Angiogenic strategy for human ischemic heart disease: Brief overview

In the Western World ischemic coronary disease is the leading cause of morbidity and mortality. Therapeutic approaches mostly aim to restore flow to a localized segment by angioplasty or bypass surgery. Therapeutic angiogenesis and or arteriogenesis describes a strategy where blood vessel formation is induced for the purposes of treating and/or preventing ischemic disease. At present, at least 17 clinical trials of myocardial angiogenesis have been presented involving over 900 patients. Therapeutic angiogenesis makes use of the administration of angiogenic growth factor protein or gene to promote the development of endogenous collateral vessels in ischemic myocardium. Most recently, interest has grown in the potential angiogenesis effects of cell therapy—such as autologous bone marrow cells or cultured stem cells—and there are now several groups initiating phase I/II trials in this area. (Mol Cell Biochem 264: 143–149, 2004)     

SR-BI in Bone Marrow Derived Cells Protects Mice from Diet Induced Coronary Artery Atherosclerosis and Myocardial Infarction

SR-BI deficient mice that are also hypomorphic for apolipoprotein E expression develop diet induced occlusive coronary artery atherosclerosis, myocardial infarction and early death. To test the role of SR-BI in bone marrow derived cells, we used bone marrow transplantation to generate SR-BI-null; apoE-hypomorphic mice in which SR-BI expression was restored solely in bone marrow derived cells. SR-BI-null; apoE-hypomorphic mice were transplanted with SR-BI^+/+apoE-hypomorphic, or control, autologous SR-BI-null; apoE-hypomorphic bone marrow. Four weeks later, mice were fed a high-fat, high-cholesterol, cholate-containing diet to induce coronary artery atherosclerosis. Mice transplanted with autologous bone marrow developed extensive aortic atherosclerosis and severe occlusive coronary artery atherosclerosis after 4 weeks of feeding. This was accompanied by myocardial fibrosis and increased heart weights. In contrast, restoration of SR-BI expression in bone marrow derived-cells reduced diet induced aortic and coronary artery atherosclerosis, myocardial fibrosis and the increase in heart weights in SR-BI-null; apoE-hypomorphic mice. Restoration of SR-BI in bone marrow derived cells did not, however, affect steady state lipoprotein cholesterol levels, but did reduce plasma levels of IL-6. Monocytes from SR-BI-null mice exhibited a greater capacity to bind to VCAM-1 and ICAM-1 than those from SR-BI^+/+ mice. Furthermore, restoration of SR-BI expression in bone marrow derived cells attenuated monocyte recruitment into atherosclerotic plaques in mice fed high fat, high cholesterol cholate containing diet. These data demonstrate directly that SR-BI in bone marrow-derived cells protects against both aortic and CA atherosclerosis.     

二维斑点追踪技术评价犬心梗后自体骨髓CD34＋干细胞移植对心肌功能的影响

目的应用二维斑点追踪成像超声心动图（2D-STE）,评价犬心梗后自体骨髓CD34＋干细胞移植对心肌功能的影响。方法 12只杂种犬行冠脉左前降支结扎术,导致前壁心肌梗死,随机分为两组,A组为对照组,结扎术后两周二次开胸手术,经心肌注射磷酸盐缓冲液（PBS）1 mL;B组为治疗组,结扎术后两周二次开胸手术,经心肌注射含自体骨髓CD34＋干细胞的磷酸盐缓冲液1 mL。应用STE对12只犬结扎术前、术后左室短轴基底段及心尖段心室节段径向应变（RS）、圆周方向应变（CS）以及局部心肌旋转（Rot）进行分析,并对对照组和治疗组治疗后的RS、CS及Rot变化进行比较。结果心肌梗死后梗死节段的RS、CS以及Rot均下降,治疗后治疗组梗死段RS及Rot较对照组好转。结论 STE能够评价左室短轴局部心肌的收缩功能,心肌梗死后梗死段短轴各方向应变减低,自体骨髓CD34＋干细胞移植能够提高局部心肌的收缩功能。     

Influence of iloprost on eicosanoid generation and lipid levels in experimental myocardial ischemia in dogs

Anaesthetized mongrel dogs were subjected to occlusion of a coronary artery. The resulting myocardial infarction was observed for three hours. One hour after occlusion, infusion of the stable prostacyclin analogue iloprost or saline was started. In the control group myocardial infarction was associated with an increase of the ratio TXB2/6-keto-PGF1a which was abolished by iloprost treatment. After occlusion in the control group, the atherosclerosis index (TC-HDLC): HDLC was increased, but in the iloprost-treated group it was significantly decreased. The results of this study suggest that the administration of iloprost is able to prevent changes in eicosanoid metabolism and lipoprotein pattern after coronary artery occlusion in dogs.     

