Investigation of Myocardial Stunning after Cardiopulmonary Resuscitation in Pigs

Objective 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. Methods 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. Results 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. Conclusion 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.

Mechanisms of Myocardial Stunning in Stress-Induced Cardiomyopathy

Stress-induced cardiomyopathy,in contrast to acute myocardial infarction,is a type of acute heart failure characterized by reversible left ventricular dysfunction.Cardiac imaging primarily reveals left ventricle myocardial stunning,81.7%of which is apical type.Emotional or psychological stress usually precedes the onset of stress-induced cardiomyopathy,which is increasingly being recognized as a unique neurogenic myocardial stunning disease.To distinguish between acute myocardial infarction and acute viral or auto-immune myocarditis,this review summarizes specific mechanisms of myocardial stunning in stress-induced cardiomyopathy,such as calcium disorders,metabolic alterations,anatomical and histological variations in different parts of the left ventricle,and microvascular dysfunction.

Hypoglycemic myocardial stunning as cause of cardiogenic shock in a patient with ischemic cardiomyopathy: A case report and review of literature

Hypoglycemia is a common complication seen in patients with diabetes mellitus and has been proven to have adverse effects on cardiovascular mortality. Hypoglycemia can potentially lead to worsening of cardiac function in patients with ischemic heart disease. We present a case of cardiogenic shock in a patient with hypoglycemia secondary to insulin accumulation due to worsening renal function with dramatic recovery of shock once his sugars normalized.

Effects of Berberineon Cardiac Function and ATPase Activity of Postischemic Myocardial Stunned Rat Hearts

This is a report of a study on the protective effect of berberine(Ber) on postischemic myocardial stunning and the role it plays in ATPase activity. Isolated working rat hearts were used with global ischemia for 30 min followed by reperfusing for 40 min. Both systolic and diastolic functions of stunned myocardium were significantly decreased. The recovery of LVSP×HR and CO was 52%±8% and 40%±8% respectively; LVEDP and T were elevated; while both Na +, K +ATPase activity and Ca 2+ , Mg 2+ ATPase activity of myocardial membrane and mitochondria were depressed. Berberine(25 mg·kg -1 ·d -1 , ip, 3 d, and 10 μmol L -1 for isolated heart perfusion) was able to enhance the percent recovery of LVSP×HR and CO to 85%±12% and 75%±11%, respectively, and reduce LVEDP from 298%±64% to 166%±44%, with an improvement in myocardial membrane Na +, K +ATPase activity and mitochondria Ca 2+ , Mg 2+ ATPase activity. This study suggested that berberine can protect cardiac function from ischemia reperfusion stunning injury by preserving ATPase activity in ischemic myocardium.

Myocardial ischemic changes of electrocardiogram in intracerebral hemorrhage: A case report and review of literature

BACKGROUND Cardiac injury may occur after acute pathology of central nervous system(CNS)without any evidence of primary cardiac diseases.The resulting structural and/or functional changes are called cerebrocardiac syndrome(CCS).The great majority of studies have been performed in patients with subarachnoid hemorrhage(SAH),while CCS data after intracerebral hemorrhage(ICH)are rare.It may cause diagnostic and therapeutic pitfalls for the clinician due to a lack of specific clinical manifestations and diagnostic methods.Understanding the underlying pathophysiological and molecular mechanism(s)following cerebrovascular incidents will help to implement prevention and treatment strategies to improve the prognosis.CASE SUMMARY A 37-year-old man with a history of hypertension presented to our department on an emergency basis because of a sudden dizziness and left limb weakness.Cerebral computed tomography(CT)suggested ICH in the occipital and parietal lobes,and the chosen emergency treatment was hematoma evacuation.Left ventricular(LV)dysfunction occurred after the next 48 h and the electrocardiogram(ECG)showed non-ST elevation myocardial infarction.CCS was suspected first in the context of ICH due to the negative result of the coronary CT angiogram.CONCLUSION Misinterpretation of ischemic-like ECGs may lead to unnecessary or hazardous interventions and cause undue delay of rehabilitation after stroke.Our objective is to highlight the clinical implications of CCS and we hope the differential diagnoses will be considered in patients with acute CNS diseases.

