ABSTRACT
Objective To confirm whether in post-resuscitation myocardial dysfunction involved in myocyte apoptosis mechanism in porcine model of cardiac arrest and apoptosis index varied from different modalities of cardiopulmonary resuscitation or not.Methods A total of 22 WZSP inbred small swine were randomly (random number) divided into sham operation group (SHAM) (n =6),defibrillation first group (DF,n =8) and chest compression first group (CF,n =8).Eight minutes after ventricular fibrillation was set up,standard CPR was carried out subsequently after defibrillation in porcine models of cardiac arrest in DF group and defibrillation after standard CPR in CF group,and hemodynamics were monitored.Twentyfour hours after restoration of spontaneous circulation (ROSC),animals were sacrificed,and myocardial specimens were examined with electron microscopy,Western blot,quantitative RT-PCR,and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.The experimental data were analyzed by SPSS 17.0.Student's t test was employed for comparisons between two groups.Differences within groups at different time intervals were compared with repeated measures ANOVA.A two-tailed value of P ＜ 0.05 was considered statistically significant.Results Myocardial function was significantly impaired after ROSC.Levels of Bcl-2,Bax and caspase-3 protein was markedly increased in the CF and DF groups than those in the SHAM group (P ＜ 0.05) at 24 h after ROSC,while Bcl-2/Bax was significantly reduced in the CF and DF group compared with the SHAM group (P ＜ 0.05),and much more apoptotic cells were observed in cardiac arrest animals in comparison with sham-operation animals (P ＜ 0.05).Six hours after ROSC,hemodynamic indicators improved significantly in group DF than those in group CF,but Bcl-2,Bax and caspase-3 protein levels and apoptotic index were not significantly different bewteen the DF group and CF group (P ＞ 0.05).Conclusions Caspase-3-mediated apoptosis might be one of the main pathological mechanisms of postresuscitation myocardial injury in a porcine model of cardiac arrest,but there was no statistically significant difference in apoptosis index between two resuscitation modalities,showing no one modality was superior over another.
ABSTRACT
ObjectiveTo observe the effects of mild hypothermia on post-resuscitation myocardial dysfunction in rabbits in order to elucidate the underlying mechanism of hypothermia.Methods After setting up rabbit model of cardiopulmonary resuscitation,20 rabbits were randomly ( random number)divided into two groups,namely normothermic resuscitation group (group A,n =10 ) and post-ROSC hypothermia group ( group B,n =10).In the group A,animals wore treated with standard CPR after cardiac arrest.In post-ROSC hypothermia group,the body temperature of animals was cooled to 32 ～ 34°C after successful ROSC.The left ventricular end-diastolic pressure (LVEDP),left ventricular pressure rise and fall rates ( ± dp/dtmax,serum concentrations of heart-type fatty acid-binding protein (H-FABP) and 8-isoprostaglandin F2a (8-iso-PGF2a) and Cyclooxygenase-2 (COX-2) were observed. Results Compared with the A group,the B group had significantly better hemodynamics,and lower serum H-FABP,8-isoPGF2a and COX-2 levels in the early stage of post-resuscitation ( both P ＜ 0.05 ).ConclusionsMild hypothermia attenuated post-resuscitation myocardial dysfunction during the early period of postresuscitation.The cryoprotective effect on myooardium is likely associated with the reduction of 8-iso-PGF2a and COX-2.
ABSTRACT
Objective To observe the effects of selective α2-adrenergic receptor agonist alpha-Methylnore-pinephrine(α-MNE) as a vasopressin agent on hemodynamics, troponin T(cTnT) and myocardium in the rabbit cardiopulmonary resuscitation. Method Eighteen health rabbits, weighing 2.5 - 3.5 kg, both male and female,were provided by Lanzhou institute of veterinary medicine. After setting up rabbit model of cardiopulmonary resuscitation, 18 rabbits were randomly divided into three groups. The rabbits in group A as a operation-control group were processed with anesthesia, endotracheal intubation, and surgery without ventricular fibrillation induced. The rabbits in group B as a epinephrine group were administered with 30 ug/kg epinephrineduring CPR. The rabbits in group C as a MNE group were administered with 100 ug/kg α-MNE during CPR. The left ventrictdar end-diastolic pressure(LVEDP), left ventricular pressure rise and fall rate(± dp/dt) and serum concentrations of BNP were measured. Statistic package of SPSS 10.0 was used for the data analysis and significant differences between means were evaluated by ANOVA analysis. Results Compared with group A, LVEDP of other two groups gradually increased respectively(P < 0. 01), and peak ± dp/dt decreased in other two groups(P<0.01). Increase in LVEDP in group C was less than that in group B(P<0.05), whereas peak ± dp/dt in group C were higher than that in group B(P<0.05), at the same stage. Compared with group A, the cTnT of the remaining two groups increased(P<0.01, respectively),and reached peak at 30 minutes. In group C, the elevation of cTnT was less than that in group B(P<0.05) during the same period. In group B and C, myocardial injury was seen under a light microscope, but the injury in group C was lighter than that in group B. Conclusion The methylnorepinephrine can lessen the myocardial dysfunction after CPR.