Effects of Shenfu Injection(参附注射液)on Inflammatory Response during Post-Resuscitation Myocardial Dysfunction after Cardiac Arrest in Swine

Objective:To investigate whether Shenfu Injection(SFI,参附注射液)can alleviate post-resuscitation myocardial dysfunction by inhibiting the inflammatory response.Methods:After 8 min of ventricular fibrillation and 2 min of basic life support,24 pigs were randomly divided into 3 groups(n=8),which were given intravenous bolus injections of SFI(1.0 mL/kg),epinephrine(EP,0.02 mg/kg)and normal saline(SA),respectively.The animals were sacrificed at 24 h after restoration of spontaneous circulation(ROSC),and serum interleuking-6(IL-6)and tumor necrosis factor-α(TNF-α)levels were measured by enzyme-linked immunosorbent assay(ELISA);expressions of Toll-like receptor 4(TLR4)/nuclear factor kappa B(NF-κB)m RNAs and proteins were determined by RT-PCR and Western blot,respectively.Results:Compared with the EP and the SA groups,the ultrastructure of myocardial cells were slightly damaged and the systolic function of the left ventricle was markedly improved in the SFI group at 24 h after ROSC(P<0.05).In addition,compared with the EP and SA groups,the SFI group also showed significantly reduced levels of serum IL-6 and TNF-α,protein and mRNA levels of myocardial NF-κB and TLR4(P<0.05).Conclusions:Activation of TLR4/NF-κB signaling pathway may be involved in the pathological mechanisms of post-resuscitation myocardial dysfunction.SFI may block NF-κB-mediated inflammatory response by reducing the activity of NF-κB and the level of TNF-α,thus playing a protective role in post-resuscitation myocardial dysfunction.

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.

Pathophysiology of sepsis-induced myocardial dysfunction

Sepsis-induced myocardial dysfunction is a common complication in septic patients and is associated with increased mortality.In the clinical setting,it was once believed that myocardial dysfunction was not a major pathological process in the septic patients,at least in part,due to the unavailability of suitable clinical markers to assess intrinsic myocardial function during sepsis.Although sepsis-induced myocardial dysfunction has been studied in clinical and basic research for more than 30 years,its pathophysiology is not completely understood,and no specific therapies for this disorder exist.The purpose of this review is to summarize our current knowledge of sepsis-induced myocardial dysfunction with a special focus on pathogenesis and clinical characteristics.

Influence of Microcirculatory Dysfunction on Myocardial Injury after Cardiopulmonary Resuscitation

Objective This study aimed to examine the effects of microcirculatory dysfunction and 654-1intervention after cardiopulmonary resuscitation on myocardial injury.Methods Landrace pigs were divided into a sham operation group(S group,n=6),ventricular fibrillation control group(VF-C group,n=8)and 654-1 intervention group(VF-I group,n=8).Hemodynamics was recorded at baseline,at recovery of spontaneous circulation(ROSC),and 1 h,2 h,4h and 6 h thereafter.Sidestream dark field(SDF)technology was used to evaluate and monitor the microcirculation flow index,total vessel density,perfusion vessel ratio,De-Backer score,and perfusion vessel density in animal viscera at various time points.Results After administration of 654-1 at 1.5 h post-ROSC,the hemodynamics in the VF-I group,as compared with the VF-C group,was significantly improved.The visceral microcirculation detected by SDF was also significantly improved in the VF-I group.As observed through electron microscopy,significantly less myocardial tissue injury was present in the VF-I group than the VF-C group.Conclusion Administration of 654-1 inhibited excessive inflammatory by improving the state of visceral microcirculation.

Coronary microembolization induced myocardial contractile dysfunction through a p38 mapk pathway

Background Cathepsin S and its endogenous inhibitor cystatin C are implicated in the pathogenesis of atherosclerosis,especially in the plaque destabilization and rupture leading to acute coronary syndrome.However, whether circulating cathepsin S and cystatin C also change in association with coronary plaque morphology is unknown yet. Methods Sprague-Dawley rats were randomly divided into three groups;Sham group,CME group and SB203580 group (n=10 per group).CME rats were produced by injection of 42μm microspheres into the left ventricle with occlusion of the ascending aorta.SB203580,a p38 MAPK inhibitor,was injected into femoral vein after finishing the injection of microspheres in SB203580 group.Left ventricular Ejection Fraction was determined by echocardiography.The level of phosphorylated and total P38 MAPK in myocardium was assessed by Western Blot.Results Left ventricular(LV) Ejection Fraction was depressed at 3 hours and until up to 12 hours in CME group.The increased p38 MAPK activation was observed in CME group.The administration of SB203580 partly inhibited the p38 MAPK activity and preserved cardiac contractile function.Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly preserve cardiac contractile function.

