Hypertrophic cardiomyopathy and left ventricular non-compaction:Distinct diseases or variant phenotypes of a single condition?

Hypertrophic cardiomyopathy(HCM)is a genetically determined myocardial disease characterized by an increased thickness of the left ventricle(LV)wall that cannot be solely attributed to abnormal loading conditions.HCM may present with an intraventricular or LV outflow tract obstruction,diastolic dysfunction,myocardial fibrosis and/or ventricular arrhythmias.Differentiating HCM from other diseases associated with LV hypertrophy,such as hypertension,aortic stenosis,or LV non-compaction(LVNC),can at times be challenging.LVNC is defined by excessive LV trabeculation and deep recesses between trabeculae,often accompanied by increased LV myocardial mass.Previous studies indicate that the LVNC phenotype may be observed in up to 5%of the general population;however,in most cases,it is a benign finding with no impact on clinical outcomes.Nevertheless,LVNC can occasionally lead to LV systolic dysfunction,manifesting as a phenotype of dilated or non-dilated left ventricular cardiomyopathy,with an increased risk of thrombus formation and arterial embolism.In extreme cases,where LVNC is associated with a very thickened LV wall,it can even mimic HCM.There is growing evidence of an overlap between HCM and LVNC,including similar genetic mutations and clinical presentations.This raises the question of whether HCM and LVNC represent different phenotypes of the same disease or are,in fact,two distinct entities.

Left ventricular non-compaction presenting as cardio-embolic stroke

A 39-year-old male with no known comorbidities presented with sudden onset right-sided weakness.On examination,blood pressure was 128/79 mmHg,National Institutes of Health Stroke Scale score was 4 and there were no signs of heart failure.Emergent computerized tomography demonstrated an ischemic infarct of the left middle cerebral artery distribution and brain magnetic resonance imaging later confirmed it(Figure 1).

Ventricular Non-Compaction: About the First Cases Reported in Lomé(Togo)

Introduction: Ventricular non-compaction, a cardiomyopathy recently described as likely to be rare, belongs to the group of unclassified cardiomyopathy according to European Society of Cardiology. Few studies have been published on the ventricular non-compaction in sub-Saharan Africa. We aim to find out the various aspects, being diagnosis, therapeutic, in Togolese patients carrying the ventricular non-compaction. Methodology: This is a three-year prospective and descriptive study conducted from January 2017 to December 2019 in the two University Hospital of Lomé. Patients having echocardiographic criteria of ventricular non-compaction were included in our study. Results: 10 patients (6 men and 4 women) were diagnosed for ventricular non-compaction during the study period. The mean age of patients was 32.3 years. The most frequent clinical manifestation was heart failure (7 patients). The main electrocardiogram anomaly was left ventricle hypertrophy (9 patients). The preferential segments were: apical (9 cases), apicolateral (8 cases), and septoapical (7 cases). The average ratio of non-compaction/compaction was 3.31. The main complication was thromboembolic event (4 patients). Angiotensin converting enzyme inhibitors and beta-blockers were essentially the medicines used. After a three (3) year follow-up, two (2) of the patients died. Conclusion: Tough ventricular non-compaction has been recently described. It is present in Togo. It displays many clinical manifestations and the prognosis is often guarded.

Do Antineoplastic Drugs Play an Additional Role in the Progression of Non-Compaction Cardiomyopathy? A Case Report

Non-compaction cardiomyopathy is a rare form of cardiomyopathy;its most common clinical manifestations are heart failure (HF), ventricular arrhythmia, thromboembolism, and sudden cardiac death. We report a rare case of a 63-year-old man with chest tightness, worsening lower leg edema, dyspnea, and decreased exercise tolerance. He had a medical history of gastric cancer treated with subtotal gastrectomy and post-operative chemotherapy with paclitaxel and fluorouracil three years ago. At that time, he was diagnosed with non-compaction cardiomyopathy, and the thickened and reticulated trabecular muscle was exclusively confined to left ventricular apex. Five months ago, he was admitted to our hospital with heart failure and treated for dilated cardiomyopathy, echocardiography revealed severe trabecular noncompact myocardium in both ventricles, which was confirmed by cardiac magnetic resonance imaging (CMR). It is generally accepted that non-compacted myocardium forms in the early embryonic stage, which raises a question in our case whether acquired factors, such as antineoplastic drugs, potentially accelerate the pathological progression of non-compaction cardiomyopathy. Considering there are disparities between current screening tools such as echocardiography and CMR regarding diagnostic criteria, multi-detector CT may be an alternative examination method that could provide a new perspective for diagnosis.

