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Objective@#To investigate the resuscitation effect of aortic balloon occlusion (ABO) on the traumatic cardiac arrest (TCA) in swine.@*Methods@#Twenty-seven male domestic swine weighing (32.7±3.8)kg were utilized. After 40% of estimated blood volume was removed within 20 minutes, the animals were subjected to 5 minutes of untreated ventricular fibrillation and then 5 minutes of cardiopulmonary resuscitation. Additionally, fluid resuscitation was initiated coincident with the beginning of cardiopulmonary resuscitation. The animals were randomly divided into model group (n=12) and ABO group (n=15). Once cardiopulmonary resuscitation was implemented, aortic balloon was concurrently inflated to stop the blood flow of descending thoracic aorta at the level of the diaphragm in the ABO group. In the model group, aortic balloon was placed in the same position without inflation. During cardiopulmonary resuscitation, the changes of coronary perfusion pressure (CPP), forehead's regional cerebral oxygen saturation (rSO2) and pressure of end-tidal CO2 (PETCO2) were continuously monitored, and the rate of return of spontaneous circulation (ROSC), duration of cardiopulmonary resuscitation, number of shocks and dose of epinephrine were recorded. At 5 minutes after successful resuscitation, the levels of arterial blood gas, lactate and jugular venous blood oxygen saturation (SjvO2) were measured.@*Results@#Compared with the model group, the values of CPP, rSO2 and PETCO2 during cardiopulmonary resuscitation were significantly increased in the ABO group [CPP: (33.5±5.6)mmHg vs. (23.1±5.2)mmHg at 1 minute, (35.3±6.0)mmHg vs. (26.8±7.4)mmHg at 2 minutes, (36.3±6.3)mmHg vs. (28.2±6.3)mmHg at 3 minutes, (40.1±7.1)mmHg vs. (30.5±6.2)mmHg at 4 minutes, (38.1±7.5)mmHg vs. (29.8±5.3)mmHg at 5 minutes; rSO2: (45.4±5.2)% vs. (39.2±5.1)% at 1 minute, (47.2±3.6)% vs. (42.0±6.4)% at 2 minutes, (47.7±3.0)% vs. (41.5±5.4)% at 3 minutes, (47.0±2.5)% vs. (42.1±5.9)% at 4 minutes, (47.1±2.0)% vs. (41.5±7.4)% at 5 minutes; PETCO2: (17.0±3.5)mmHg vs. (12.7±4.2)mmHg at 1 minute, (18.5±3.7)mmHg vs. (14.5±2.7)mmHg at 2 minutes, (20.7±5.3)mmHg vs. (15.5±3.2)mmHg at 3 minutes, (18.7±4.5)mmHg vs. (14.9±3.5)mmHg at 4 minutes, (18.2±3.2)mmHg vs. (14.5±4.2)mmHg at 5 minutes] (all P<0.05). The rate of ROSC was significantly higher in the ABO group than in the model group[100%(15/15) vs. 75%(9/12)] (P<0.05). Additionally, shorter duration of cardiopulmonary resuscitation, less number of shocks and lower doses of epinephrine were observed in the ABO group when compared with the model group[duration of cardiopulmonary resuscitation: 5(5, 5)minutes vs. 5(5, 12.5)minutes, number of shocks: 1(1, 1)times vs. 1(1, 4)times, dose of epinephrine: 0.62(0.62, 0.74)mg vs. 0.64(0.59, 2.59)mg] (all P<0.05). At 5 minutes after resuscitation, the level of arterial lactate was significantly decreased and the value of SjvO2 was significantly increased in the ABO group compared with the model group[Lactate: (9.6±0.8)mmol/L vs. (10.8±1.4)mmol/L; SjvO2: (50.0±8.6)% vs. (37.9±16.3)%] (both P<0.05).@*Conclusions@#In a swine model of TCA, ABO can increase cardiac and cerebral perfusion during cardiopulmonary resuscitation and improve the efficacy of cardiopulmonary resuscitation. It might provide a novel and effective method for the resuscitation of TCA in the clinical setting.