Comparison between primary angioplasty and thrombolytic therapy on erectile dysfunction after acute ST elevation myocardial infarction

Acute ST elevation myocardial infarction has high mortality and morbidity rates. The majority of patients with this condition face erectile dysfunction in addition to other health problems. In this study, we aimed to investigate the effects of two different reperfusion strategies, primary angioplasty and thrombolytic therapy, on the prevalence of erectile dysfunction after acute myocardial infarction. Of the 71 patients matching the selection criteria, 45 were treated with primary coronary angioplasty with stenting, and 26 were treated with thrombolytic agents. Erectile function was evaluated using the International Index of Erectile Function in the hospital to characterize each patient＇s sexual function before the acute myocardial infarction and 6 months after the event. The time required to restore blood flow to the artery affected by the infarct was found to be associated with the occurrence of erectile dysfunction after acute myocardial infarction. The increase in the prevalence of erectile dysfunction after acute myocardial infarction was 44.4% in the angioplasty group and 76.9% in the thrombolytic therapy group （P= 0.008）. In conclusion, this study has shown that reducing the time of reperfusion decreases the erectile dysfunction prevalence, and primary angioplasty is superior to thrombolytic therapy for decreasing the prevalence of erectile dysfunction after acute myocardial infarction.

The Incidence of Myocardial Diastolic Dysfunction in Patients with Decompensated Liver Disease

Introduction: There is a debate about whether the occurrence is of systolic, diastolic dysfunction, or both in patients with liver cirrhosis. Aim of the work was to investigate the diastolic and systolic function changes prevalence in Acute decompensated on top of chronic liver disease. Patients and methods: The studywas performed on three hundred patients with Hepatitis C virus (HCV) associated liver cirrhosis;patients with a history of cardiac disease were excluded from the study about complete liver function tests. Abdominal ultrasound and echo-doppler were done for all patients and control. They were subdivided according to compensation into two groups: Group A was 150 patients with Compensated Liver Cirrhosis Disease (child A), and Group B was 150 patient with Decompensate Liver Cirrhosis (child B & C) and Control group of twenty, with no hepatic abnormality and no cardiac dysfunction. Echocardiography was done to all patients to detect left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), ejection fraction (EF%) and E/A ratio to detect the presence of diastolic dysfunction. Results: In this study, reversed E/A ratio as an indicator for diastolic dysfunction was found in 120 (40%) patients while patients had standard E/A rate was 180 (60%). E/A ratio decreased and decreased in the LVESD and EF% in patients with decompensated liver cirrhosis more than those with compensated liver cirrhosis. Conclusion: Decompensated liver cirrhosis is associated with diastolic and systolic dysfunctions.

Left Ventricular Diastolic Dysfunction and Silent Myocardial Ischemia amongst Asymptomatic Type 2 Diabetic Patients in Two Referral Hospitals in Cameroon

Background: Cardiovascular events, the leading cause of death among diabetic patients, are usually under-diagnosed due to subclinical presentation. Methods: We conducted a cross-sectional study from March-2019 to September-2020, in two reference hospitals in Yaoundé, Cameroon, to assess the prevalence of asymptomatic Left Ventricular Diastolic Dysfunction (LVDD) and Silent Myocardial Infarction (SMI) and potentially associated factors. Results: Out of 95 participants (mean age ± SD: 43 ± 7 years;M/F sex-ratio 1.6), 22 (23.1%;95% CI: 15.8% - 32.6%) had LVDD and fewer (n = 13, 13.6%;95% CI: 8.2% - 22.0%) had SMI, p = 0.86. Though not statistically significant, patients with ≥5 years diabetes duration, as well as patients with HbA1C ≥ 7.5% had two-fold increased risk of LVDD (p = 0.22 and p = 0.15 respectively). LVDD was significantly higher in patients with SMI (29% vs 6.3%, p Conclusion: The significant presence of asymptomatic cardiovascular manifestations in this population entails mandatory preventive screening, especially, in patients with long standing diabetes and poor glycemic control, to allow timely detection and management.

Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis

BACKGROUND We studied the protective effects of Qingyi decoction(QYD)(a Traditional Chinese Medicine)against severe acute pancreatitis(SAP)-induced myocardial infarction(MI).AIM To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP.METHODS Ultrasonic cardiography,hematoxylin and eosin staining,immunohistochemistry,qRT-PCR,western blot,enzyme-linked immunosorbent assays,and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats.RESULTS Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms,mortality rate,and ultrasonic cardiography outputs among the different groups compared to the control.The expression of serum cytokines[interleukin(IL)-1?,IL-6,IL-8,IL-12,amyloidβ,and tumor necrosis factor-α]were significantly higher in the SAP versus QYD treated group(P<0.05 for all).STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage(P<0.001).There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups.The SAP group had a significantly higher apoptosis index score compared to the QYD group(P<0.001).CONCLUSION QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression(STIM1 and Orai1).

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.

Accuracy of myocardial viability imaging by cardiac MRI and PET depending on left ventricular function

AIM To compare myocardial viability assessment accuracy of cardiac magnetic resonance imaging(CMR)compared to[^(18)F]-fluorodeoxyglucose(FDG)-positron emission tomography(PET)depending on left ventricular(LV)function.METHODS One-hundred-five patients with known obstructive coronary artery disease(CAD)and anticipated coronary revascularization were included in the study and examined by CMR on a 1.5T scanner.The CMR protocol consisted of cine-sequences for function analysis and late gadolinium enhancement(LGE)imaging for viability assessment in 8 mm long and contiguous short axis slices.All patients underwent PET using[^(18)F]-FDG.Myocardial scars were rated in both CMR and PET on a segmental basis by a 4-point-scale:Score 1=no LGE,normal FDG-uptake;score 2=LGE enhancement<50% of wall thickness,reduced FDG-uptake(≥50% of maximum);score 3=LGE≥50% ,reduced FDG-uptake(<50% of maximum);score 4=transmural LGE,no FDG-uptake.Segments with score 1 and 2 were categorized"viable",scores 3 and 4 were categorized as"non-viable".Patients were divided into three groups based on LV function as determined by CMR:Ejection fraction(EF),<30% :n=45;EF:30% -50% :n=44;EF>50% :n=16).On a segmental basis,the accuracy of CMR in detecting myocardial scar was compared to PET in the total collective and in the three different patient groups.RESULTS CMR and PET data of all 105 patients were sufficient for evaluation and 5508 segments were compared in total.In all patients,CMR detected significantly more scars(score 2-4)than PET:45% vs 40% of all segments(P<0.0001).In the different LV function groups,CMR found more scar segments than PET in subjects with EF<30% (55% vs 46% ;P<0.0001)and EF 30% -50% (44% vs 40% ;P<0.005).However,CMR revealed less scars than PET in patients with EF>50% (15% vs 23% ;P<0.0001).In terms of functional improvement estimation,i.e.,expected improvement after revascularization,CMR identified"viable"segments(score 1 and 2)in 72% of segments across all groups,PET in 80% (P<0.0001).Also in all LV function subgroups,CMR judged less segments viable than PET:EF<30% ,66% vs 75% ;EF=30% -50% ,72% vs 80% ;EF>50% ,91% vs 94% .CONCLUSION CMR and PET reveal different diagnostic accuracy in myocardial viability assessment depending on LV function state.CMR,in general,is less optimistic in functional recovery prediction.

