犬心肺复苏后心肌凋亡的变化及纳洛酮的干预作用

目的：观察犬心跳骤停复苏后心肌细胞凋亡的变化以及纳洛酮(NLX)的干预作用。方法：体外电击诱发犬室颤，3min后复苏，18只犬随机分为3组，CPR组，NLX组，空白对照组，每组6只，6小时后取心肌组织，TUNEL法检测心肌组织凋亡的形态学改变。结果：CPR组心肌细胞凋亡指数高于空白对照组，使用NLX后心肌细胞凋亡指数下降。结论：犬室颤复苏后心肌细胞凋亡增加，纳洛酮可以减少心肌细胞凋亡，对复苏后心肌具有保护作用。     

犬心搏骤停复苏后心功能不全与TNF-α、IL-6的相关性研究

目的观察犬心跳骤停复苏后血流动力学和细胞因子的变化。方法12只犬随机分为2组：常规治疗组(CPR组)和正常对照组；每组6只，CPR组通过体外电击诱发犬室颤，3min后复苏。采用Swan-Ganz漂浮导管监测复苏前和复苏后6h的心输出量(c0)和肺毛细血管楔压(PAWP)，同时抽血检测血清肿瘤坏死因子-α(TNF-α)，白细胞介素．6(IL-6)水平(放免法)，6h后取心肌组织进行TNF-α mRNA、IL-6 mRNA表达的测定。结果两组各血流动力学指标在心跳骤停前差异无显著性，CPR组的MAP在复苏成功即时高于正常对照组，随后开始下降，在复苏后4、6h低于正常对照组。CO、CI、SV和LVSWI在复苏成功后随时间延长而下降，6h降至最低，复苏后各观察点均低于正常对照组和电击前。TNF-α、IL-6浓度在复苏后2h开始出现明显的升高，并随时间的延长而增高，与本组电击前及同时间的正常对照组比较差异有显著性。细胞因子TNF-a和IL-6与反映心功能的指标CO、CI、SV和LVSWI之间呈负相关。心肌细胞因子mRNA表达在CPR组高于正常对照组。结论电击诱发室颤犬复苏成功后存在着心功能不全，心肺复苏后升高的TNF-α和IL-6水平与复苏后心功能不全密切相关。     

心跳骤停犬复苏后血流动力学及心肌MDA、SOD的研究

目的 :观察心跳骤停犬心肺复苏 (CPR )后血流动力学和心肌MDA、SOD的变化。方法 :体外电击诱发犬室颤 ,3min后复苏 ,12只犬随机分为 2组 ,CPR组、正常对照组 ,每组 6只 ,采用Swan Ganz漂浮导管监测复苏前和后 6h的CO和PAWP。 6h后取心肌组织 ,匀浆测SOD和MDA的活性。结果 :CPR组的平均动脉压在复苏后4、6h低于正常对照组 (P <0 0 5～ 0 0 1)。CO、CI、SV和LVSWI在心跳骤停前 2组无统计学差异 ,复苏成功后 0～ 6hCPR组的各指标均低于正常组 (P <0 0 1)。复苏后 6hCPR组心肌组织SOD活性低于正常对照组 (P <0 0 5 ) ,而MDA高于正常对照组 (P <0 0 1)。结论 :诱发室颤犬复苏成功后存在氧自由基的产生增多和内源性抗氧化机制的削弱 ,缺血再灌注损伤及心肌损害 ,从而导致心功能不全     