A Case Report of Isolated Left Ventricular Non-Compaction Presenting with Congestive Heart Failure and Intramural Thrombus

Isolated left ventricular non-compaction is recently described as a rare form of cardiomyopathy that is associated with a heart failure, life threatening cardiac arrhythmia and thromboembolic complications. The diagnosis is based on echocardiography demonstration of spongy myocardium. Here we report a case of 74 years old female patient diagnosed as an isolated left ventricular non-compaction with congestive heart failure, intramural thrombus and hypertension. There is no specific treatment for LVNC;therapeutic measures are directed towards the patient’s symptom (heart failure, arrhythmia and thrombotic events) and consideration of an implantable cardioverter defibrillator and cardiac transplantation.

七氟醚可逆性下调糖尿病模型大鼠心肌生物钟蛋白BMAL1的表达

目的观察七氟醚(SEV)对糖尿病大鼠心肌生物钟基因芳香烃受体核转运样蛋白1(BMALl1)表达的影响,并探讨其变化规律。方法雄性SD大鼠60只,体质量200~250 g,将正常大鼠分为吸氧组(NC)、吸七氟醚组(SEV);常规建立糖尿病模型,建立成功后分为吸氧组(DM)、吸七氟醚组(DM+SEV),吸入时间5 h(n=15)。4组试验动物分别在停止麻醉后0、12和24 h处死,分离心肌组织。用Western blot测定生物钟基因BMAL1与其活化酶泛素特异性肽酶9X(USP9X)的表达;HE染色观察心肌组织病理特征以及免疫荧光共定位观察USP9X与BMAL1之间的相互关系。结果停止麻醉后0、12 h,与DM组比较,DM+SEV组BMAL1、USP9X表达均明显下调(P<0.05);停止麻醉后24 h,与DM组比较,DM+SEV组BMAL1、USP9X表达水平的变化差异无统计学意义。HE染色光镜下显示:DM+SEV组在停止麻醉后0、12 h时心肌组织纤维结构排列发生改变,且在停止麻醉后0 h时这种改变最为显著,但在24 h时心肌组织结构排列整齐。免疫荧光共定位结果显示:USP9X与BMAL1蛋白主要分布于心肌细胞质中,两者存在重叠部分。且受七氟醚影响,在停止麻醉后0、12 h两者重叠部分较少,而在24 h时两者重叠部分较多,接近于DM组。结论七氟醚可逆性改变糖尿病大鼠心肌生物钟基因BMAL1表达,该作用在停止麻醉后12 h仍然存在,而在停止麻醉后24 h该作用明显减弱。

CMR评价急性心肌梗死PCI后远程心肌应变影响因素

目的 采用心脏磁共振特征追踪技术(CMRFT)评价急性心肌梗死(AMI)患者经皮冠状动脉介入治疗(PCI)后远程心肌(RM)的收缩功能,并探讨远程心肌收缩功能的影响因素。方法回顾性分析141例因AMI行急诊P CI治疗患者RM的C MR应变参数,比较RM应变受损组和RM应变保留组间临床及影像参数的差异。采用多因素Logistic回归分析确定RM收缩功能的影响因素。结果 141例患者共识别423个RM节段,其中54例、102个RM节段周向应变受损。两组间年龄(P=0.035)、高脂血症史(P=0.049)及罪犯血管(P<0.001)的差异有统计学意义。多因素Logisti c回归分析显示,年龄增高是RM周向应变受损的独立保护因素,高脂血症史是RM周向应变受损的独立危险因素。罪犯血管为回旋支及右冠状动脉患者发生RM周向应变受损的风险高于左前降支者,差异有统计学意义。结论AMI后RM收缩功能存在受损风险,高脂血症史、罪犯血管、年龄是RM收缩功能的影响因素。

Hypoxia induces PGC-la expression and mitochondrial biogenesis in the myocardium of TOF patients

PGC-1α, a potent transcriptional coactivator, is the major regulator of mitochondrial biogenesis and activity in the cardiac muscle. The dysregulation of PGC-la and its target genes has been reported to be associated with congenital and acquired heart diseases. By examining myocardium samples from patients with Tetralogy of Fallot, we show here that PGC-1α expression levels are markedly increased in patients compared with healthy controls and positively correlated with the severity of cyanosis. Furthermore, hypoxia significantly induced the expression of PGC-1α and mitochondrial biogenesis in cultured cardiac myocytes. Mechanistic studies suggest that hypoxia-induced PGC-1α expression is regulated through the AMPK signaling pathway. Together, our data indicate that hypoxia can stimulate the expression of PGC-1α and mitochondrial biogenesis in the cardiac myocytes, and this process might provide a potential adaptive mechanism for cardiac myocytes to increase ATP output and minimize hypoxic damage to the heart.

