Effect of ginsenoside Rh1 on myocardial injury and heart function in isoproterenol-induced cardiotoxicity in rats

The present study was designed to investigate the effect of ginsenoside Rh1 on myocardial injury and heart function in isoproterenol-induced cardiotoxicity in rats. Sprague–Dawley rats were subcutaneously injected with isoproterenol (20?mg/kg). Cardiac marker enzymes in serum, antioxidative parameters and inflammatory cytokines in left ventricles were measured. Hemodynamic parameters were monitored and recorded as well. Histopathological examination of left ventricles was performed. It was found that creatine kinase-MB (CK-MB) activity and troponin T level in isoproterenol-treated rats were significantly increased. Isoproterenol caused declines of left ventricular systolic pressure, positive and negative maximal values of the first derivative of left ventricular pressure, and an elevation of left ventricular end diastolic pressure. Isoproterenol enhanced the content of malondialdehyde (MDA), tumor necrosis-α (TNF-α), interleukin-1β (IL-1β) and decreased the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-Px) in left ventricles. Ginsenoside Rh1 significantly ameliorated myocardial injury and heart function impairment induced by isoproterenol. The cardioprotective effect of ginsenoside Rh1 was further confirmed by histopathological examination. Ginsenoside Rh1 also partially inhibited the increase of MDA, TNF-α, IL-1β contents and the decrease of SOD, catalase, and GSH-Px activities in left ventricles. The results indicated that ginsenoside Rh1 possessed the effect against isoproterenol-induced cardiotoxicity, and that the mechanism of pharmacological action was related to regulating the activities of SOD, catalase, and GSH-Px and decreasing the contents of TNF-α and IL-1β.     

金属硫蛋白对异丙肾上腺素心肌损伤的保护作用

在大鼠ｓｃ异丙肾上腺素（Ｉｓｏ）４０ｍｇ·ｋｓ－１·ｄ－１造成的心肌损伤模型上，观察外源性金属硫蛋白（ＭＴ）和锌诱导内源性ＭＴ对心脏的保护作用．结果发现：外源性和内源性ＭＴ均可减少Ｉｓｏ引起的心肌丙二醛和心肌组织钙的聚集，同时发现内源性ＭＴ可减少血浆组织蛋白酶Ｄ的活性。提示：ＭＴ保护Ｉｓｏ心肌损伤的机制可能与其清除自由基、抗脂质过氧化、减少细胞内钙超载、稳定溶酶体膜等作用有关。     

Effects of diesel exhaust particles on left ventricular function in isoproterenol-induced myocardial injury and healthy rats

The associations between ambient particulate matter with an aerodiameter less than 2.5 mu m (PM(2.5)) and congestive heart failure (CHF) have been reported. However, the underlying mechanisms remain unclear. We investigated the effect of diesel exhaust particles (DEPs) on left ventricular function in isoproterenol (ISO)-induced myocardial injury and healthy rats. Male Sprague-Dawley (SD) rats were injected with ISO or normal saline. Seven days later, both groups were further assigned to receive either DEPs or normal saline by intratracheal instillation (IT). Echocardiography was used to measure fractional shortening (FS) and left ventricular end-diastolic diameter (LVDd) 24 h before and after IT in each rat. Fractional shortening (FS) was significantly decreased in SD rats treated with ISO as compared to those treated with normal saline (p < .05, t-test). When FS and LVDd before and after treatment were compared in each rat, there was no difference for normal saline treatment in healthy or ISO groups. However, there was significantly lower FS before and after DEPs exposure in both groups (p < .05, paired t-test). When using SD rats treated with normal saline as a reference group, both SD rats treated with DEPs and ISO rats treated with normal saline had lower FS (p < .05 and .0001, respectively, t-test), while ISO rats treated with DEPs had the lowest FS (p < .0001, t-test). Echocardiographic assessment revealed that left ventricular function was impaired by acute DEPs exposure, and this LV function was further compromised in rats with preexisting ISO-induced myocardial injury.     

Effect of Piper betle on cardiac function,marker enzymes,and oxidative stress in isoproterenol-induced cardiotoxicity in rats

The present study was designed to investigate the cardioprotective potential of Piper betle (P. betle) against isoproterenol (ISP)-induced myocardial infarction in rats. Rats were randomly divided into eight groups viz. control, ISP, P. betle (75, 150, and 300?mg/kg) and P. betle (75, 150, and 300?mg/kg) + ISP treated group. P. betle leaf extract (75, 150, or 300?mg/kg) or saline was orally administered for 30 days. ISP (85?mg/kg, s.c.) was administered at an interval of 24?h on the 28^th and 29^th day and on day 30 the functional and biochemical parameters were measured. ISP administration showed a significant decrease in systolic, diastolic, mean arterial pressure (SAP, DAP, MAP), heart rate (HR), contractility (+LVdP/dt), and relaxation (?LVdP/dt) and increased left ventricular end-diastolic pressure (LVEDP). ISP also caused significant decrease in myocardial antioxidants; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and myocyte injury marker enzymes; creatine phosphokinase-MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH) along with enhanced lipid peroxidation; thiobarbituric acid reacting species (TBARS) in heart. Pre-treatment with P. betle favorably modulated hemodynamic (SAP, DAP, and MAP) and ventricular function parameters (?LVdP/dt and LVEDP). P. betle pre-treatment also restored SOD, CAT, GSH, and GPx, reduced the leakage of CK-MB isoenzyme and LDH along with decreased lipid peroxidation in the heart. Taken together, the biochemical and functional parameters indicate that P. betle 150 and 300?mg/kg has a significant cardioprotective effect against ISP-induced myocardial infarction. Results of the present study suggest the cardioprotective potential of P. betle.     