Serum uric acid in patients with acute ST-elevation myocardial infarction

BACKGROUND:Few studies investigated serum uric acid levels in patients with acute STelevation myocardial infarction(STEMI).The study was to assess the clinical value of serum uric acid levels in patients with acute ST-elevation myocardial infarction(STEMI).METHODS:Totally 502 consecutive patients with STEMI were retrospectively studied from January 2005 to December 2010.The level of serum lipid,echocardiographic data and in-hospital major adverse cardiovascular events(MACE) in patients with hyperuricemia(n=119) were compared with those in patients without hyperuricemia(n=383).The relationship between the level of serum uric acid and the degree of diseased coronary artery was analyzed.All data were analyzed with SPSS version 17.0 software for Student's t test,the Chi-square test and Pearson's correlation coefficient analysis.RESULTS:Serum uric acid level was positively correlated with serum triglyceride level.Hyperlipidemia was more common in hyperuricemia patients than in non-hyperuricemia patients(43.7%vs.33.7%,P=0.047),and serum triglyceride level was significantly higher in hyperuricemia patients(2.11±1.24 vs.1.78±1.38,P=0.014).But no significant association was observed between serum uric acid level and one or more diseased vessels(P>0.05).Left ventricular end-diastolic diameter(LVEDd) was larger in hyperuricemia patients than in non-hyperuricemia patients(53.52±6.19 vs.52.18±4.89,P=0.041).The higher rate of left systolic dysfunction and diastolic dysfunction was discovered in hyperuricemia patients(36.4%vs.15.1%,P<0.001;68.2%vs.55.8%,P=0.023).Also,hyperuricemia patients were more likely to have in-hospital MACE(P<0.05).CONCLUSIONS:Serum uric acid level is positively correlated with serum triglyceride level,but not with the severity of coronary artery disease.Hyperuricemia patients with STEMI tend to have a higher rate of left systolic dysfunction and diastolic dysfunction and more likely to have more in-hospital MACE.

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.

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.

Why is there a need for an interdisciplinary approach to assess erectile dysfunction?

Erectile dysfunction is a prevalent complaint among men. The majority of patients suffering erectile dysfunction exhibit various risk factors of vascular diseases. Erectile dysfunction used to be recognised as one of the consequences of vascular diseases in patients suffering heart attack or myocardial infarction. During the last decade, however, the role of endothelial dysfunction in the occurrence of erectile dysfunction has been signifi ed, and it has been suggested that erectile dysfunction may not be simply a consequence of vascular diseases but an indicator of future vascular problems. Erectile dysfunction has been known as "the tip of iceberg" of a generalised vascular dysfunction, which typically happens before serious vascular problems. Considerable evidence shows a link between erectile dysfunction and vascular disorders. Several theories have been considered for the association between erectile dysfunction and vascular diseases. One of them is the "artery size" theory focusing on the differences between the diameter of the penile artery and other arteries. Another theory is based on "endothelial dysfunction", which highlights inappropriate vasoconstriction as a cause of erectile dysfunction and vascular diseases. "Age" has also been reported to have pivotal role in the development of vascular dysfunction resulting in erectile dysfunction and ultimately vascular diseases. Another theory explaining the pathophysiology of erectiledysfunction and its relationship with vascular diseases focuses on the formation of atherosclerosis plaques. This article endeavours to review the current literature and discuss why a multidisciplinary approach is needed while assessing erectile dysfunction.

Transplantation of CD34+cells for myocardial ischemia

CD34+cells are multipotent hematopoietic stem cells also known as endothelial progenitor cells and are useful in regenerative medicine.Naturally,these cells are mobilized from the bone marrow into peripheral circulation in response to ischemic tissue injury.CD34+cells are known for their high proliferative and differentiation capacities that play a crucial role in the repair process of myocardial damage.They have an important paracrine activity in secreting factors to stimulate vasculogenesis,reduce endothelial cells and cardiomyocytes apoptosis,remodel extracellular matrix and activate additional progenitor cells.Once they migrate to the target site,they enhance angiogenesis,neovascularization and tissue regeneration.Several trials have demonstrated the safety and efficacy of CD34+cell therapy in different settings,such as peripheral limb ischemia,stroke and cardiovascular disease.Herein,we review the potential utility of CD34+cell transplantation in acute myocardial infarction,refractory angina and ischemic heart failure.

