ABSTRACT
Objective To observe the effect of mild hypothermia on myocardial β-adrenergic receptor (β-AR) signal pathway after cardiopulmonary resuscitation (CPR) in pigs with cardiac arrest (CA) and explore the mechanism of myocardial protection. Methods Healthy male Landraces were collected for reproducing the CA-CPR model (after 8-minute untreated ventricular fibrillation, CPR was implemented). The animals were divided into two groups according to random number table (n = 8). In the mild hypothermia group, the blood temperature of the animals was induced to 33 ℃ and maintained for 6 hours within 20 minutes after return of spontaneous circulation (ROSC) by using a hypothermia therapeutic apparatus. In the control group, the body temperature of the animals was maintained at (38.0±0.5)℃ with cold and warm blankets. The heart rate (HR), mean arterial pressure (MAP), the maximum rate of increase or decrease in left rentricular pressure (+dp/dt max)were measured during the course of the experiment. The cardiac output (CO) was measured by heat dilution methods before CA (baseline), and 0.5, 1, 3, 6 hours after ROSC respectively, the venous blood was collected to detect the concentration of cTnI. Left ventricular ejection fraction (LVEF) was measured with cardiac ultrasound before CA and 6 hours after ROSC. Animals were sacrificed at 6 hours after ROSC and the myocardial tissue was harvested quickly, the mRNA expression of β1-AR in myocardium was detected by reverse transcription-polymerase chain reaction (RT-PCR), the contents of adenylate cyclase (AC) and cyclic adenosine monophosphate (cAMP) were detected by enzyme linked immunosorbent assay (ELISA), the protein content of G protein-coupled receptor kinase 2 (GRK2) was detected by Western Blot. Results After successful resuscitation, the HR of both groups were significantly higher than the baseline values, CO, ±dp/dt max were significantly decreased, MAP were not significantly changed, serum cTnI levels were significantly increased. Compared with the control group, HR at 0.5, 1, 3 hours after ROSC were significantly decreased in mild hypothermia group (bpm: 142.80±12.83 vs. 176.88±15.14, 115.80±11.48 vs. 147.88±18.53, 112.60±7.40 vs. 138.50±12.02, all 1 < 0.01), CO was significantly increased at 1 hours and 3 hours after ROSC (L/min: 3.97±0.40 vs. 3.02±0.32, 4.00±0.11 vs. 3.11±0.59, both 1 < 0.01), +dp/dt max at 3 hours and 6 hours was also significantly increased after ROSC [+dp/dt max (mmHg/s): 3 402.5±612.7 vs. 2 130.0±450.6, 3 857.5±510.4 vs. 2 562.5±633.9; -dp/dt max (mmHg/s): 2 935.0±753.2 vs. 1 732.5±513.6, 3 520.0±563.6 vs. 2 510.0±554.3, all 1 < 0.05], the cTnI was significantly decreased at 3 hours and 6 hours afher ROSC (μg/L: 1.39±0.40 vs. 3.24±0.78, 1.46±0.35 vs. 3.78±0.93, both 1 < 0.01). The left at 6 hours after ROSC in both groups was decreased as compared with that before CA. The LVEF in the mild hypothermia group was higher than that in the control group (0.52±0.04 vs. 0.40±0.05, 1 < 0.05). The mRNA expression of β1-AR, and concentrations of AC and cAMP in hypothermia group were significantly higher than those in control group [β1-AR mRNA (2-ΔΔCT): 1.18±0.39 vs. 0.55±0.17, AC (ng/L):197.0±10.5 vs. 162.0±6.3, cAMP (nmol/L): 1 310.58±48.82 vs. 891.25±64.95, all 1 < 0.05], GRK2 was lower than that in the control group (GRK2/GAPDH: 0.45±0.05 vs. 0.80±0.08, 1 < 0.05). Conclusion Mild hypothermia can reduce the degree of cardiac function injury after CPR, and its mechanism may be related to the reduction of impaired myocardial β-AR signaling after CPR.