纳洛酮对心肺复苏后犬血流动力学和心肌氧自由基、一氧化氮的影响

目的 观察纳洛酮(naloxone，NLX)对犬心跳骤停复苏后血流动力学和心肌氧自由基及一氧化氮(NO)的影响。方法体外电击诱发犬室颤，3min后复苏，18只犬随机分为3组：CPR组、NLX组、正常对照组，每组6只。采用Swan-Ganz漂浮导管监测复苏前和复苏后6h的CO和PAWP。6h后取心肌组织，匀浆检测超氧化物岐化酶(SOD)、丙二醛(MDA)和一氧化氮(NO)。结果CPR组的平均动脉压在复苏后4、6h低于正常对照组，而NLX组在复苏后2、4、6h高于CPR组，与正常对照组无差异。CO、Cl、SV和LVS,W1在心跳骤停前三组间差异无统计学意义，复苏成功后0-6h NLX组和CPR组的各指标均低于正常组，而NLX组的CO、CI、SV和LVSWI在复苏后1．6h高于CPR组。复苏后6h CPR组和NLX组心肌组织SOD活性则低于正常对照组，而MDA和NO高于正常对照组，NLX组心肌组织MDA和NO含量较CPR组降低，而SOD活力较CPR组升高。结论诱发室颤犬复苏成功后存在心功能不全、氧自由基和NO产生增加和内源性抗氧化机制的削弱，NLX能予以改善。     

复苏后心功能不全与炎症因子关系的实验研究

目的:观察犬心跳骤停复苏后血流动力学和细胞因子的变化及其关系。方法:体外电击诱发犬室颤,3min后复苏,12只犬随机分为2组,常规治疗组(CPR组)和正常对照组,每组6只,采用Swan-Ganz漂浮导管监测复苏前和复苏后6h的心输出量(CO)和肺动脉楔压(PAWP),同时抽血检测血清肿瘤坏死因子-α(TNF-α),白介素-6(IL-6)和白介素-10(IL-10)水平(放免法)。结果:两组各血流动力学指标在心跳骤停前差异无统计学意义,CPR组的MAP在复苏成功即时高于正常对照组,随后开始下降,在复苏后4、6h低于正常对照组。CPR组的PAWP从心跳骤停前的(5.0±1.26)mmHg一直上升,到复苏后达高峰(28.83±4.79)mmHg,各观察点均高于正常对照组,CO在复苏成功后随时间延长而下降,6h降至最低,复苏后各观察点均低于正常对照组和电击前。TNF-α、IL-6浓度在复苏后即时和2h开始出现明显的升高,并随时间的延长而增高,与本组电击前及同时间的正常对照组比较差异有统计学意义。在整个实验过程均未能检测到IL-10的浓度。细胞因子TNF-α和IL-6与CO之间呈负相关。结论:电击诱发室颤犬复苏成功后存...     

血红素氧合酶对复苏后心功能不全的保护作用

目的 探讨诱导血红素氧合酶表达对复苏后心肌损伤的保护作用,为复苏后心功能不全探索新的治疗手段.方法 采用窒息法制作大鼠心跳骤停与心肺复苏(CPR)模型.实验动物分为4组:假手术组、CPR组、血晶素组(Hemin组)、血晶素+锌原卟啉组(Hemin+ZnPP组),各复苏组又分复苏后6 h及24 h 2个亚组.各实验组记录血流动力学资料;测定血清肌酸肌酶同功酶(CPK-MB)、乳酸脱氢酶(LDH)含量;测定心肌组织匀浆HO-1含量;观察心肌超微结构变化.对结果进行方差分析.结果 各复苏组复苏后平均动脉压(MBP)显著低于复苏前(均P＜0.05),但组间比较差异无统计学意义.CPR组、Hemin+ZnPP组复苏后各时相点dp/dt40值、-dp/dt值均显著低于复苏前(P＜0.05),但Hemin组复苏前后dp/dt40值无显著性变化,-dp/dt值仅复苏后0.5 h和1 h低于复苏前(P＜0.05);Hemin组复苏后各时相点dp/dt40值、-dp/dt值均高于其他两组(P＜0.05).复苏后6h及24 h血清CPK-MB、LDH水平,Hemin组均低于CPR组及Heroin+ZnPP组(P＜0.05),但CPR组和Hemin+ZnPP组两组之间比较差异无统计学意义.Hemin组复苏后6 h心肌超微结构完整性明显优于CPR组及Hemin+ZnPP组.复苏后6 h及24 h心肌组织匀浆HO-1水平,Hemin组均高于CPR组及Hemin+ZnPP组(均P＜0.05),但CPR组和Hemin+ZnPP组两组之间差异无统计学意义(P＞0.05).结论 诱导HO-1表达可有效改善复苏后心功能不全,减轻心肌损伤,保存心肌细胞超微结构的完整性,为复苏后心功能不全的治疗提供了新的手段.     

