通过建立大鼠心跳骤停与复苏模型，探讨亚低温治疗可能通过保护心脏功能，改善模型动物生存预后。

雄性SD大鼠18只，随机分为常温对照组和亚低温治疗组。通过建立经右室电诱发室颤模型，对复苏后大鼠实施亚低温治疗。用超声评估复苏后大鼠的第1～4小时动物左室射血分数(EF)和心肌表现指数(MPI)等心脏功能变化；观察复苏后大鼠第24小时、72小时生存率，及每24小时神经功能缺损评分。

两组共18只动物全部复苏成功，ROSC成功率、心肺复苏时间、首次除颤成功率等均无显著性差异。复苏后心脏彩超示，对照组动物在复苏后1～4小时心功能进行性受损，左室射血分数(EF)从基础值的(74.9±2.2)%，降低至(59.8±6.52)%，(50.4±4.4)%，(48.8±4.8)%，(47.8±6.1)%。而低温治疗组动物EF值从(73.9±2.5)%变化为(76.2±3.0)%，(75.1±3.5)%，(71.9±4.7)%，(64.1±3.1)%，两组间由统计学差异；心肌表现指数(MPI)，对照组动物从基础值的0.6±0.1增高至1.1±0.1，1.2±0.1，1.3±0.2，1.4±0.3，较亚低温治疗组动物显著恶化，而低温组MPI则从0.6±0.1升高至0.7±0.1，0. 8±0.1，0.8±0.1，0.9±0.1。亚低温治疗组动物在复苏后72小时存活数显著高于对照组，复苏后24、48、72小时的神经功能缺损评分均显著性低于对照组。

在本大鼠心跳骤停与复苏模型中，亚低温治疗能够显著保护心脏功能，从而显著改善动物生存及神经功能预后。

To establish a rat model with cardiac arrest and resuscitation to study the role of mild hypothermia in protecting the post-resuscitation heart function and improving their survival outcomes.

Eighteen male SD rats were enrolled in the study and randomly divided into control group (normal temperature) and mild hypothermia group. Ventricular fibrillation model was induced electrically and the resuscitated rats were treated with mild hyperthermia. Heart function indices including ejection fraction and myocardial performance index were monitored by ultrasound at 1-4 hours after resuscitation. Neurological deficit score (NDS) was evaluated every 24 hours after resuscitation. The 24-hour and 72-hour survival rates were compared between two groups.

All 18 rats were successfully resuscitated. There were no significant differences in success rate of ROSC, resuscitation time and success rate of first defibrillation. The heart function was worsened obviously in the rats of the control group at 1-4 hours after resuscitation, with left ventricular ejection fraction decreasing from baseline (74.9±2.2)% to (59.8±6.52)%, (50.4±4.4)%, (48.8±4.8)%, (47.8±6.1)%. While the left ventricular ejection fraction was changed from (73.9±2.5)% to (76.2±3.0)%, (75.1±3.5)%, (71.9±4.7)%, (64.1±3.1)%, with statistical difference between two groups. The myocardial performance index was increased from the baseline 0.6±0.1 to 1.1±0.1, 1.2±0.1, 1.3±0.2, 1.4±0.3 in the control group but increased from baseline 0.6±0.1 to 0.7±0.1, 0. 8±0.1, 0.8±0.1, 0.9±0.1, with worse results in the control group. The 72-hour survival animals in the mild hyperthermia group were significantly more than those in the control group. NDS at 24, 48 and 72 hours after resuscitation in the mild hyperthermia group was significantly lower than that in the control group.

In this model, mild hypothermia can protect the heart function and improve the neurological and survival outcomes of the resuscitated rats.