ABSTRACT
Objective Gasp was defined as a pathology respiration during cardiac arrest. This study was to investigate its effect on hemodynamics during CPR. Method Twelve domestic pigs, weighening (30 ± 1) kg,were anaesthetized. After tracheal intubation and mechanical ventilation, continuous respiratory variables were recorded. An artery catheter was inserted for reference blood samples and measuring aortic artery pressure (AOP).Right atrial pressure (RAP) and cardiac output (CO) were detected by Swan-Ganz catheter. Ventricular fibrillation (VF) was induced by programmed electrical stimulation instruments. After 4 minutes untreated VF, standard 30:2 CPR was done for 12 minutes and the parameters were recorded. Results pH, PaCO2 and lactic acid increased and PaO2 decreased progressively during CPR, whereas PaO2 was up to 50mmHg during the whole protocol. Gasps were observed in 10 animals, but weaken gradually; the left 2 animals with no gasp did not restore of spontaneous circulation (ROSC). Standard CPR could produce passive ventilation more than dead space (VD), but its tidal volume decreased gradually, which led to the percentage of rescue ventilation increased progressively. Positive correlations were found between CO, coronary perfusion pressure (CPP) and minute ventilation of gasps (MVg) (r was 0.736 and 0.721 respectively, both P ＜0.01); negative correlation were found between RAP and MVg (r= -0. 744, P ＜ 0.01). Conclusions Standard CPR could maintain 12 minutes oxygenation of body; compressions could produce enough passive ventilation more than VD; gasps were benefit to ROSC by increasing CO, CPP and decreasing RAP.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate cardiac function and myocardial perfusion during 48 h after cardiopulmonary resuscitation (CPR), further to test myocardial stunning and seek indicators for long-term survival after CPR.</p><p><b>METHODS</b>After 4 min of untreated ventricular fibrillation, fifteen anesthetized pigs were studied at baseline and 2 h, 4 h, 24 h, and 48 h after restoration of spontaneous circulation (ROSC). Hemodynamic data, echocardiography and gated-single photon emission computed tomography myocardial perfusion images were carried out.</p><p><b>RESULTS</b>Mean arterial pressure (MAP), coronary perfusion pressure (CPP) and cardiac troponin I (CTNI) showed significant differences between eventual survival animals and non-survival animals at 4 h after ROSC (109.2 ± 10.7 mmHg vs. 94.8 ± 12.3 mmHg, P=0.048; 100.8 ± 6.9 mmHg vs. 84.4±12.6 mmHg, P=0.011; 1.60 ± 0.13 ug/L vs. 1.75 ± 0.10 ug/L, P=0.046). Mitral valve early-to-late diastolic peak velocity ratio, mitral valve deceleration time recovered 24 h; ejection faction and the summed rest score recovered 48 h after ROSC.</p><p><b>CONCLUSION</b>Cardiac systolic and early active relaxation dysfunctions were reversible within survival animals; cardiac stunning might be potentially adaptive and protective after CPR. The recovery of MAP, CPP, and CTNI could be the indicators for long-term survival after CPR.</p>
Subject(s)
Animals , Male , Blood Pressure , Cardiopulmonary Resuscitation , Coronary Circulation , Heart Arrest , Hemodynamics , Myocardial Contraction , Physiology , Myocardial Stunning , Swine , Time Factors , Ventricular FibrillationABSTRACT
Objective To investigate the microstructure and ultrastructure changes of cardiac muscle, pallium, lung, liver and kidney tissue and hemodynamic effects after the success of cardiac arrest (CA)-cardiopulmonary resuscitation(CPR) of swine. Method A total of 16 Beijing swine(weight 29 ～ 35 kg)were randomly (random number) divided into normal-control group ( n = 8) and standard CPR group ( n = 8). The swine of the former group were only given anesthetized and intubated, without ventricular fibrillation and CPR. The swine of the latter group were given standard CPR after 4 min of untreated VF, from 10 min after restoration of spontaneous cirkg) and keep for 6 h. And cardiac output (CO), left ventricular maximal rate of systolic pressure ( + dp/dtmax),maximum reduction of left ventricular diastolic velocity ( - dp/dtmax), heart rate (HR) and mean arterial pressure (MAP) of these animals before ventricular fibrillation and 0.5 h, 2 h, 4 h, 6 h after ROSC have been monitored.All swine were put to death after 6 h,and got their cardiac apex, pallium, left lung, right lobe of liver and upper pole of left kidney quickly for microstructure and ultrastructure studies. Statistical analysis was performed using two paired samples t test. Results At different time points after restoration of spontaneous circulation, the cardiac output (CO),left ventricular maximal rate of systolic pressure ( + dp/dtmax), maximum reduction of left ventricular diastolic velocity (- dp/dtmax) were significantly lower than before ventricular fibrillation, with significant difference ( P ＜ 0.05). And HR of different time points were increased significantly ( P ＜ 0.05), with no significantly difference between MAP of each time points ( P ＞ 0.05). Compared with the normal-control group, the cardiac muscle, pallium, lung, liver and kidney tissue of the swine in standard CPR group were found different degree of damages in their microstructure and ultrastructure sections. The damages of the cardiac muscle, pallium, and lung tissue were more obviously. Conclusions Sudden cardiac arrest(CA)-cardiopulmonary resuscitation(CPR) could cause different degree of damages and hemodynamic effects on the body, through our ROSC 6 h model, the damages of the cardiac muscle, pallium and lung were more severity, the damages of liver and kidney were lighter.