线粒体在δ阿片药物性心肌冬眠保护复苏后心功能作用中的研究

目的:在线粒体水平研究心跳骤停与心肺复苏期间,激动δ阿片受体诱导药物性心肌冬眠保护复苏后心功能的机制.方法:交流电致颤法诱发大鼠心室颤动,8 min的室颤后开始包括胸外按压和机械通气的心肺复苏,6 min后电击除颤.动物随机分为3组:(1)心肺复苏组;(2)δ阿片受体激动剂组;(3)δ阿片受体拮抗剂+δ阿片受体激动剂组.δ阿片受体拮抗剂在室颤前15 min预先给药,δ阿片受体激动剂或者生理盐水在室颤5 min时给药.动态监测血流动力学,在复苏成功后6h处死动物电镜观察心肌线粒体损伤情况.结果:δ阿片受体激动剂组复苏后心功能明显改善,δ阿片受体拮抗剂预处理完全取消其保护作用;和心肺复苏组和δ阿片受体拮抗剂组相比较,δ阿片受体激动剂组动物心肌的线粒体超微结构的完整性明显保存完好.结论:在心跳骤停与心肺复苏期间激动δ阿片受体诱导药物性心肌冬眠通过保护心肌线粒体超微结构的完整性,从而减轻复苏后心功能损伤.     

纳洛酮对心肺复苏犬脑组织S100蛋白表达的影响

目的　通过检测心搏骤停犬复苏后及给予纳洛酮干预后脑组织中S1 0 0蛋白表达情况 ,了解纳洛酮对脑复苏的影响。方法　 1 8只健康杂种犬 ,随机分成 3组 ,每组 6只 ,予体外电击诱发室颤 ,对照组 :心搏停后予标准心肺复苏术 ;实验组 :心搏骤停后予标准心肺复苏术 +纳洛酮 ;空白组 :不诱发室颤 ,于复苏后 6h取脑海马组织行脑形态学检查 ,及S1 0 0蛋白表达的测定。结果　实验组S1 0 0蛋白表达明显低于对照组 (P <0 0 1 ) ,实验组脑组织的病理损害低于对照组。结论　使用纳洛酮后心肺复苏犬脑组织的病理损害有所减轻 ,脑组织S1 0 0蛋白的生成也显著减少 ,纳洛酮可能通过减少S1 0 0蛋白的表达而减轻心肺复苏后脑的再灌流损伤     

心肺复苏后犬脑组织一氧化氮浓度的变化及纳络酮的干预

目的:探讨犬心肺复苏(CPR)后6h脑组织形态学和一氧化氮(NO)浓度的变化以及纳络酮对两者的影响。方法:18只健康杂种犬随机分成三组(n=6),空白组:不诱发室颤,6h后取脑组织;对照组:心跳骤停后予常规心肺复苏术;纳络酮组:心跳骤停后予常规心肺复苏术并使用纳络酮。对照组和纳络酮组于复苏后6h取脑组织行NO浓度测定以及形态学检查。结果:对照组脑组织NO的含量高于空白组和纳络酮组,均P<0.01。纳络酮组的病理损害低于对照组。结论:纳络酮可减轻心肺复苏后脑组织NO的生成,减轻神经元的再灌注损伤。     

