ABSTRACT
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, 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.
ABSTRACT
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, 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.
ABSTRACT
Objective To investigate the effects of hydrogen on post - cardiac arrest brain injury in rabbits.Method Sixty New Zealand rabbits were randomly divided into two groups,namely experiment group ( group A,n =30 ) and control group ( group B,n =30 ).Inhalation of 2％ hydrogen gas was conferred to rabbits immediately at the end of cardiac arrest modeling for 72 hours in the group A. Air instead was given to rabbits in the group B.Blood samples were collected before cardiac arrest (CA),and 4,12,24 and 72 hours after restoration of spontaneous circulation (ROSC) in all rabbits for determining the levels of hydrogen,tumor necrosis factor - α ( TNF - α),neuron - specific enolase (NSE) and protein S100β.At the same time,rectal temperature,mean arterial pressure,heart rate and respiration rate were recorded,and the neurologic deficit scoring (NDS) was carried out.The rate of systemic inflammatory response syndrome ( SIRS ) and the rate of survival of rabbits were analyzed. Results There was no significant difference in level of TNF - α activation between group A and group B within12 h of cardiopulmonary resuscitation (CPR).In group A,TNF - α level and the rate of SIRS peaked at 24 hours after CPR,which were higher than those in group B,and then decreased gradually,and the rate of survival was higher than that in group B in 72 hours after ROSC,the NSE was lower than that in group B at 24 hours after ROSC.In group B,S100β level began to increase significantly 4 hours after CPR,which was higher than that in group A,the level of NDS in group B was higher than that in group A 72 hours after ROSC.Conclusions Inhalation of hydrogen gas lessened inflammation and alleviated the brain injury after CPR.