Efficient Gene Delivery to Myocardium with Ultrasound Targeted Microbubble Destruction and Polyethylenimine

The aim of present study was to evaluate the feasibility and efficiency of enhanced green fluorescent protein （EGFP） gene delivery to myocardium in vivo by ultrasound targeted microbubble destruction （UTMD） and polyethylenimine （PEI）. SonoVue/DNA and PEI/DNA/SonoVue complexes were prepared. Gel electrophoresis analysis was performed to determine the structural integrity of plasmid DNA or PEI/DNA after UTMD. Solutions of plasmid DNA, SonoVue/DNA, PEI/DNA complexes or PEI/DNA/SonoVue complexes were respectively transduced into BALB/c mice hearts by means of transthoracic ultrasound irradiation. Mice undergoing PBS injection, plasmid injection or PEI/DNA complexes injection without ultrasound irradiation served as controls. Gene expression in myocardium was detected 4 days after treatment. Cryosections and histological examinations were conducted. Electrophoresis gel assay showed no damage to DNA or PEI/DNA complexes after UTMD. When the heart was not exposed to ultrasound, the expression of EGFP was observed in the subendocardial myocardium obviously. The strongest expression was detected in the anterior wall of the left ventricle when the heart was exposed to ultrasound alone. Injection of PEI/DNA complexes and UTMD resulted in the highest transfection efficiency and the distributional difference of EGFP was not obvious. No tissue damage was seen histologically. In conclusion, a combination of UTMD and PEI was highly effective in transfecting mice hearts without causing any apparently adverse effect. It provides an alternative to current clinical gene therapy and opens a new concept of non-viral gene delivery for the treatment of cardiac disease.

Experimental study on the relationship of bile acids and myocardium damage in obstructive jaundice

AIM To investigate the morphologic changes of the myocardium and its relationship to serum bile acids in obstructive jaundice. METHODS Part Ⅰ: 35 rats were randomly assigned to three groups: Group Ⅰ (BDL1, n =11), the common bile duct (CBD) was ligated and severed and killed after one week. Group Ⅱ (BDL2, n =11), the CBD was ligated and severed and killed after two weeks. Group Ⅲ (SO, n =13), the CBD was simply isolated. The hearts were taken for morphologic studies and blood was taken to determine the total serum bile acids (TAB). Part Ⅱ: 13 rats received gastric intubation of 10% 4ml/kg of sodium cholate, and their serum TBA and the morphologic changes of the heart were examined. RESULTS One to two weeks after the CBD was ligated and severed, the mitochondrium of the myocardium was damaged and the serum TBA obviously increased. When the rats were administered sodium cholate to make their peak blood concentration close to the average blood concentration in BDL2, their myocardium was damaged in a similar degree. CONCLUSION The myocardium was damaged in obstructive jaundice and the endogenous bile acids was one of the factors.

Parthenolide attenuates LPS-induced activation of NF-κB in a time-dependent manner in rat myocardium

Parthenolide （PTN）, a selective nuclear factor kappa B （NF-κB） inhibitor, has been used extensively to inhibit NF-κB activation. The duration of the inhibitory effect of PTN on NF-kB in vivo remains unclear. This study was to determine whether a lipopolysaccharide （LPS） challenge 6, 12 and 24 h after the administration of PTN could activate NF-κB. Rats were devided into five groups. The rats in the PTN, PTN＋LPS and DMSO groups were injected intraperitoneally with PTN or DMSO. After 6, 12 or 24 h, LPS was administered in LPS and PTN＋LPS groups. The expressions of NF-κB p50, IκBα and p-IκBα were inhibited in both PTN and PTN＋LPS group at end of 6 and 12 h and no effects at 24 h. In summary, myocardial NF-κB expression occurs 1 h after the administration of LPS. PTN blocks this effect given at 6 h and no inhibitory effect 24 h after administration in vivo.

