Objective: 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, both P < 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.
Conclusions: Inhalation of H2 alleviates cardiac dysfunction and myocardial injury after CPR.