摘要目的 探讨氢气(H2)干预对兔心搏骤停(CA)后心肌损伤及心功能不全的影响.方法 按随机数字表法将雄性新西兰白兔分为吸入H2治疗组和空气对照组,每组30只.两组均经口气管插管行机械通气,采用电刺激心外膜法建立兔CA模型,CA 6 min后进行心肺复苏(CPR),待自主循环恢复(ROSC)后停机.H2治疗组置于含2％H2空气的笼中饲养,持续至ROSC 72 h;空气对照组则吸入100％空气72 h.观察72 h后动物存活情况;记录CA前及ROSC后的心率和室性期前收缩(室早)发生数,测定全血心肌肌钙蛋白I(cTnI)、左室射血分数(LVEF)、B型钠尿肽(BNP)、血乳酸(Lac)水平;电镜下观察心肌组织超微结构改变.结果 两组均有28只动物ROSC;ROSC 72 h时,H2治疗组存活动物数多于空气对照组(只:15比7,χ2=4.791,P=0.029).ROSC初期,两组动物心率减慢、室早发生数增多,之后逐渐恢复;ROSC 48 h,H2治疗组心率较空气对照组恢复更快(次/min:319±63比362±40,P<0.05);ROSC 72 h,H2治疗组室早发生数较空气对照组明显减少(次/min:9.1±4.3比15.0±8.0,P<0.05).ROSC后两组动物均有不同程度的心肌损害及心功能不全,随时间延长均有所恢复.与空气对照组比较,H2治疗组ROSC 24 h BNP水平明显降低(ng/L:385±98比488±174,P<0.05);ROSC 48 h cTnI和Lac明显降低〔cTnI(μg/L):1.83±0.68比2.83±0.98,Lac(mmol/L):5.5±1.6比7.9±2.6,均P<0.01〕,72 h LVEF略增加(0.690±0.040比0.650±0.041,P=0.051).电镜下观察显示,H2治疗组心肌组织病理改变较空气对照组减轻.结论 吸入H2可减轻CA兔心肌损伤,缩短心肌顿抑及功能障碍的病程,改善组织灌注,提高动物存活率.

abstractsObjective To investigate the effects of hydrogen (H2) on myocardium injury post-cardiac arrest (CA) in rabbits.Methods Sixty New Zealand rabbits were randomly divided into H2 treatment group (n = 30) and control group (n = 30) by random number table. The rabbit CA model was established by means of electrical stimulation of external membrane, both groups were mechanically ventilated. Cardiopulmonary resuscitation (CPR) was performed after 6 minutes of nonintervention, and stopped after restoration of spontaneous circulation (ROSC). Inhalation of 2％ H2 gas was conferred to rabbits immediately at the end of CA modeling for 72 hours in H2 treatment group. Air was given to rabbits in control group instead. The survival rate of rabbits was analyzed. Heart rate, ventricular premature beat frequency, and the levels of blood samples cardiac troponin I (cTnI), left ventricular ejection fraction (LVEF), B-type natriuretic peptide (BNP), and blood lactic acid (Lac) were collected before CA and after ROSC in all rabbits. Rabbits were sacrificed and microstructure injury was observed by electric microscope after ROSC 72 hours.Results There were 28 animals ROSC in both groups; the survival number in H2 treatment group was higher than that in control group at 72 hours after ROSC (number: 15 vs. 7,χ2 = 4.791,P = 0.029). In the early stage of ROSC, the heart rate of two groups slowed down, the number of premature ventricular increased, and then gradually recovered; the heart rate in H2 treatment group was returning to normal more quickly than that in control group at 48 hours after ROSC (bpm: 319±63 vs. 362±40,P < 0.05); the ventricular premature beat frequency was lower than that in control group at 72 hours after ROSC (times per minutes: 9.1±4.3 vs. 15.0±8.0,P < 0.05). The animals of two groups had different degrees of myocardial damage and cardiac insufficiency after ROSC, and restored with the extension of time. Compared with control group, the level of BNP in H2 treatment group was significant decreased at 24 hours after ROSC (ng/L: 385±98 vs. 488±174,P < 0.05), the levels of cTnI and Lac were significant decreased at 48 hours after ROSC [cTnI (μg/L:1.83±0.68 vs. 2.83±0.98, Lac (mmol/L): 5.5±1.6 vs. 7.9±2.6, bothP < 0.01], the LVEF was slightly higher than that at 72 hours after ROSC (0.690±0.040 vs. 0.650±0.041,P = 0.051). Compared with control group, less damage to myocardial ultra structure was found in H2 treatment group at 72 hours after ROSC.Conclusion Inhalation of H2 alleviates cardiac dysfunction and myocardial injury after CPR.