刺槐素对大鼠心肌缺血再灌注损伤的保护作用与机制研究

摘要 目的：探讨刺槐素对大鼠心肌缺血再灌注损伤(MIRI)的作用以及可能的作用机制。方法：对24只Sprague-Dawley (SD)大鼠进行随机分组,分为：假手术组、模型组、刺槐素给药组、刺槐素+AG490给药组,每组6只,通过结扎冠状动脉左前降支,缺血30 min,再灌注120 min复制心肌缺血再灌注损伤模型。利用氯化三苯基四氮唑测定心肌梗死面积,紫外分光光度计和酶联免疫法检测血清中肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）的活性,蛋白印迹法分别检测心肌组织中Bcl-2、Bax、Stat3和p-Stat3蛋白相对表达水平。结果：与假手术组比较,模型组大鼠血清中CK-MB、LDH活性明显升高（P＜0.01）,心肌梗死面积百分比显著增加（P＜0.01）,p-Stat3/Stat3比率、Bcl-2/Bax比率显著下降（P＜0.01）;与模型组相比,刺槐素给药组中CK-MB、LDH的活性,以及心肌梗死面积百分比显著降低（P＜0.01）,Bcl-2/Bax比率和p-Stat3/Stat3比率显著提高（P＜0.05）。然而在刺槐素+AG490药物组中刺槐素对于受损心肌的保护作用被AG490消除。结论：刺槐素可减轻MIRI大鼠心肌损伤,发挥心肌保护作用,其机制可能与活化Jak2/Stat3信号通路进而抑制心肌细胞凋亡有关。     

Simulation of coronary circulation with special regard to the venous bed and coronary sinus occlusion

The vascular beds of the left circumflex and the left anterior descending coronary arteries are modelled by means of coupled differential equations that consider an arterial, a capillary and a venous section. In a stepwise procedure, experimental data from normal coronary perfusion and coronary sinus occlusion are used to assess the model parameters. For venous distensibility, a non-linear form of pressure-volume relationship proved vital to reproduce the characteristics of the rise in venous pressure after the onset of coronary sinus occlusion. Numerical integration was carried out for normal perfusion and for coronary sinus occlusion, yielding time courses of flows, volumes and pressures within large coronary arteries, capillaries and coronary veins. Coronary sinus occlusion reduces total mean flow by 18% and divides intramyocardial flow between the capillaries and the veins into a forward component of 3.03 mls⁻¹ and a backward component of − 1.54 mls⁻¹. This result represents a prediction for a haemodynamic quantity which is therapeutically important but inacessible to measurement. Varying degrees of systolic myocardial squeezing are studied to display the impact of myocardial contractility and vessel collapse on the mean values and phasic components of intra-myocardial flows.     

ST段抬高性和非ST 段抬高性急性心肌梗死患者的冠状动脉病变特点比较

目的:比较ST段抬高性和非ST段抬高性急性心肌梗死患者的冠状动脉病变特点。方法:选取100例在我院接受24h动态心电图和冠状动脉造影检查的急性心肌梗死患者,根据心电图结果分为观察组和对照组各50例。对照组为ST段抬高性心肌梗死(STEMI)患者,观察组为非ST段抬高性心肌梗死(NSTEMI)患者,比较两组患者冠状动脉病变的差异。结果:对照组LAD(左前降支)闭塞血管比例(52.00%)显著高于观察组(18.00%),差异具有统计学意义(P0.05)。对照组LCX(回旋支)闭塞血管比例(8.00%)显著低于观察组(50.00%),差异具有统计学意义(P0.05)。对照组RCA(右冠脉主干)闭塞血管比例(40.00%)和观察组(30.00%)比较,差异无统计学意义(P0.05)。对照组单支病变比例(46.00%)明显高于观察组(12.00%),对照组三支病变比例(20.00%)明显低于观察组(48.00%)比较,差异均具有统计学意义(P0.05)。对照组二支及正常血管比例与观察组比较,差异均无统计学意义(P0.05)。对照组罪犯血管狭窄程度在76%-90%、91%-99%及完全闭塞的比例与观察组比较差异均具有统计学意义(P0.05)。罪犯血管狭窄程度在50%及50%-75%时,两组差异无统计学意义(P0.05)。两组并发症发生情况比较,差异无统计学意义(P0.05)。结论:1NSTEMI罪犯血管闭塞以LCX多见,STEMI罪犯血管闭塞以LAD多见;2NSTEMI以三支血管病变较多见,STEMI以单支病变较多见。     