Cardioprotective effect of erythropoietin on sepsisinduced myocardial injury in rats

BACKGROUND:Sepsis-induced myocardial injury is one of the major predictors of morbidity and mortality of sepsis.The cytoprotective function of erythropoietin(EPO) has been discovered and extensively studied.However,the cardioprotective effects of EPO on sepsis-induced myocardial injury in the rat sepsis model has not been reported.METHODS:The rat models of sepsis were produced by cecal ligation and perforation(CLP)surgery.Rats were randomly(random number) assigned to one of three groups(n=8 for each group):sham group,CLP group and EPO group(1000 lU/kg erythropoietin).Arterial blood was withdrawn at3,6,12,and 24 hours after CLP.cTnl,BNP,CK-MB,LDH,AST,TNF-a,IL-6,IL-10,and CRP were tested by the ELISA assay.Changes of hemodynamic parameters were recorded at 3,6,12,24 hours after the surgery.Histological diagnosis was made by hematoxylin and eosin.Flow cytometry was performed to examine cell apoptosis,myocardium mitochondrial inner membrane potential,and NF-κB(p65).Survival rate at 7 days after CLP was recorded.RESULTS:In the CLP group,myocardial enzyme index and inflammatory index increased at3,6,12 and 24 hours after CLP compared with the sham group,and EPO significantly blocked the increase.Compared with the CLP group,EPO significantly improved LVSP,LV +dpldt_(max) LV-dp/dt_(min),and decreased LVEDP at different time.EPO blocked the reduction of mitochondrial transmembrane potential,suppressed the cardiomyocyte apoptosis,inhibited the activation of NF-κB,and reduced the production of proinflmmatory cytokines.No difference in the survival rate at 7 days was observed between the CLP group and the EPO group.CONCLUSION:Exogenous EPO has cardioprotective effects on sepsis-induced myocardial injury.

Knockdown of 11β-hydroxysteroid dehydrogenase type 1 alleviates LPS-induced myocardial dysfunction through the AMPK/SIRT1/PGC-1αpathway

Sepsis-induced myocardial dysfunction is primarily accompanied by severe sepsis,which is associated with high morbidity and mortality.11β-hydroxysteroid dehydrogenase type 1(11β-HSD1),encoded by Hsd11b1,is a reductase that can convert inactive cortisone into metabolically active cortisol,but the role of 11β-HSD1 in sepsis-induced myocardial dysfunction remains poorly understood.The current study aimed to investigate the effects of 11β-HSD1 on a lipopolysaccharide(LPS)-induced mouse model,in which LPS(10 mg/kg)was administered to wild-type C57BL/6J mice and 11β-HSD1 global knockout mice.We asscessed cardiac function by echocardiography,performed transmission electron microscopy and immunohistochemical staining to analyze myocardial mitochondrial injury and histological changes,and determined the levels of reactive oxygen species and biomarkers of oxidative stress.We also employed polymerase chain reaction analysis,Western blotting,and immunofluorescent staining to determine the expression of related genes and proteins.To investigate the role of 11β-HSD1 in sepsis-induced myocardial dysfunction,we used LPS to induce lentivirus-infected neonatal rat ventricular cardiomyocytes.We found that knockdown of 11β-HSD1 alleviated LPS-induced myocardial mitochondrial injury,oxidative stress,and inflammation,along with an improved myocardial function;furthermore,the depletion of 11β-HSD1 promoted the phosphorylation of adenosine 5′-monophosphate-activated protein kinase(AMPK),peroxisome proliferator-activated receptor gamma coactivator 1α(PGC-1α),and silent information regulator 1(SIRT1)protein levels both in vivo and in vitro.Therefore,the suppression of 11β-HSD1 may be a viable strategy to improve cardiac function against endotoxemia challenges.