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Objective To investigate the resuscitation effect of aortic balloon occlusion (ABO) on the traumatic cardiac arrest (TCA) in swine.Methods Twenty-seven male domestic swine weighing (32.7 ± 3.8) kg were utilized.After 40％ of estimated blood volume was removed within 20 minutes,the animals were subjected to 5 minutes of untreated ventricular fibrillation and then 5 minutes of cardiopulmonary resuscitation.Additionally,fluid resuscitation was initiated coincident with the beginning of cardiopulmonary resuscitation.The animals were randomly divided into model group (n =12) and ABO group (n =15).Once cardiopulmonary resuscitation was implemented,aortic balloon was concurrently inflated to stop the blood flow of descending thoracic aorta at the level of the diaphragm in the ABO group.In the model group,aortic balloon was placed in the same position without inflation.During cardiopulmonary resuscitation,the changes of coronary perfusion pressure (CPP),forehead's regional cerebral oxygen saturation (rSO2) and pressure of end-tidal CO2 (PETCO2) were continuously monitored,and the rate of return of spontaneous circulation (ROSC),duration of cardiopulmonary resuscitation,number of shocks and dose of epinephrine were recorded.At 5 minutes after successful resuscitation,the levels of arterial blood gas,lactate and jugular venous blood oxygen saturation (SjvO2) were measured.Results Compared with the model group,the values of CPP,rSO2 and PETCO2 during cardiopulmonary resuscitation were significantly increased in the ABO group [CPP:(33.5 ± 5.6)mmHg vs.(23.1 ± 5.2)mmHg at 1 minute,(35.3 ± 6.0) mmHg vs.(26.8 ± 7.4) mmHg at 2 minutes,(36.3 ± 6.3) mmHg vs.(28.2 ± 6.3) mmHg at 3 minutes,(40.1 ± 7.1) mmHg vs.(30.5 ± 6.2) mmHg at 4 minutes,(38.1 ±7.5)mmHg vs.(29.8 ±5.3)mmHg at 5 minutes;rSO2:(45.4±5.2)％ vs.(39.2 ±5.1)％ at 1 minute,(47.2 ±3.6)％ vs.(42.0±6.4)％ at 2 minutes,(47.7 ±3.0)％ vs.(41.5 ±5.4)％ at 3 minutes,(47.0±2.5)％ vs.(42.1 ±5.9)％ at4 minutes,(47.1 ±2.0)％ vs.(41.5 ±7.4)％ at 5 minutes;PETCO2:(17.0 ± 3.5) mmHg vs.(12.7 ± 4.2) mmHg at 1 minute,(18.5 ± 3.7) mmHg vs.(14.5 ±2.7)mmHg at 2 minutes,(20.7 ±5.3)mmHg vs.(15.5 ±3.2)mmHg at 3 minutes,(18.7 ±4.5) mmHg vs.(14.9 ± 3.5) mmHg at 4 minutes,(18.2 ± 3.2) mmHg vs.(14.5 ± 4.2) mmHg at 5 minutes] (all P ＜0.05).The rate of ROSC was significantly higher in the ABO group than in the model group[100％ (15/15) vs.75％ (9/12)] (P ＜0.05).Additionally,shorter duration of cardiopulmonary resuscitation,less number of shocks and lower doses of epinephrine were observed in the ABO group when compared with the model group [duration of cardiopulmonary resuscitation:5 (5,5) minutes vs.5 (5,12.5) minutes,number of shocks:1 (1,1) times vs.1 (1,4) times,dose of epinephrine:0.62(0.62,0.74) mg vs.0.64 (0.59,2.59) mg] (all P ＜ 0.05).At 5 minutes after resuscitation,the level of arterial lactate was significantly decreased and the value of SjvO2 was significantly increased in the ABO group compared with the model group [Lactate:(9.6 ± 0.8) mmol/L vs.(10.8 ± 1.4) mmol/L;SjvO2:(50.0±8.6)％ vs.(37.9±16.3)％] (bothP＜0.05).Conclusions In a swine model of TCA,ABO can increase cardiac and cerebral perfusion during cardiopulmonary resuscitation and improve the efficacy of cardiopulmonary resuscitation.It might provide a novel and effective method for the resuscitation of TCA in the clinical setting.