不同年龄鼠骨髓干细胞移植治疗心梗后心衰的实验研究

目的：通过对比观察不同年龄鼠骨髓干细胞在体外的生长状态和移入受损心肌后对心肌梗死大鼠心功能的影响,说明年龄对骨髓干细胞的增殖能力和对移植效果的影响。方法：分别分离培养3日龄,1月龄,6月龄,12月龄Wister雄鼠骨髓干细胞,观察细胞生长状态,描记生长曲线。将60只大鼠用结扎冠状动脉前降支的方法制成心肌梗死模型后两周,随机分为三组：Ⅰ组：3日龄组（n=20只）：给予3日龄的5-溴脱氧尿嘧啶（Brdu）标记的鼠骨髓干细胞;Ⅱ组：6月龄组（n=20只）：给予6月龄的Brdu标记的鼠骨髓干细胞;Ⅲ组：对照组（n=20只）：给予培养液。各组均于治疗前及治疗后4周进行心脏超声检查评价心功能改善情况。处死动物取出心脏,进行直接测量后取左心室作石蜡切片,行苏木素-伊红（HE）染色及免疫组化检测,鉴定植入的细胞和心肌、毛细血管再生情况。结果：不同年龄鼠骨髓干细胞培养结果示3日龄及1月龄组增殖能力均高于6月龄及12月龄组,但3日龄与1月龄组之间无统计学差异,12月龄组在原代培养后期即死亡。治疗前超声心动图显示Ⅰ、Ⅱ、Ⅲ组心功能无显著差异（P〉0.05）,治疗之后四周超声心动图检查结果示：Ⅰ、Ⅱ组LVEF、FS、IVST、LVPW和LVESD较治疗前均有明显提高,且显著高于Ⅲ组;Ⅰ组LVEF、FS、IVST、LVPWs和LVESD又明显高于Ⅱ组;Ⅰ、Ⅱ、Ⅲ组LVEDD与治疗前比较无统计学意义。心脏直测结果显示Ⅰ、Ⅱ组的Wh、Wh、Wb、L、I度均较第Ⅲ组有所增加,其中Ⅰ组又明显高于Ⅱ组。免疫组化结果显示：Ⅰ、Ⅱ组于梗死周边均发现Brdu（＋）细胞存在,心肌特异性抗体阳性,且Ⅰ组阳性率明显高于Ⅱ组。毛细血管密度检测结果显示Ⅰ组毛细血管增生情况明显优于Ⅱ组。结论：不同年龄鼠骨髓干细胞的体外增殖能力不同,年龄越小,增殖能力越强。骨髓干细胞移植可以改善心肌梗死后大鼠的心脏功能,增加梗死区毛细血管密度,抑制心室重构,且年龄与移植效果成反比。     

Atresia of the right atrial ostium of the coronary sinus

A case of asymptomatic congenital occlusion of the ostium of the coronary sinus is described. The myocardial venous drainage was maintained via a persistent left superior vena cava as well via ectatic, widened atrial veins of the dorsal wall of the left atrium. The study shows that complete ostial occlusion of the coronary sinus does not reduce cardiac venous drainage. The view of the literature allows a comparison with the comprehensive classification of coronary sinus anomalies.     

Autologous vascular smooth muscle cell-based myocardial gene therapy to induce coronary collateral growth