实时监测颅内微循环的犬心脏骤停模型建立

目的 建立可以实时观察颅内微循环变化的犬室颤心脏骤停(CA)模型.方法 6只比格犬开颅后采用交流电诱发室颤,同时观察犬诱发室颤前、自主循环恢复(ROSC)后2 h内动脉内平均压(MAP)、右颈总动脉平均流量(Q)、耳及颅内微循环灌注量.结果 犬全部诱发室颤,无干预3 min后开始心肺复苏,6只比格犬均复苏成功.ROSC 30 min颅内微循环最高均值,与其余各时点差异均有统计学意义(P<0.05).ROSC 5 min MAP低值与ROSC 105 min高值差异有统计学意义(P<0.05).经相关分析表明CA前MAP与Q呈负相关(r=-0.941,P=0.005).ROSC后,耳与颅内微循环正相关(r=0.269,P=0.049);而耳微循环与MAP(r=-0.454,P=0.001)、Q(r=-0.440,P=0.001)呈负相关;MAP与Q呈正相关(r=0.297,P=0.029).结论 开颅窗比格犬CA模型,可动态观察颅内微循环变化,为心肺脑复苏(CPCR)提供更直接更可靠的观察手段和方法.颅内微循环在复苏后30 min时存在高灌注.复苏后2 h内耳与颅内微循环灌注量正相关.     

A selective alpha(2)-adrenergic agonist for cardiac resuscitation

The effects of selective alpha(2)-adrenergic agonist alpha-methylnorepinephrine on the initial success of resuscitation and postresuscitation myocardial function were compared with nonselective alpha- and beta-adrenergic epinephrine in a swine model of cardiac arrest. Epinephrine, the primary pharmacological intervention in the treatment of cardiac arrest, improves immediate outcome. However, epinephrine increases the severity of myocardial dysfunction after cardiac resuscitation. Both inotropic and chronotropic actions provoke disproportionate increases in myocardial oxygen consumption by the ischemic heart, prompting this study, in which we hypothesized that a selective alpha(2)-adrenergic agonist, alpha-methylnorepinephrine (alpha-MNE), would moderate these adverse effects of epinephrine and minimize postresuscitation myocardial dysfunction. After 7 minutes of untreated ventricular fibrillation (VF) in 14 anesthetized male domestic pigs, precordial compression at a fixed rate of 80 compressions/min was begun, along with mechanical ventilation. Either alpha-MNE (100 microg/kg) or epinephrine (20 microg/kg) was administered as a bolus after 2 minutes of precordial compression. After an additional 4 minutes of precordial compression, defibrillation was attempted. Left ventricular systolic and diastolic function was quantitated with the use of transesophageal echo-Doppler imaging. Comparable increases in coronary perfusion pressure to 15 mm Hg were observed after the administration of both drugs. All animals were successfully resuscitated; epinephrine and alpha-MNE were equally quick in restoring spontaneous circulation after 7 minutes of untreated VF. Ejection fraction was reduced by 35% and 14% by epinephrine and alpha-MNE, respectively, after resuscitation. Epinephrine and alpha-MNE increased postresuscitation heart rate by 38% and 15%, respectively. Accordingly, significantly less postresuscitation impairment followed the administration of alpha-MNE. alpha-MNE, a selective alpha-adrenergic agonist, was as effective as epinephrine in restoring spontaneous circulation after 7 minutes of untreated VF in a porcine model for CPR and demonstrated lesser postresuscitation myocardial injury.     

Ultrastructural evidence of mitochondrial abnormalities in postresuscitation myocardial dysfunction

Objectives

Though there is evidence to implicate that the mitochondrion may play an important role in the development of postresuscitation myocardial dysfunction, limited data are available regarding the ultrastructural alterations of the mitochondria, mitochondrial energy-producing ability, and their relationship to postresuscitation myocardial dysfunction. This study was designed to determine whether mitochondrial abnormalities contribute to the development of postresuscitation myocardial dysfunction.