Autonomic neurocardiogenic syndrome is stonewalled by the universal definition of myocardial infarction

Myocardial infarction(MI)is defined as myocardial cell death due to prolonged myocardial ischemia.Clinically,troponin rise and/or fall have become the“defining feature of MI”according to the universal definition of MI(UD-MI).Takotsubo syndrome(TS)and TS-related disease conditions also cause troponin elevation with typical rise and/or fall pattern but through a mechanism other than coronary ischemia.By strict application of the clinical diagnostic criteria for type-1 MI,type-2 MI,type-3 MI,and MI with non-obstructive coronary arteries according to the UD-MI including the fourth one published recently,TS and most of the 26 other causes of troponin elevation mentioned in the fourth UD-MI may erroneously be classified as MI.The existing evidence argues for the case that TS by itself is not a MI.Hyper-activation of the autonomic-sympathetic nervous system including local cardiac sympathetic hyper-activation and disruption with nor-epinephrine churn and spillover is the most probable cause of TS.This autonomic neuro-cardiogenic(ANCA)mechanism results in myocardial“cramp”(stunning),the severity and duration of which depend on the degree of the sympathetic-hyperactivation and nor-epinephrine spillover.The myocardial cramp may squeeze the cytosolic free troponin pools causing mild to moderate troponin elevation in TS and TS-related disease conditions.This ANCA syndrome,which has hitherto been enveloped by the UD-MI over more than one decade,may occur in acute,recurrent,and chronic forms.In this critical review,the controversies of UD-MI,evidence for ANCA syndrome,and a hypothetical mechanism for the troponin elevation in ANCA syndrome are provided.

The effect of stunned myocardium on heart function and the protection of fructose－1，6－diphosphate on it

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Effects of sevoflurane preconditioning and postconditioning on rat myocardial stunning in ischemic reperfusion injury

Ischemic preconditioning and postconditioning distinctly attenuate ventricular arrhythmia after ischemia without affecting the severity of myocardial stunning. Therefore, we report the effects of sevofiurane preconditioning and postconditioning on stunned myocardium in isolated rat hearts. Isolated rat hearts were underwent 20 min of global ischemia and 40 min of reperfusion. After an equilibration period （20 min）, the hearts in the preconditioning group were exposed to sevoflurane for 5 min and next washout for 5 min before ischemia. Hearts in the sevoflurane postconditioning group underwent equilibration and ischemia, followed immediately by sevoflurane exposure for the first 5 min of reperfusion. The control group received no treatment before and after ischemia. Left ventricular pressure, heart rate, coronary flow, electrocardiogram, and tissue histology were measured as variables of ventricular function and cellular injury, respectively. There was no significant difference in the duration of reperfusion ventricular arrhythmias between control and sevoflurane preconditioning group （P=0.195）. The duration of reperfusion ventricular arrhythmias in the sevoflurane postconditioning group was significantly shorter than that in the other two groups （P〈0.05）. ＋（dPIdt）max in the sevoflurane preconditioning group at 5, 10, 15, 20, and 30 min after reperfusion was significantly higher than that in the control group （P〈0.05）, and there were no significant differences at 40 min after reperfusion among the three groups （P〉0.05）. As expected, for a 20-min general ischemia, infarct size in heart slices determined by 2,3,5-triphenyltetrazolium chloride staining among the groups was not obvious. Sevofiurane postconditioning reduces reperfusion arrhythmias without affecting the severity of myocardial stunning. In contrast, sevoflurane preconditioning has no beneficial effects on reperfusion arrhythmias, but it is in favor of improving ventricular function and recovering myocardial stunning. Sevoflurane preconditioning and postconditioning may be useful for correcting the stunned myocardium.