For therapeutic angiogenesis to achieve clinical relevance, it must be effective, with minimal side effects to other end organ systems. We developed a cardiac-specific gene delivery mechanism by transfecting autologous vascular smooth muscle cells (VSMC) with VEGF and administering these cells via intracoronary injection. We evaluated the efficacy of this protocol by its ability to stimulate angiogenesis in the presence of a subthreshold stimulus for collateralization. A modified canine repetitive coronary occlusion model was utilized in these experiments with left anterior descending coronary artery occlusions for 2 min every 2 h four times per day for 21 days. An intramyocardial catheter in the perfusion territory of the left anterior descending coronary artery measured proteins in the myocardial interstitial fluid. VSMC from jugular vein explants were isolated, amplified in culture for 3 wk, and transfected with a plasmid expressing VEGF-165 and/or enhanced green fluorescent protein. Cells were injected before commencement of occlusions. VEGF levels in myocardial interstitial fluid were significantly higher in VEGF-transfected animals than in sham (repetitive occlusions without cell transplantation) and control (repetitive occlusions with enhanced green fluorescent protein-transfected cells) animals at the onset of occlusions (P < 0.05). In the VEGF group, collateral flow was increased at day 7 and remained higher than in sham and control groups thereafter. We found that intracoronary administration of VEGF-transfected autologous VSMC effectively promotes collateral development. This approach may provide a way to confine delivery of a gene to a specified organ, thus minimizing complications related to gene transfection in nontargeted organ systems.     

Autologous stem cell transplantation for myocardial repair

Current therapies for heart failure due to transmural left ventricular (LV) infarction are limited. We have developed a novel patch method for delivering autologous bone marrow stem cells to sites of myocardial infarction for the purpose of improving LV function and preventing LV aneurysm formation. The patch consisted of a fibrin matrix seeded with autologous porcine mesenchymal stem cells labeled with lacZ. We applied this patch to a swine model of postinfarction LV remodeling. Myocardial infarction was produced by using a 60-min occlusion of the left anterior descending coronary artery distal to the first diagonal branch followed by reperfusion. Results were compared between eight pigs with stem cell patch transplantation, six pigs with the patch but no stem cells (P), and six pigs with left anterior descending coronary artery ligation alone (L). Magnetic resonance imaging data collected 19 +/- 1 days after the myocardial infarction indicated a significant increase of LV systolic wall thickening fraction in the infarct zone of transplanted hearts compared with P or L hearts. Blue X-gal staining was observed in the infarcted area of transplanted hearts. PCR amplification of specimens from the X-gal-positive area revealed the Ad5 RSV-lacZ vector fragment DNA sequence. Light microscopy demonstrated that transplanted cells had differentiated into cells with myocyte-like characteristics and a robust increase of neovascularization as evidenced by von Willebrand factor-positive angioblasts and capillaries in transplanted hearts. Thus this patch-based autologous stem cell procedure may serve as a therapeutic modality for myocardial repair.     

The Protective Effect of Mitochondrial ATP-Sensitive K<Superscript>+</Superscript> Channel Opener,Nicorandil, Combined With Na<Superscript>+</Superscript>/Ca<Superscript>2+</Superscript> Exchange Blocker KB-R7943 on Myocardial Ischemia–Reperfusion Injury in Rat

To study the protective effect of mitochondrial ATP-sensitive K⁺ channel (mitoK_ATP channel) opener, nicorandil, combined with Na⁺/Ca²⁺ exchange blocker KB-R7943 on myocardial ischemia–reperfusion injury in isolated rat hearts; the isolated rat heart was perfused by modified Langendorff device, after 15-min balanced perfusion, 45-min ischemia (about left and right coronary perfusion flow reduced to 5% of the original irrigation flow), and 2-h reperfusion were performed. Forty Wistar rats were randomly divided into four groups: control group, nicorandil group, KB-R7943 group, and the combination of nicorandil and KB-R7943 group. After 45-min ischemia and then 2-h reperfusion, the myocardial infarct size was 34.31% in control group, 26.35% in nicorandil group, 28.74% in KB-R7943 group, and 19.23% in combination of nicorandil and KB-R7943 group. SOD activity in coronary perfusion fluid was the highest in the combination of nicorandil and KB-R7943 group, and MDA content was the lowest. In the combination drug group compared with the control group, myocardial ultrastructural injury was significantly reduced. The combination of nicorandil and KB-R7943 significantly reduced myocardial infarct size, significantly reduced myocardial ultrastructural damage, could increase coronary perfusion fluid SOD activity, and reduced MDA levels.     