Protective effects of erythropoietin pretreatment on myocardium with hypoxia/reoxygenation injury in rats

Objective: To establish the rat model with myocardial hypoxia/reoxygenation (H/R) injury, and investigate the protective effect of EPO pretreatment on the myocardium. Methods: Sixty male adult Wistar rats were randomly divided into 3 groups: control group, H/R group, and EPO group, 20 in each group. The rats in EPO group accepted injection of 5 000 U/kg recombinant human erythropoietin (RHuEPO) through vein, and the other rats accepted the injection of the same volume of saline. Twenty-four hours after the injection, rats in the EPO and H/R groups were put into the hypoxia environment for 12 h and then returned to the normoxic environment for 2 h, and then the samples of blood and myocardium were collected. Serum myocardial enzyme activity, apoptosis, ultrastructure, myocardial MDA contents, EPO receptor (EPOR) expression in cardiac myocytes and cardiac functions were tested. Results: EPOR expression was positive in cardiac myocytes of adult rat according to the result of immunonistochemitry assaying. Compared to those in H/R group, rats in EPO group presented lighter injury of myocardial ultrastructure, the reduction of serum myocardial enzyme activity, inhibition of apoptosis, the better recovery of cardiac functions, and the less production of oxygen-derived free radicals. Conclusion: Adult rat cardiac myocytes could express EPOR, and EPO pretreatment produced protective effects on myocardium with H/R injury.

In vivo mechanical study of helical cardiac pacing electrode interacting with canine myocardium

Cardiac pacing is a medical device to help human to overcome arrhythmia and to recover the regular beats of heart. A helical configuration of electrode tip is a new type of cardiac pacing lead distal tip. The helical electrode attaches itself to the desired site of heart by screwing its helical tip into the myocardium. In vivo experiments on anesthetized dogs were carried out to measure the acute interactions between helical electrode and myocardium during screw-in and pull-out processes. These data would be helpful for electrode tip design and electrode/myocardium adherence safety evaluation. They also provide reliability data for clinical site choice of human heart to implant and to fix the pacing lead. A special design of the helical tip using strain gauges is instrumented for the measurement of the screw-in and pull-out forces. We obtained the data of screw-in torques and pull-out forces for five different types of helical electrodes at nine designed sites on ten canine hearts. The results indicate that the screw-in torques increased steplike while the torque-time curves presente saw-tooth fashion. The maximum torque has a range of 0.3-1.9 Nmm. Obvious differences are observed for different types of helical tips and for different test sites. Large pull-out forces are frequently obtained at epicardium of left ventricle and right ventricle lateral wall, and the forces obtained at right ventricle apex and outflow tract of right ventricle are normally small. The differences in pull-out forces are dictated by the geometrical configuration of helix and regional structures of heart muscle.

Clinical study of applying fructose-1,6-diphosphate and captopril to enhance the protective effects of cardioplegia solution on ischemic myocardium

In the present experiment,fructose-1,6-diphosphate（FDP）and captopril（Cap）wereadded to the cold potassium cardioplegia solution and the levels of malondialdehyde（MDA）,cre-atine phosphokinase MB（CPK-MB）,thromboxane B（TXB2）and 6-keto-PGF1α in plasma weremeasured during open-heart surgery.Quantitative study of myocardial ultrastructure and obser-vation of cardiac resuscitation were also undertaken.The findings suggested that FDP,especiallywhen combined with Cap could significantly strengthen the protective effects of cold potassiumcardioplegia solution on ischemic myocardium.

Chronic stress causes protein kinase C epsilon-aldehyde dehydrogenase 2 signaling pathway perturbation in the rat hippocampus and prefrontal cortex,but not in the myocardium