Gastrin attenuates sepsis-induced myocardial dysfunction by down-regulation of TLR4 expression in macrophages

Myocardial dysfunction is the most serious complication of sepsis.Sepsis-induced myocardial dysfunction(SMD)is often associated with gastrointestinal dysfunction,but its pathophysiological significance remains unclear.The present study found that patients with SMD had higher plasma gastrin concentrations than those without SMD.In mice,knockdown of the gastrin receptor,cholecystokinin B receptor(Cckbr),aggravated lipopolysaccharide(LPS)-induced cardiac dysfunction and increased inflammation in the heart,whereas the intravenous administration of gastrin ameliorated SMD and cardiac injury.Macrophage infiltration plays a significant role in SMD because depletion of macrophages by the intravenous injection of clodronate liposomes,48 h prior to LPS administration,alleviated LPSinduced cardiac injury in Cckbr-deficient mice.The intravenous injection of bone marrow macrophages(BMMs)overexpressing Cckbr reduced LPS-induced myocardial dysfunction.Furthermore,gastrin treatment inhibited toll-like receptor 4(TLR4)expression through the peroxisome proliferator-activated receptor a(PPAR-a)signaling pathway in BMMs.Thus,our findings provide insights into the mechanism of the protective role of gastrin/CCKBR in SMD,which could be used to develop new treatment modalities for SMD.

大鼠单次完全可逆缺血/再灌注心肌顿抑模型的改进

目的:改进和完善大鼠单次完全可逆缺血/再灌注心肌顿抑的模型。方法:采用成年SD大鼠28只,分为对照组和实验组,用操作简单、损伤小、出血少的手术方法阻断大鼠左冠状动脉的前室间支,15min后完全恢复其血流,再灌注2h。同时检测大鼠心电图的变化并进行组织学检查。结果:实验组阻断左冠状动脉的前室间支后,心电图出现异常,表现为S-T间期延长,T波倒置,而光镜下组织结构正常。结论:该模型符合心肌顿抑的特点;该方法操作简单,结果可靠,可重复性强,是一种建立在体大鼠单次完全可逆缺血/再灌注模型的可靠方法。

超声二维斑点追踪显像技术检测犬顿抑心肌跨壁力学状态的变化

目的应用超声二维斑点追踪显像技术检测犬顿抑心肌心内、外膜纵向的应变变化,探讨顿抑心肌的跨壁力学变化及其随时间的变化规律。方法 12只犬左冠状动脉前降支结扎20min,再灌注120min,分别于结扎前、结扎期间、再灌注后即刻、30、60、90、120min采集心尖切面图像。应用超声二维斑点追踪显像技术检测缺血及非缺血节段心内膜、心外膜、整体节段应变参数:纵向峰值应变(LSpeak)、峰值应变延迟时间(TPSLS),并进行比较分析。结果犬心肌左冠状动脉前降支结扎后、再灌注后即刻缺血节段心内、外膜、整体节段LSpeak明显减低,TPSLS延长,且LSpeak以心内膜下心肌减低更明显;随再灌注时间延长,二维应变逐渐恢复,心外膜下心肌恢复更快,缺血节段整体心肌恢复正常时,心内膜下心肌仍未恢复正常。非缺血节段在左冠状动脉前降支结扎后、再灌注后即刻心内、外膜下LSpeak明显增加,TPSLS延长,再灌注30min恢复正常。结论超声二维斑点追踪显像技术可检测犬顿抑心肌在缺血及再灌注阶段心内、外膜下心肌二维应变变化。

一氧化氮在家兔缺血再灌注心肌顿抑中的作用及左旋精氨酸干预

目的 探讨一氧化氮 (NO)在家兔缺血再灌注心肌顿抑中的作用及左旋精氨酸 (L -Arg)对其影响。方法 2 0只家兔随机均分为对照组和L -Arg组 ,制备心肌缺血再灌注模型 ,于缺血前、缺血 40分钟及再灌注 2 0分钟取血检测NO水平 ,相应时点监测心功能。结果 心肌缺血再灌注期间 ,NO显著下降 ,心肌舒缩功能明显降低 ,尤以再灌注 2 0分钟为著 ,L -Arg可逆转上述指标。结论 缺血再灌注心肌顿抑与NO水平下降有关 ,L