Methods

Fifteen anesthetized male Sprague-Dawley rats were randomized to: (1) global myocardial ischemia/reperfusion, in which 8 min of ventricular fibrillation was induced and successful defibrillation was achieved after 6 min of cardiopulmonary resuscitation (CPR); (2) global myocardial ischemia, in which ventricular fibrillation and CPR were performed without defibrillation attempt; and (3) sham control.

Results

Myocardial function was significantly impaired after resuscitation. Mitochondria were massively swollen in global ischemic hearts and mildly swollen in the resuscitated hearts. Concomitantly, ATP levels abruptly declined during global ischemia and partially recovered after resuscitation. Furthermore, mitochondrial abnormalities were supported by the incapability of utilizing energy substrates manifested by the accumulations of intramyocellular lipid droplets and glycogen deposits.

Conclusions

In this model of cardiac arrest and CPR, the presence of ultrastructural mitochondrial abnormalities, further evidenced by the incapability of utilizing energy substrates and impairment of energy-production, might, in part, contribute to the development of postresuscitation myocardial dysfunction.     

Cardiopulmonary resuscitation ameliorates myocardial mitochondrial dysfunction in a cardiac arrest rat model

PurposePrevious studies implicate that the mitochondrial injury may play an important role in the development of post-resuscitation myocardial dysfunction, however few of them are available regarding the ultrastructural alterations of myocardial mitochondria, mitochondrial energy producing and utilization ability in the stage of arrest time (no-low) and resuscitation time (low-flow). This study aimed to observe the dynamic changes of myocardial mitochondrial function and metabolic disorders during cardiac arrest (CA) and following cardiopulmonary resuscitation (CPR).MethodsA total of 30 healthy male Sprague-Dawley rats were randomized into three groups: 1) VF/CPR: Ventricular fibrillation (VF) was electrically induced, and 5 min of CPR was performed after 10 min of untreated VF; 2) Untreated VF: VF was induced and untreated for 15 min; and 3) Sham: Rats were identically prepared without VF/CPR. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 min were calculated from ECG signals. The rats' hearts were quickly removed at the predetermined time of 15 min after beginning the procedure to gather measurements of myocardial mitochondrial function, high-energy phosphate stores, lactate, mitochondrial ultrastructure, and myocardial glycogen.ResultsThe mitochondrial respiratory control ratios significantly decreased after CA compared to sham group. CPR significantly increased respiratory control ratios compared with untreated VF animals. A significant decrease of myocardial glycogen was observed after CA, and a more rapid depletion of myocardial glycogen was observed in CPR animals. CPR significantly reduced the tissue lactate. The mitochondrial ultrastructure abnormalities in CPR animals were less severe than untreated VF animals. AMSA decayed during untreated VF; however, it was significantly greater in CPR group than the untreated VF group. In addition, AMSA was clearly positively correlated with ATP, but negatively correlated with myocardial glycogen.ConclusionImpairment of myocardial mitochondrial function and the incapability of utilizing glycogen were observed after CA. Furthermore, optimal CPR might, in part, preserved mitochondrial function and enhanced utilization of myocardial glycogen.     

Levosimendan improves postresuscitation myocardial dysfunction after beta-adrenergic blockade

In earlier studies, we found that a nonselective beta-adrenergic blocking agent, propranolol, facilitated cardiac resuscitation, reduced postresuscitation myocardial ectopy, and improved postresuscitation survival. However, the potential adverse effects and specifically the negative inotropic actions of propranolol prompted our further investigation of the potential value of a non-beta-adrenergic inotropic drug, levosimendan, in conjunction with propranolol, for minimizing postresuscitation myocardial dysfunction after successful resuscitation from cardiac arrest. Ventricular fibrillation was induced and untreated for 7 minutes in 15 domestic pigs, which were divided into propranolol, propranolol plus levosimendan, and control groups. Propranolol was administered as a bolus dose of 0.1 mg/kg during cardiac arrest. Electrical defibrillation was attempted after 12 minutes of cardiac arrest including 5 minutes of precordial compression. Levosimendan was administered at 10 minutes after successful resuscitation in a dose of 20 microg/kg and followed by infusion of 0.4 microg/kg/min over the ensuing 220 minutes. Propranolol reduced energies or numbers of defibrillatory shocks and postresuscitation myocardial ectopy, and it improved postresuscitation myocardial dysfunction. When levosimendan was added, postresuscitation myocardial contractile function was improved even more.     