Study of the impact of intramyocardial implantation of stem cells on myocardial perfusion and contractility in patients with coronary heart disease concurrent with postinfarct cardiosclerosis and chronic heart failure

OBJECTIVE: to study of intramyocardial implantation of cultured bone marrow stem cells on myocardial perfusion and contractility in the surgical treatment of patients with coronary heart disease (CHD) and chronic heart failure (CHF), by synchronized single-photon emission computed tomography (SSPECT) of the myocardium. SUBJECTS AND METHODS: The study included 11 patients. Intramyocardial injection of cell injections into the myocardial periscarring areas was made at coronary bypass surgery. All the patients underwent 99mTc myocardial SSPECT MIBI before and 3, 6, 12 months after surgery. RESULTS AND CONCLUSIONS: Implantation of bone marrow stem cells into the left ventricular myocardium favorably affects left ventricular remodeling and contributes to the improvement of myocardial perfusion and contractility, as evidenced by 99mTc.     

Relationship between HIF-1α and apoptosis in rats with traumatic brain injury and the influence of traditional Chinese medicine Sanqi

Objective To explore the expression of HIF-1α, neuronal apoptosis and the influence of traditional Chinese medicine Sanqi on hematoma after brain injury in rats. Methods Ninety SD rats were divided into 3 groups randomly: blank control group, traumatic brain injury (TBI) group and Sanqi intervention group, and they were decapitated after brain injury at different time points: 6 h, 1 d, 2 d, 3 d, 5 d, 7 d. The model of cerebral hemorrhage was made by autologous non-coagulation in stereotactic locator, the expression of HIF-1α and TUNEL-positive cells (apoptotic cells) in the perihematomal area was detected by immunohistochemistry. Results In blank control group, a small amount of HIF-1α was expressed and apoptotic cells were observed. The expression of HIF-1α was up-regulated in the brain injury group from 6 h, and the apoptotic cells increased in abundance. The peak of HIF-1α was reached at 3 d, then decreased, and remained at the high level on the 7 d. Compared with blank control group, the TBI group was statistically significant (P < 0.05). The Chinese medicine Sanqi intervention group significantly up-regulated HIF-1α’expression and decreased neuronal apoptosis, which was statistically significant (P < 0.05). Conclusion HIF-1α’s expression was up-regulated around the hematoma after brain injury, and the apoptosis of nerve cells was obviously increased. The traditional Chinese medicine Sanqi can significantly increase the expression of HIF-1α, reduce the apoptosis around the hematoma, and thus play a neuroprotective role.     

Intra-arterial transplantation of bone marrow mononuclear cells immediately after reperfusion decreases brain injury after focal ischemia in rats

AIMS: Transplantation of bone marrow cells has been reported to exert neuroprotection against cerebral ischemia. However, the effect of bone marrow mononuclear cells (BMMCs) administered immediately after reperfusion has rarely been investigated. The present study was designed to examine whether brain injury in response to transient focal ischemia can be ameliorated by BMMC administration immediately after reperfusion in rats, and to determine whether there are differences in the route of administration. MAIN METHODS: Autologous BMMCs were obtained from each rat. Rats were then subjected to transient focal ischemia followed by BMMC administration via the ipsilateral carotid artery (IA group) or the femoral vein (IV group) immediately after reperfusion. Control rats underwent the same procedure but received vehicle injection. Infarct volume was compared among the groups 24 h and 7 days after reperfusion. BMMCs were fluorescently labeled with PKH26 prior to administration to track transplanted cells. KEY FINDINGS: Total infarct volume decreased in the IA group, but not in the IV group, when compared to the vehicle group. In the ipsilateral hemisphere, PKH26 positive cell count was greater in the IA group than in the IV group. Motor function, assessed with a rotarod test, improved in the IA group compared to the vehicle group. SIGNIFICANCE: These results show significant neuroprotection after transient focal ischemia by 1x10(7) autologous BMMCs administered intra-arterially, but not intravenously, immediately after reperfusion in rats. The larger number of transplanted BMMCs in the brain during the early stage of reperfusion may be responsible for the protective effect.     

Effect of the beta-adrenoblockader atenolol on the extent of myocardial necrosis in transient and permanent coronary occlusion

It has been demonstrated in experiments on rats that atenolol in a dose of 10 mg/kg exerts an antiischemic action in transitory coronary occlusion lasting 30 minutes followed by reperfusion for 23h and 30 min. The effect manifested in the diminution of the relative area and mass of myocardial necrosis zone and in the dilatation of the left ventricle. Atenolol also produced an antiischemic action in permanent coronary occlusion for 24 h. However, the effect in the latter case was less marked than in transitory occlusion. When injected for permanent occlusion, atenolol (10 mg/kg i. v.) led to a 1.59-fold decrease in the necrosis area and a 2.1-fold decrease (p less than 0.001) when administered for transitory occlusion. The mass of the myocardial necrosis zone also dropped (by 1.65-fold and 2.3-fold, respectively), whereas the degree of dilatation by 2.1- and 2.3-fold, respectively.     