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Objective To evaluate the effect of mild hypothermia on inositol-requiring enzyme 1 (IRE1) signaling pathway during myocardial injury after cardiac arrest and resuscitation in swine.Methods Twenty-one healthy male white swine,weighing 33-41 kg,were divided into 3 groups using a random number table method:sham operation group (group S,n =5),cardiac arrest-cardiopulmonary resuscitation group (group CA-CPR,n=8),and mild hypothermia group (group MH,n=8).The model of cardiac arrest and resuscitation was established based on the previously reported method.The catheters placed in the left femoral artery and right internal jugular vein were connected to the PiCCO Monitor system,and another pacing catheter was advanced from the right external jugular vein into the right ventricle.Ventricular fibrillation was induced by using a 1 mA alternating current through the pacing catheter.Once ventricular fibrillation was successfully induced,mechanical ventilation was discontinued for 8 min,and then cardiopulmonary resuscitation was initiated.Epinephrine 20 μg/kg was administered at 2.5 min of resuscitation followed by repetition every 3 min.Defibrillation was delivered at 5 min of resuscitation,and then spontaneous circulation was evaluated.If return of spontaneous circulation was not achieved,cardiopulmonary resuscitation was immediately resumed for 2 min and then defibrillation was delivered again.Mechanical ventilation was continued for 30 h after successful resuscitation.Animals in group S only underwent surgical preparation without experiencing cardiac arrest and resuscitation.At 5 min after successful resuscitation,body temperature was cooled down to 33 ℃ by using a cooling blanket,and then maintained at this level until 24 h after resuscitation,followed by 5 h of re-warming at a rate of 1 ℃/h in group MH.The temperature was maintained at 37.5-38.5 ℃ with the aid of surface cooling blanket in the other two groups.At 1,6,12,24 and 30 h after resuscitation (T1-5),the values of stroke volume (SV) and global ejection fraction (GEF) were recorded,and meanwhile 2 ml of blood samples was obtained via the femoral vein to measure the concentration of serum cardiac troponin Ⅰ (cTnI) (by enzyme-linked immunosorbent assay) and activity of serum creatine kinase-MB (CK-MB) (by immunosuppression).The swine were sacrificed at 30 h after resuscitation,and then myocardial specimens from the left ventricle were obtained for determination of the expression of caspase-3 (by immunohistochemistry),cell apoptosis (by TUNEL),and expression of IRE1 and casepase-12 (by Western blot).Apoptosis index was calculated.Results Compared with group S,SV and GEF were significantly decreased and the serum CK-MB activity was increased at T1-5,the concentration of serum cTnI was increased at T2-5,the expression of IRE1,caspase-12 and caspase-3 in myocardium was up-regulated,and apoptosis index was increased in CA-CPR and MH groups (P＜0.05).Compared with group CA-CPR,the SV and GEF were significantly increased and the concentration of serum cTnI was decreased at T2-5,the activity of serum CK-MB was decreased at T3-5,the expression of IRE1,caspase-12 and caspase-3 in myocardium was down-regulated,and apoptosis index was decreased in group MH (P＜0.05).Conclusion The mechanism by which mild hypothermia mitigates myocardial injury after cardiac arrest and resuscitation may be related to inhibiting IRE1 signaling pathway in swine.
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Objective To detect the dynamic change of N-terminal pro-B-type natriuretic peptide (NT-proBNP) in patients with major trauma and measure its relation to the outcome.Methods Sixty patients with major trauma were measured with serum NT-proBNP level at 1,3,and 7 days postinjury.According to the prognosis,the patients were allocated to survival group (n =47) and death group (n =13).Changes in NT-proBNP was detected and compared between the two groups.Correlation of NT-proBNP level with acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) and ISS was analyzed at each time point.Receiver operating characteristic curve (ROC) was developed to determine the prognostic value of NT-proBNP.Results Overall NT-proBNP level revealed no statistical difference at each time point and kept within normal reference range.NT-proBNP level in death group increased gradually,whereas in survival group the increase was followed by a reduction.Moreover,NT-proBNP level was higher in death group than in survival group at each time point.Area under the ROC of NT-proBNP had no statistical difference with that of APACHE Ⅱ and ISS at each time point.Conclusions Obviously high or continuously increased NT-proBNP level may indicate an unfavorable prognosis of major trauma patients.NT-proBNP can be used as a marker to dynamically predict prognosis of major trauma patients.
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ObjectiveTo detect the serum NT-proBNP level in patients with severe trauma 24 hours after injury in order to find the possible correlated factors for the evaluation of the clinical application.MethodsSixty patients with severe trauma admitted to the emergency ICU were enrolled. Serum NTproBNP level was detected 24 hours after injury for comparison between survivors and nonsurvivors. The validity of NT-proBNP for predicting outcome was analyzed by receiver operating characteristic ( ROC )curve. The factors with significant correlation between NT-proBNP level and the length of ICU stay as well as the duration of mechanical ventilation support were determined in those survivors with correlation and stepwise linear regression analysis. These factors included injury severity score (ISS), head abbreviated injury score (AIS), acute physiology and chronic health evaluation Ⅱ ( APACHE I ), Glasgow coma score (GCS), creatine kinase-MB (CK-MB), cardiac troponin-I (cTn-I) and central venous pressure. Results The median NT-proBNP levels were 762 pg/ml (IQR, 400-1131 pg/mL) in nonsurvivors versus 200 pg/ml (IQR, 80-383 pg/mL) in survivors (Z =-3. 972, P ＜0.01 ). The area under ROC curve of NTproBNP was not statistically different to that of ISS and that of APACHE Ⅱ. The best threshold value of NTproBN to predict the outcome was 384 pg/ml ( sensitivity 0. 846, specifity 0. 766). A positive correlation was found between NT-proBNP and the length of ICU stay ( r =0. 32, P ＜ 0. 05 ) as well as the duration of mechanical ventilation ( r =0. 37, P ＜ 0. 05 ) in survivors. Stepwise linear regression analysis indicated there were significant correlations between APACHE Ⅱ, CK-MB and NT-proBNP.ConclusionsSerum NT-proBNP level 24 hours after injury is correlated with the severity and outcome of patients with severe trauma. It may be used as a complementary biomarker for the rapid assessment of the severity of trauma.