The difference in myocardial injuries and mitochondrial damages between asphyxial and ventricular fibrillation cardiac arrests

Introduction

Ventricular fibrillation (VF) and asphyxia account for most cardiac arrests but differ in cardiac arrest course, neurologic deficit, and myocardial damage. In VF resuscitation, cardiac mitochondria were known to be damaged via excess generation of reactive oxygen species. This study evaluated the difference of cardiac mitochondrial damages between VF and asphyxial cardiac arrests.

Methods

In the VF + electrical shock (ES) group, VF was induced and untreated for 5 minutes, followed by 1 minute of cardiopulmonary resuscitation (CPR) and 1 ES of 5 J. Animals were killed immediately after ES. In the asphyxia group, cardiac arrest was induced by airway obstruction, and then pulselessness was maintained for 5 minutes, followed by 1 minute of CPR. The animals were killed immediately after CPR. The histology and ultrastructural changes of myocardium and complex activities and respiration of mitochondria were evaluated. The mitochondrial permeability transition pore opening was measured based on mitochondrial swelling rate.

Results

The histopathologic examinations showed myocardial necrosis and mitochondrial damage in both cardiac arrests. Instead of regional damages of myocardium in the VF + ES group, the myocardial injury in the asphyxia group distributed diffusely. The asphyxia group demonstrated more severe mitochondrial damage than the VF + ES group, which had a faster mitochondrial swelling rate, more decreased cytochrome c oxidase activity, and more impaired respiration.

Conclusions

Both VF and asphyxial cardiac arrests caused myocardial injuries and mitochondrial damages. Asphyxial cardiac arrest presented more diffuse myocardial injuries and more severe mitochondrial damages than VF cardiac arrest.     

Tumor necrosis factor-alpha is associated with early postresuscitation myocardial dysfunction

OBJECTIVE: Left ventricular dysfunction after successful cardiopulmonary resuscitation contributes to early death following resuscitation. The stress-induced proinflammatory cytokines, particularly tumor necrosis factor-alpha and interleukin-1beta, are known to depress myocardial function. We hypothesized that tumor necrosis factor-alpha and interleukin-1beta, synthesized and released in response to the stress of global ischemia accompanying cardiac arrest, play a role in development of postresuscitation left ventricular dysfunction. METHODS: Hemodynamic variables, tumor necrosis factor-alpha , interleukin-1beta, interleukin-6 (enzyme-linked immunosorbent assay method), and ionized calcium were measured in ten anesthetized swine before and after 7 mins of cardiac arrest and during the early postresuscitation period (60-90 mins). RESULTS: Tumor necrosis factor-alpha increased three-fold within 15 mins of restoration of circulation and remained elevated throughout the observation period. A significant negative correlation was observed between tumor necrosis factor-alpha and left ventricular systolic change in pressure over time (r = -.54, p <.001). Interleukin-1beta was undetectable before and after resuscitation, and interleukin-6 was detectable in only two animals after resuscitation. Although a significant decline in ionized calcium was observed and correlated with left ventricular systolic change in pressure over time, an independent role for ionized calcium in postresuscitation left ventricular dysfunction was not demonstrated. CONCLUSION: Tumor necrosis factor-alpha increases during the early postresuscitation period and may play a role in postresuscitation myocardial dysfunction.     