Intrathecal cell therapy with autologous stromal cells increases cerebral glucose metabolism and can offer a new approach to the treatment of Alzheimer's type dementia

Background aimsAfter recent observations that intrathecal administration of autologous bone marrow mesenchymal stromal cells (MSCs) increases cerebral metabolism in patients with severe traumatic brain injury (TBI), we examined this type of cell therapy in Alzheimer's type dementia.MethodsThree patients with clinical diagnosis of Alzheimer's disease received every 3 months 100million autologous MSCs by intrathecal route, until a total dose of 300million.ResultsDuring cell therapy the patients showed arrest in neurological deterioration and two of them manifested clear improvement of previous symptoms. A global increase in cerebral glucose metabolism, measured using 18F-fluorodeoxyglucose positron emission tomography (18F-FDG-PET), was observed after every administration of cell therapy.ConclusionsOur present findings suggest that intrathecal administrations of autologous MSCs can be a new strategy for the treatment of Alzheimer's dementia.     

Phagocyte activation in coronary artery disease

Abstract Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Granulocytes can release a variety of molecules mediating tissue injury which act synergistically with other molecules and cells. The aim of our investigation was to evaluate the granulocyte function in patients affected by coronary artery disease (CAD) and during coronary angioplasty (PTCA). We studied 20 patients suffering from CAD. The PMN's aggregating activity was greater in the coronary sinus than in the aorta ( P <0.01). The increase in aggregating activity was evident in patients who were smokers: their cells release significantly lower quantities of leukotriene C₄ ( P <0.025). In the 20 patients who underwent coronary angioplasty we analyzed superoxide release after stimulation with phorbolmyristate-acetate (PMA). The results showed a greater decrease of PMN's superoxide production in the coronary sinus than in the aorta ( P <0.05). In all patients affected by CAD we evaluated the PMN's expression of CD11b/CD18 membrane integrins. In these patients the increase in expression of CD11b/CD18 was statistically significant in comparison with the controls ( P <0.01). This increase in expression correlates with a higher aggregation (r=0.87, P <0.001). The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in the pathophysiology of myocardial injury due to regional ischemia and reperfusion is an area of intense investigation. This paper presents studies carried out in vivo which have been instrumental in demonstrating the role of granulocytes as mediators of myocardial ischemia.     

Cardioprotection from ischemia and reperfusion injury by Withania somnifera: a hemodynamic, biochemical and histopathological assessment

The efficacy of Withania somnifera (Ws) to limit myocardial injury after ischemia and reperfusion was explored and compared to that of Vit E, a reference standard known to reduce mortality and infarct size due to myocardial infarction. Wistar rats (150-200 g) were divided into six groups and received orally saline (sham, control group), Ws-50/kg (Ws control and treated group) and Vit E-100 mg/kg (Vit E control and treated group) respectively for 1 month. On the 31st day, rats of the control, Vit E and Ws treated groups were anesthetized and subjected to 45 min occlusion of the LAD coronary artery followed by 60 min reperfusion. Hemodynamic parameters: systolic, diastolic and mean arterial pressure (SAP, DAP, MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), left ventricular peak (+)LVdP/dt and (-)LVdP/dt were monitored. Hearts were removed and processed for histopathological and biochemical studies: Myocardial enzyme viz, creatin phosphokinase (CPK), and antioxidant parameters: malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx) were estimated. Postischemic reperfusion produced significant cardiac necrosis, depression of left ventricular functions (MAP, LVEDP, (+) and (-)LVdP/dt) and a significant fall in GSH (p < 0.01), SOD, CAT (p < 0.05), LDH and CPK (p < 0.01) as well as an increase in MDA level (p < 0.05) in the control group rats as compared to sham group. The changes in levels of protein and GPx was however, not significant. Ws and Vit E favorably modulated most of the hemodynamic, biochemical and histopathological parameters though no significant restoration in GSH, MAP (with Vit E) were observed. Ws on chronic administration markedly augmented antioxidants (GSH, GSHPx, SOD, CAT) while Vit E did not stimulate the synthesis of endogenous antioxidants compared to sham. Results indicate that Ws significantly reduced myocardial injury and emphasize the beneficial action of Ws as a cardioprotective agent.