铁死亡在脓毒症心肌损伤中的研究进展

铁死亡是一种与铁积累和脂质过氧化相关的程序性细胞死亡形式,具有独特的形态、遗传和生化特征。脓毒症是一种危及生命的多器官功能障碍综合征,由人体对感染的免疫反应失调引起。脓毒症心肌损伤是脓毒症的一种严重并发症,是加剧患者死亡的重要因素,给社会和家庭造成极大负担。铁死亡与脓毒症心肌损伤的发生密切相关。本文对铁死亡与脓毒症心肌损伤的机制进行综述,探讨铁死亡在脓毒症心肌损伤中的研究进展,以期为脓毒症心肌损伤的治疗提供新思路。

血必净注射液对脓毒症性心肌功能障碍的临床干预效果

目的:观察脓毒症性心肌功能障碍患者接受血必净注射液干预的有效性。方法:选取2021年3月—2023年3月贵州省人民医院收治的脓毒症心肌功能障碍患者92例作为研究对象,以随机数字表法分为普通干预组和实践干预组,各46例。普通干预组采用基础抗感染及抗休克治疗,实践干预组在对照组基础上给予血必净注射液治疗。比较两组患者ICU治疗时间、心功能与血浆脑钠尿肽、血清炎性因子与肾功能、治疗有效率。结果:实践干预组ICU治疗时间短于普通干预组,差异有统计学意义(P=0.035);干预后,两组左心室舒张末期内径、左室射血分数、每分心输出量与血浆脑钠尿肽均优于干预前,实践干预组优于普通干预组,差异有统计学意义(P<0.05);干预后,实践干预组白细胞介素-10、白细胞介素-6、肿瘤坏死因子-α、白蛋白及血肌酐均优于普通干预组,差异有统计学意义(P<0.05);实践干预组治疗有效率高于普通干预组,差异有统计学意义(P=0.001)。结论:脓毒症性心肌功能障碍的临床治疗中应用血必净注射液干预效果显著,可有效改善患者心功能、肾功能、炎性因子,降低血浆脑钠尿肽水平,促进康复。

心脏能量代谢在脓毒症心功能障碍中的研究进展

生理条件下,心脏中脂质、葡萄糖、酮体和氨基酸等能量物质代谢活动保持动态平衡,以满足心脏的能量需求。而在脓毒症期间,一些化学介质如内毒素、一氧化氮等引发的炎症反应以及某些信号通路的激活或抑制都会导致心脏能量代谢的改变,这既是机体代偿的过程,也是造成器官功能障碍的原因。本篇综述将着重探讨脓毒症期间的能量代谢变化,特别是心脏的能量代谢,旨在为治疗脓毒症所导致的心功能障碍提供新的研究方向和策略。

抑制TRAF6调节炎症和自噬改善脓毒症小鼠的心肌损伤和心功能

目的 探索抑制TRAF6后对脓毒症小鼠心肌细胞自噬、炎症反应和心功能的改善作用。方法 (1)昆明雄性小鼠24只,随机分为4组,分别为假手术(sham)组、假手术+C25-140(sham+C)组、盲肠结扎穿刺术(CLP)组、盲肠结扎穿刺术+C25-140(CLP+C)组。sham+C组、CLP+C组术后腹腔注射C25-140。术后24 h超声评估LVEF、LVFS;ELISA测血清TNF-α、IL1-β;HE染色评估心肌炎症反应;透射电镜观察心肌细胞自噬小体、线粒体微结构;qPCR检测心肌组织TRAF6 mRNA;WB检测TRAF6、P62、Beclin-1、LC3B蛋白的表达;(2)予3-MA抑制自噬观察C25-140对脓毒症小鼠心肌损伤的影响。结果 (1)与sham组比,CLP组心肌组织TRAF6mRNA及TRAF6蛋白显著升高(P <0.05);血清TNF-α、IL1-β浓度显著升高(P <0.05);心肌组织HE染色见炎症细胞浸润;LVEF、LVFS显著降低(P <0.05);(2)与CLP组比,CLP+C组TRAF6 mRNA及TRAF6蛋白表达减少(P <0.05);血清TNF-α、IL1-β下降(P <0.05);心肌组织病理心肌炎症细胞浸润减少;LVEF、LVFS升高(P <0.05);电镜见线粒体肿胀减轻、自噬小体增多;Beclin-1、LC3Ⅱ/Ⅰ表达增加,P62表达减少(P <0.05);予3-MA抑制自噬后,与CLP+C组比,CLP+C+3-MA组小鼠心肌病理见炎症细胞浸润明显,LVEF、LVFS降低(P <0.05)。结论 抑制TRAF6改善脓毒症小鼠心肌炎症损伤和心功能障碍;抑制TRAF6促进心肌细胞自噬参与保护脓毒症诱导的心肌损伤。