万爽力对顿抑心肌能量代谢及功能的恢复作用

目的 :应用兔冠脉前降支结扎缺血再灌模型 ,观察万爽力对顿抑心肌能量代谢及功能的影响并分析其可能机制。方法 :18只日本大耳白兔随机分为对照组、心肌顿抑组和万爽力组。结扎兔冠脉左前降支 2 0min ,再灌36 0min ,观察血流动力学、抗氧化酶、脂质过氧化物、血清游离脂肪酸、乳酸以及心肌组织ATP含量和超微结构的变化。结果 :①万爽力可缓解顿抑心肌收缩舒张功能明显降低 ;②万爽力可抑制顿抑组血清游离脂肪酸 (FFA)、乳酸 (LD)、丙二醛 (MDA)水平明显升高 ,超氧化物歧化酶 (SOD)活性明显下降 ;③顿抑组心肌组织ATP含量较对照组明显下降 ,万爽力可升高顿抑心肌组织ATP含量 (P <0 .0 1) ;④万爽力可减轻顿抑心肌损伤。结论 :万爽力对顿抑心肌功能与能量代谢的恢复作用与其直接参与心肌细胞脂肪酸代谢有关。

环磷腺苷葡胺联合地高辛治疗脓毒症致心肌顿抑性心力衰竭的疗效分析

目的探讨环磷腺苷葡胺联合地高辛治疗脓毒症致心肌顿抑性心力衰竭的疗效。方法选取2013年1月—2015年6月安徽医科大学附属宿州医院急诊科和全科医学科收治的脓毒症致心肌顿抑性心力衰竭患者58例,采用随机数字表法分为治疗组29例和对照组29例,两组均予常规对症治疗,治疗组在常规治疗基础上加用5%葡萄糖注射液250 ml+环磷腺苷葡胺180 mg+胰岛素4 U,静脉滴注;地高辛0.125 mg,口服,1次/d。对照组加用地高辛0.125mg,口服,1次/d。两组患者分别于治疗前、治疗后第7天抽静脉血和/或动脉血查心肌肌钙蛋白I(c Tn-I)、脑钠肽(BNP)、C反应蛋白(CRP)、血乳酸(Lac)、降钙素原(PCT),并进行急性生理与慢性健康状况评分系统Ⅱ(APACHEⅡ评分)及床旁彩超检测左心室射血分数(LVEF)。结果两组患者治疗前c Tn-I、BNP、CRP、Lac、PCT水平、APACHEⅡ评分、LVEF比较,差异均无统计学意义(P>0.05);治疗后治疗组c Tn-I、BNP、CRP、Lac、PCT水平、APACHEⅡ评分低于对照组,LVEF高于对照组(P<0.05)。两组不良反应发生率比较,差异无统计学意义[44.8%(13/29)与51.7%(15/29),χ~2=0.276,P=0.599];两组2周后病死率比较,差异有统计学意义[34.5%(10/29)与10.3%(3/29),χ~2=4.858,P=0.028]。结论环磷腺苷葡胺联合地高辛治疗脓毒症致心肌顿抑性心力衰竭,可明显减轻心肌损伤及全身炎性反应,改善心功能,降低病死率。

心肌顿抑的防治机制新进展

心肌顿抑是短暂心肌缺血血流恢复后收缩功能延迟恢复的现象。它的发生严重影响各种心脏治疗的成功率。因此,减少心肌顿抑的发生率成为现今缺血-再灌注损伤新的热点之一。近年来有许多有关预防和治疗心肌顿抑的研究报道,这些研究报道将为临床上心肌顿抑的防治提供一些理论和实验依据。