Left Ventricular Function after Monophasic and Biphasic Waveform Defibrillation: The Impact of Cardiopulmonary Resuscitation Time on Contractile Indices

Previous work has suggested that low-energy biphasic waveform defibrillation (BWD) is followed by less post-resuscitation left ventricular (LV) dysfunction when compared with higher-energy monophasic waveform defibrillation (MWD). To the best of the authors' knowledge, the effect of cardiopulmonary resuscitation (CPR) duration and total ischemia time on LV function after countershock, controlling for waveform type, has not been evaluated. OBJECTIVE: To determine the effect of CPR duration on LV function after MWD and BWD. METHODS: VF was electrically induced in anesthetized and instrumented swine. After 5 minutes of VF, the animals were randomized to MWD (n = 22) or one of two BWDs (n = 46). If countershock terminated VF but was followed by a nonperfusing rhythm, conventional manual CPR without drug therapy was performed until restoration of spontaneous circulation (ROSC), defined as a systolic arterial pressure >60 mm Hg for 10 minutes without vasopressor support. Systolic LV pressure (LVP), LV dP/dt (first derivative of pressure measured over time), and cardiac output (CO) were measured at intervals for 60 minutes postresuscitation. CPR times (times to ROSC) and hemodynamic variables for the three groups were compared. Multivariable linear regression was performed to assess the contribution of defibrillation waveform, total joules, and CPR time on LVP, LV dP/dt, and CO at 15, 30, and 60 minutes postresuscitation. RESULTS: When analyzed as groups, significant differences in median number of shocks to terminate VF, total joules, or CPR time were not observed between waveform groups. Regression analysis demonstrated that increasing CPR time was associated with a significant effect on indices of LV function at 15 and 30 minutes postresuscitation. Global LV function was not influenced by waveform type or total joules. CONCLUSIONS: Adjustment for CPR time, a determinant of total myocardial ischemia time, is necessary when defibrillation waveforms are compared for their effect on postresuscitation cardiac function and short-term outcome.     

Shen-fu injection reduces postresuscitation myocardial dysfunction in a porcine model of cardiac arrest by modulating apoptosis

ABSTRACT: Shen-Fu injection (SFI) following cardiac arrest exhibits cardioprotective effects, but its effect on myocardial dysfunction, a critical issue following resuscitation, is unclear. This study sought to examine whether SFI reduces postresuscitation myocardial dysfunction in a porcine model of cardiac arrest by modulating apoptosis. After 8 min of untreated ventricular fibrillation and 2 min of basic life support, 24 pigs were randomized divided into three groups, which received central venous injection of either Shen-Fu (SFI group; 1.0 mL/kg), epinephrine (EP group; 0.02 mg/kg), or saline (SA group). After successful return of spontaneous circulation (ROSC), hemodynamic status and blood samples were obtained at 0, 30, 120, and 360 min after ROSC. Surviving pigs were killed at 24 h after ROSC, and the hearts were removed for analysis by electron microscopy, Western blotting, quantitative real-time polymerase chain reaction, and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) assay. Compared with the EP and SA groups, animals treated with SFI had improved left ventricular function (P < 0.05), lower troponin T levels (P < 0.01), and increased tissue perfusion and oxygen metabolism (P < 0.05). Shen-Fu injection was associated with a reduction in (i) Bcl-2, Bax, and caspase 3 protein expression (P < 0.05); (ii) caspase 3 mRNA upregulation; and (iii) apoptosis, compared with the EP and SA groups. Caspase 3-mediated apoptosis occurs following myocardial injury after cardiopulmonary resuscitation in pigs. Shen-Fu injection decreased myocardial injury; improved myocardial ultrastructure; inhibited Bcl-2, Bax, and caspase 3 expression; and reduced myocardial apoptosis. Therefore, SFI could significantly attenuate postresuscitation myocardial dysfunction by modulating apoptosis.