目的 观察不同时机行轻度低温干预对室颤兔心肌组织能量、超微结构和血清心肌肌钙蛋白(cTNI)、肿瘤坏死因子α (TNF-α)水平以及近期死亡率的影响.方法 雄性新西兰兔54只,随机分为5组;常温(39.0±0.5℃)对照组(n=8),低温(33.5±0.5℃)对照组(n=8),常温(39.0±0.5℃)复苏组(n=14),复苏前低温(33.5±0.5℃)组(n=10),复苏后低温(33.5±0.5℃)组(n=14).采用心外膜电刺激致颤法制备兔心肺复苏模型.复苏后4h采血检测血清cTNI、TNF-α水平；低温各组均持续控温4h后自然复温,观察各组存活情况至复苏后48h,将兔处死后行左室心尖组织电镜检查和三磷腺苷(ATP)、二磷酸腺苷(ADP)、磷酸腺苷(AMP)含量测定,计算心肌能荷(EC).结果 复苏后低温组和两对照组48h存活率均为100％,高于常温复苏组和复苏前低温组(60.0％和44.4％,P＜0.05),复苏前低温组48h存活率低于常温复苏组(P＜0.05).各复苏组血清cTNI水平均高于两对照组,复苏前低温组血清cTNI水平低于常温复苏组和复苏后低温组(P＜0.05)；常温复苏组血清TNF-α水平明显高于其他各组(P＜0.05),两低温复苏组间及两对照组间无统计学差异(P＞0.05).复苏前和复苏后低温组心肌组织ATP含量均高于常温复苏组,复苏后低温组和常温复苏组心肌组织ATP含量均较对照组明显减低(P＜0.05)；常温复苏组EC明显低于两对照组和复苏前低温组(P＜0.05)；复苏后低温组EC与复苏前低温组及两对照组间无统计学差异(P＞0.05).复苏前和复苏后低温组复苏后48h心肌超微结构损害均较常温复苏组轻(P＜0.05).结论 室颤兔自主循环恢复后存在心肌组织损害和能量代谢异常；自主循环恢复后轻度低温干预可减轻心肌组织结构损害,降低48h死亡率,其保护机制与改善心肌细胞能量代谢、抑制炎症反应有关；室颤前轻度低温处理不能降低48h死亡率.%Objective To determine the effects of mild pre- and post-arrest therapeutic hypothermia on the post-resuscitation myocardium of rabbit cardiac arrest model. Methods Fifty-four rabbits were randomly assigned into 5 groups: normothermic control group (NTC, n=8, 39.0 ± 0.5 ℃), hypothermia control group (HTC, n=8, 33.5 ± 0.5℃), normothermic resuscitation group (NTR, n=14, 39.0 ± 0.5℃), pre-arrest hypothermia group (HPRA, n=10,33.5 ± 0.5℃) and post-arrest hypothermia group (HPOA, n=14, 33.5 ± 0.5℃). Ventricular fibrillation cardiac arrest was induced in rabbits by transcutaneous epicardium electrical stimulation. The body temperature of rabbits in hypothermia groups was maintained by surface cooling for 4 hours. Mortality was recorded at 48h, and blood was then drawn to measure the levels of cTNI and TNF- a . The survived rabbits were sacrificed and myocardium tissues were harvested for ultrastructural observation by electronic microscopy. The contents of ATP, ADP and AMP in the tissue samples were measured by high performance liquid chromatography (HPLC), and myocardial energy charge (EC) was calculated. Results The 48-hour survival rates were 100% in NTC, HTC and HPOA groups, respectively, and they were significantly higher than that of NTR and HPRA groups (60.0% and 44.4%). Higher levels of cTNI were observed in NTR, HPRA and HPOA groups when compared with those in NTC and HTC groups, and the cTNI level in HPRA group was lower than that in NTR and HPOA groups. The level of TNF- a. was higher in NTR group than in other 4 groups, and no difference was found in the level of TNF- a between HPRA and HPOA group. The levels of ATP in myocardium tissue were higher in HPRA and HPOA groups than in NTR group, while the levels of ATP were found to be lower in NTR and HPOA groups than in the two control groups. No significant difference was found in ATP levels between HPRA and control groups. The levels of EC were lower in NTR group than in HPRA and control groups, while no significant difference in EC levels was found among NTC, HTC, HPOA and HPRA groups. Compared with NTC and HTC groups, in the remaining 3 groups with cardiac arrest destruction of myocardial ultrastructure was found in 48h, but the damage was ameliorated in HPOA and HPRA groups. Conclusions Therapeutic hypothermia may attenuate the myocardial injury of ventricular fibrillation in cardiac arrest model of rabbits; it preserves more ATP and decreases inflammatory reaction. Following the restoration of spontaneous circulation, a mild post-arrest therapeutic hypothermia may increase the 48h survival rate of rabbits with cardiac arrest, but pre-arrest therapeutic hypothermia may not.
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