Chronic stress is strongly associated with the occurrence and development of depression and cardiovascular disease.Stress can induce altered mitochondrial function and activation of apoptosis in the cardio-cerebral system.However,it is unknown whether the protein kinase C ε（PKCε）-aldehyde dehydrogenase 2（ALDH2） pathway is altered under chronic stress,and this study sought to address this question.A rat model of depression was established using a chronic unpredictable mild stress（CUMS） protocol.After experiencing CUMS for 4 weeks,the sucrose preference test and the forced swim test verified depressive-like behaviors.Enzyme linked immunosorbent assays showed that ALDH2 activity was decreased in the rat hippocampus and prefrontal cortex,but was not altered in the myocardium.Western blot assays demonstrated reduced levels of ALDH2 and PKCε,but increased levels of 4-hydroxy-2-nonenal（4 HNE） adducts.Caspase-3 expression did not obviously alter,but active forms of caspase-3 were increased in the hippocampus and prefrontal cortex.In the myocardium,expression of ALDH2,PKCε and 4 HNE adducts did not remarkably alter;while caspase-3 expression was reduced and the active forms of caspase-3 were upregulated.Pearson＇s correlation test demonstrated that expression of 4 HNE adducts was positively correlated with levels of the active forms of caspase-3 in the hippocampus and prefrontal cortex,but not in the myocardium.In conclusion,chronic stress can damage the PKCε-ALDH2 signaling pathway in the hippocampus and prefrontal cortex,but not in the myocardium.Moreover,4 HNE is associated with active forms of caspase-3 in the hippocampus and prefrontal cortex.

Effects of PPAR-y in the Myocardium on the Development of Ventricular Septation

Ventricular septum defects(VSDs)are common types of congenital heart diseases caused by developmental defect;they contribute to 25%-30%of all adult congenital heart diseases.The peroxisome proliferator-activated receptor gamma(PPAR-y)is widely expressed in mammalian tissues and in the immune system,regulating cell differentiation and immune and inflammatory responses.The PPAR-y gene has recently been found crucial for heart development,but the mechanism of action is not clear.This study aims to investigate the effects of the PPAR-y gene in the myocardium on the development of ventricular septation.In this study,we applied Cre-loxP recombination enzyme(CRE)technology to downregulate the expression of the PPAR-y gene in different cardiac tissues,RT-PCR to examine the expression of the c-fos and TGF-B!genes,and histology staining to check the defect of embryonic heart at embryonic day 14.5(E14.5).We found that the downregulation of the PPAR-p gene resulted in a ventricular membranous septation defect of the embryonic heart at E14.5.Furthermore,only conversion of a Tnt:Cre,but not Mef2c:Cre,Tie2:Cre,or Wnt:Cre PPAR-T floxed allele to a null allele resulted in VSD.PPAR-/mi-Orv+embryos showed increascs in atrioventricular(AV)-cushion cells and the expression of c-fos gene but no change in the expression of TGF-B1 at E10.5.Our study demonstrates PPAR-N in the myocardium is required for ventricular septation through regulation of AV-cushion cell proliferation by a Tntc-fos signal.

Changes of Expression of Stretch-activated Potassium Channel TREK-1 mRNA and Protein in Hypertrophic Myocardium

The expression of stretch activated potassium channel TREK-1 mRNA and protein of hypertrophic myocardium was measured. Using a model of hypertrophy induced by coarctation of abdominal aorta in male Wistar rats, the expression of TREK-1 mRNA and protein was detected by using semi quantitative RT-PCR and Western blot respectively. At 4th and 8th week after constriction of the abdominal aorta , rats developed significant left ventricular hypertrophy. As compared to sham-operated group, stretch-activated potassium channel TREK-1 mRNA was strongly expressed and protein was up regulated in operation groups （P〈0.05）. It was concluded that the expression of TREK-1 was up-regulated in hypertrophic myocardium induced by chronic pressure overload in Wistar rats.

A VIEWPOINT TO MEASURE OF NON-COMPACTNESS OF OPERATORS IN BANACH SPACES

This article is committed to deal with measure of non-compactness of operators in Banach spaces.Firstly,the collection C(X)(consisting of all nonempty closed bounded convex sets of a Banach space X endowed with the uaual set addition and scaler multiplication)is a normed semigroup,and the mapping J from C(X)onto F(Ω)is a fully order-preserving positively linear surjective isometry,whereΩis the closed unit ball of X^*and F(Ω)the collection of all continuous and w^*-lower semicontinuous sublinear functions on X^*but restricted toΩ.Furthermore,both EC=JC-JC and EK=JK-JK are Banach lattices and EK is a lattice ideal of EC.The quotient space EC/EK is an abstract M space,hence,order isometric to a sublattice of C(K)for some compact Haudorspace K,and(FQJ)C which is a closed cone is contained in the positive cone of C(K),where Q:EC→EC/EK is the quotient mapping and F:EC/EK→C(K)is a corresponding order isometry.Finally,the representation of the measure of non-compactness of operators is given:Let BX be the closed unit ball of a Banach space X,thenμ(T)=μ(T(BX))=||(F QJ)T(BX)||C(K),∀T∈B(X).