心肌顿抑中的氧化应激作用及氨基胍干预的效果

背景氧化应激的超氧阴离子(O-.2)可与细胞一氧化氮合酶(NOS)释出的一氧化氮(NO)结合,生成过氧亚硝酸阴离子(ONOO-)。ONOO-是氧化应激各种产物[如O2.-、H2O2、羟自由基(.OH)等]之一,统称为反应性氧族(ROS)。ROS在心肌顿抑中的作用研究不多,氨基胍作为NOS抑制剂对ROS的作用也不清楚。目的探讨ONOO-在心肌顿抑发生中的作用和机制以及氨基胍的干预作用。方法24条雄性杂种犬,随机分为4组:1)短顿抑组[左前降支冠状动脉(LAD)阻断15min/再灌注120min];2)长顿抑组(LAD阻断60min/再灌注120min);3)氨基胍组[LAD阻断60min/再灌注120min加一氧化氮合酶抑制剂氨基胍(100mg/kg)干预];4)假手术组。在不同观察时间点测定超声心功能和冠状静脉窦血浆NO浓度。实验完毕后心肌标本行电镜检查,并行硝基酪氨酸免疫组化检查以证实是否有ONOO-生成。结果1)LAD结扎后缺血心肌节段收缩期增厚百分率和左室射血分数显著下降,缺血心肌节段表现为矛盾运动;再灌注开始后心肌节段收缩功能和左室射血分数呈进行性改善,短顿抑组和氨基胍组心功能的恢复快于长顿抑组。2)短顿抑组和长顿抑组再灌注期血浆NO浓度明显升高,氨基胍组再灌注期血浆NO浓度无显著升高。3)短顿抑组顿抑心肌硝基酪氨酸免疫组化染色见阳性染色的心肌细胞灶;长顿抑组见较大、较多的强阳性染色心肌细胞灶,主要是胞浆尤其横纹处染色较深;氨基胍组顿抑心肌偶见心肌细胞弱阳性染色。4)透射电镜观察发现,短顿抑组心肌细胞偶见线粒体轻度脱颗粒;长顿抑组心肌细胞部分肌丝断裂,收缩带溶解,线粒体肿胀、脱颗粒,胞质水肿;氨基胍组心肌超微结构保存良好。结论1)顿抑心肌生成NO增多伴ONOO-形成;2)ONOO-主要攻击的蛋白质对象是肌丝上的蛋白质;3)氨基胍抑制顿抑心肌过多的NO生成,显著减少ONOO-形成,并对顿抑心肌的超微结构和功能有明显保护作用。

超速驱动诱发大鼠离体心脏心肌顿抑的研究

目的:通过电超速驱动模拟运动负荷诱发心肌顿抑现象,建立离体大鼠心脏运动性心肌顿抑模型。方法:将36只SPF级成年雄性SD大鼠随机分6组,用电刺激模拟运动负荷的方法来对大鼠离体心脏施加超速驱动,并根据驱动时间的不同进行分组,再分别测量记录各组驱动前后各指标的变化情况加以分析。结果:(1)各组左心室收缩压、发展压在驱动全过程呈下降趋势,舒张压呈上升趋势,而驱动前组间室内压无明显差异。(2)各组冠状动脉流出液CK、LDH在驱动前无明显差异,驱动后各实验组水平均高于对照组。(3)驱动20min组和30min组的心肌坏死率明显高于其他组,而其他组两两比较无组间差异。结论:(1)运动性心肌顿抑存在。(2)过长的高心率负荷将不再发生心肌顿抑现象而出现大面积心肌坏死。(3)本实验中,运动性心肌顿抑存在于5min组和10min组中。

米力农联合多巴胺用于重症心内直视术停机过程

目的 :观察米力农联合多巴胺对重症瓣膜置换术后脱离体外循环 (CPB)过程全身血流动力学及氧供需平衡影响 ,以评价联合用药对这类病人的治疗效果。方法 :重症瓣膜置换手术病人 2 0例 ,随机分成两组 ,于心脏复跳、建立稳定的自主心律后 ,分别应用小剂量 (A组 )或较大剂量 (B组 )米力农联合多巴胺 ,停机过程经人工心肺机输血、补液维持PADP相对稳定。结果 :A、B两组停机后 ,CI分别较基础值增加 5 0 %和 80 %。B组用药后SVRI的下降幅度明显超过A组 ,同时MAP显著降低 ,多数病人因MAP <8kPa需单次静注去氧肾上腺素治疗。HR变化均不明显 ,PVRI、MPAP及PAWP虽显著降低 ,但两组间差异无显著性。停机后两组病人DO2 I显著增加 ,VO2 I无明显变化 ,而VO2 /DO2 显著降低。结论 :米力农与多巴胺联合应用可明显改善重症心脏手术后心肌收缩功能 ,提高氧的利用率而对全身氧耗无明显影响。但考虑到对MAP的影响 ,在脱离CPB过程 。