dynamic change in NACHT, LRR and PYD domains?containing protein 3 inflammasome components was determined by western blot analysis and immunohistochemistry. Neuronal death and apoptosis were measured via TUNEL assays. In the CA rat models, increasing the duration of CA before cardiopulmonary resuscitation was found to aggravate the neural deficit and increase the incidence of inflammation. Following ROSC, the expression level of the inflammasome components was observed to increase in CA rat models, which was accompanied by increased secretion of IL?18 and IL?1β, indicating the promotion of inflammation. In addition, the study identified the beneficial role of spontaneous hypothermia in ameliorating the ROSC?induced inflammation and neurologic deficit in CA rat models, including the downregulation of inflammasome components and attenuating neuronal apoptosis. The present study contributes to the understanding of underlying mechanisms in CA?evoked inflammation and the subsequent neurologic damage following ROSC. A novel potential therapeutic strategy that may increase survival times and the quality of life for patients suffering from post?CA syndrome is proposed in the present study.