| Objective:Recently,the incidence of cardiac arrest is increasing,accounting for almost 50%of deaths from heart disease.In recent years,with the advancement of CPR technology,the improvement of advanced life support systems has led to agradual increase in the recovery rate of spontaneous circulation,but the overall survival rate has not been significantly improved due to organ dysfunction after resuscitation.Cardiac dysfunction after resuscitation is the main cause of high mortality within 72 hours after ROSC.Interventions aimed at improving cardiac dysfunction after ROSC can be clinically beneficial.In recent years,studies have found that mild hypothermia has a certain protective function on the heart and has received extensive attention.The cardiac β-adrenergic signaling pathway plays an important role in the regulation of the diastolic function of the myocardium.Studies have shown that the heart’s β-renal superiority signaling pathway is significantly impaired after cardiopulmonary resuscitation,leading to impairment of cardiac function after ROSC.This study investigated the protective effect of mild hypothermia on cardiopulmonary resuscitation in cardiopulmonary resuscitation and its effect on myocardial β-adrenergic receptor signaling pathway.Methods:Male healthy Landrace pigs were selected and ventricular fibrillation was induced by programmed electrical stimulation and CPR was taken place in 8 minutes later.16 trials with successful resuscitation were divided into control group(n=8)and mild hypothermia group(n=8)using random number table method.During the experiment,the monitor continuously monitors heart rate(HR),mean arterial pressure(MAP),and continuously monitors left ventricular isovolumic systolic blood pressure maximum change rate(dp/dtmax)and left ventricular diastolic pressure decrease with the BL420 biological function system.Cardiac output(CO)was measured by thermodilution before and at post-ROSC 0.5 h,1 h,3 h,and 6 h,respectively,and venous blood was collected to determine the concentration of troponin I(cTnI)in the serum.Left ventricle ejection fraction(LVEF)was measured with echocardiography before and at 6 hours after resuscitation.Six hours after ROSC,animals were sacrificed by euthanasia and take off myocardial tissue specimens.RT-PCR was used to detect the mRNA expression of β1-adrenergic receptor(β1-AR)in myocardial tissue.ELISA was used to detect the contents of AC and cAMP in myocardium.Western blot was used to detect the protein content of G protein-coupled receptor kinase 2(GRK2)in myocardium.Results:There was no significant difference in hemodynamic parameters,cTnI,and LVEF between the mild hypothermia group and the control group.After successful resuscitation,the heart rate was significantly higher than the baseline value between the two group(P<0.05),while in the two group the CO and ±dp/dt max values were significantly decreased(P<0.05).Compared with the control group,the HR of the mild hypothermia group was significantly reduced at 0.5h,lh,3 h after ROSC,and the CO at 1 h and 3 h after ROSC was significantly increased,and the 1h 3 h and 6 h after the ROSC dp/dt max were significantly increased(P<0.05).And the 3 h and 6 h after the ROSC-dp/dt max were significantly increased(P<0.05).There was no significant change in MAP between the two groups(all P>0.05).After successful resuscitation,cTnI was lower than the control group at 3 and 6 hours after ROSC(p<0.05).At 6h after recovery of spontaneous circulation,the expression of LVEF and β1-AR mRNA and AC and cAMP levels,compared with control group,in the mild hypothermia group were significantly higher(P<0.05),while the concentration of GRK2 was significantly lower than that in the control group(P).<0.05).Conclusion:Mild hypothermia can reduce the degree of myocardial damage after resuscitation,and its mechanism may be related to the reduction of adrenergic receptor signaling pathway damage. |
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