IMPLANTATION OF AUTOLOGOUS BONE MARROW MONONUCLEAR CELLS INTO ISCHEMIC MYOCARDIUM ENHANCES CORONARY CAPILLARIES AND SYSTOLIC FUNCTION IN MINISWINE

Objective To investigate the therapeutic effectiveness of intracoronary implantation of autologous bone marrow mononuclear cells (BM-MNC) in miniswine model of reperfused myocardial infarction. Methods Sixteen miniswine myocardial ischemic reperfusion injury models made by ligation of the distal one third segment of left anterior descending artery for 90 minutes were randomized into 2 groups. In BM-MNC group (n = 9), (3.54±0.90)×108 BM-MNC were intracoronary injected, and in the control group (n = 7), phosphate buffered saline was injected by the same way. Echocardiographic and hemodynamic results, vessel density, and myocardial infarction size were evaluated and compared before and 4 weeks after cell transplantation. Results In BM-MNC group, there were no differences between before and 4 weeks after transplantation in aspects of left ventricular ejection fraction (LVEF), interventricular septal thickness, left ventricular lateral and anterior septal wall thickness, cardiac output, or +dp/dtmax. In control group, LVEF, interventricular septal thickness, left ventricular lateral and anterior septal wall thickness, cardiac output, and +dp/dtmax decreased significantly 4 weeks after transplantation (P < 0.05). Left ventricular end-diastolic pressure and –dp/dtmax did not change significantly before and after cell transplantation in both groups. Capillary density in BM-MNC group was greater than that in control group [(13.39 ± 6.96)/high power field vs. (3.50 ± 1.90)/high power field, P < 0.05]. Infarction area assessed by tetrazolium red staining and the infarction percentage decreased in BM-MNC group compared with those in control group (P < 0.05). Conclusions Transplantation of BM-MNC into myocardium with ischemic reperfusion injury increases capillary density and decreases infarction area. It has significantly beneficial effect on cardiac systolic function rather than on diastolic function.

Effect of protective myocardium by allitridum from decreasing apoptosis in rats with ischemia/reperfusion injury

Objective: Previous studies have shown t hat allitridum can protect myocardium from ischemia/reperfusion (I/R) injury, bu t whether allitridum had the effect of anti-apoptosis is unclear. The aim of th is study was to investigate whether allitridum had the effects of pharmacologica l preconditioning and decreasing myocardium apoptosis after ischemic insult. Methods: Pentobarbital sodium-anesthetized Sprague-Dawley (SD) rats underwent 30 min of left anterior descending (LAD) coronary occlusion foll owed by 120 min of reperfusion. Thirty-six rats were divided into three groups randomly: Control group, I/R group and allitridum (G) group. The control and I/R groups with saline, G group with allitridum were administrated 24 h before oper ation. Control group underwent only sham operation; the other two groups underwe nt I/R operation. Infarcted size (IS/AAR %) was measured in I/R and G groups. Ma londialdehyde (MDA), Creatine kinase isoenzyme-MB (CK-MB ), Superoxide dismuta se (SOD)and the apoptosis index (AI) by TUNEL staining were measured in each gro up. In addition, DNA fragmentation by agarose gel electrophoresis was conducted on DNA isolated from these groups. Results: Allitridum p retreatm ent decreased the infarcted size compared with I/R group in IS/ AAR%[(21.85±1. 49)% vs. ( 44.65±4.65)%, P<0.01], CK-MB [(986.40±94.01) vs. (2044.2 5±1 07.28) U/L, P<0.01] and MDA [(3.26±0.35) vs. (4.96±0.46) nmol/mg pro, P<0.01], and SOD level in G group was higher than that of I/R group [(140 .20±12.89)vs. (73.16±11.22) U/mg pro, P<0.01]. AI of I/R group was highe r than that of G group [(13.99±3.05)% vs. (6.97±1.23)%, P<0.01], which was consistent with that in DNA fragmentation by agarose gel electrophoresis. Conclusion: This study indicated that allitridum had the effect of protecting myocardium against I/R injury and decreasing infarcted zone. The e ffect was probably through decreasing myocardium apoptosis in I/R injury.