三味檀香散对异丙肾上腺素所致心肌缺血大鼠血流动力学的影响

目的研究三味檀香散对异丙肾上腺素(Iso)致心肌缺血大鼠心电图和血流动力学的影响。方法采用ip Iso诱导大鼠致急性心肌缺血的动物模型。实验大鼠随机分为Iso模型组、阳性对照组和三味檀香散大、小剂量组,测定各组大鼠心电图ST段变化、血流动力学指标平均动脉压(MBP)、左心室收缩压(LVSP)、左心室舒张末压(LVEDP)、左心室等容期压力最大变化速率(±dp/dtmax)和心率(HR)。结果大、小剂量的三味檀香散组大鼠心电图ST段移位和HR明显低于模型组(P<0.01),血流动力学指标±dp/dtmax、LVSP-、LVEDP明显高于模型组(P<0.05或P<0.01),但对大鼠MBP无影响。结论藏药三味檀香散对Iso致心肌缺血大鼠的心脏舒缩功能有一定的保护作用。     

Intermedin~(1-53)保护异丙基肾上腺素诱导的心肌损伤

目的在异丙基肾上腺素(isoproterenol,ISO)诱导的大鼠急性心肌损伤的模型上探讨Intermedin153(IMD153)对心肌损伤的保护作用。方法用ISO建立大鼠缺血损伤模型,观察IMD153对心脏功能和心肌组织损伤影响;半定量RTPCR检测心室肌降钙素受体样受体(calcitoninreceptorlikereceptor,CL)、受体活性修饰蛋白(receptoractivitymodifyingprotein,RAMP)1/2/3的mRNA表达水平;放射免疫法测定心肌cAMP的含量和放射配基法测定心肌浆膜IMD受体结合位点。结果与对照组比较ISO组大鼠的左室内压变化速率(±LVdp/dtmax)分别降低23%和44%(均P<0.01),左室舒张末压(leftventricularenddiastolicpressure,LVEDP)增高7.8倍(P<0.01),心室肌CL、RAMP1/2/3的mRNA水平均明显上调(除RAMP2P<0.05,均P<0.01),ISO组心肌浆膜IMD受体Bmax值升高118%〔(83.05±5.75)vs(38.10±1.85)pmol·g-1Pro,P<0.01〕;与单纯ISO组比较,IMD可呈剂量依赖性减轻心内膜下心肌缺血损伤,改善心功能,高剂量Intermedin治疗组大鼠优于低剂量组。结论ISO诱导的缺血损伤心肌的IMD受体上调,而IMD153对心肌缺血损伤具有明显的保护作用。     

Effect of atorvastatin treatment on isoproterenol-induced myocardial infarction in rats

In the present study, chronic treatment of atorvastatin was evaluated on isoproterenol-induced myocardial infarction. Male Sprague-Dawley rats (200 +/- 25 g) were randomized into the following four groups: (1) control group, (2) isoproterenol-treated group, (3) atorvastatin-treated group, and (4) isoproterenol- and atorvastatin-treated group. Various serum and tissue parameters as well as histopathological studies were carried out in all groups. Isoproterenol administration produced severe myocardial damage and oxidative stress in rats. Atorvastatin treatment reduced myocardial infarction which has been reflected by improvement in serum parameters, ATPase activities and histopathological lesions. However, it could not reduce oxidative stress and hypertrophy induced by isoproterenol. Hence, it can be concluded that atorvastatin may protect myocardial infarction induced by isoproterenol independent of its antioxidant properties.     

Efficacy of grape seed proanthocyanidins on serum and heart tissue lipids in rats subjected to isoproterenol-induced myocardial injury

The present study was aimed to evaluate the preventive role of grape seed proanthocyanidins (GSPs) on serum and tissue lipid enzymes in isoproterenol (ISO)-induced myocardial injury in male Wistar albino rats. GSP was administered orally to rats (150-180 g) in three different doses, by gastric gavage (50, 100 and 150 mg/kg GSP), 6 days a week for 5 weeks. At the end of this period, all the rats, except the normal untreated rats that served as the control group, were administered ISO, 85 mg/kg subcutaneously, for 2 consecutive days to induce myocardial injury. After 48 h, rats (n=6 per group) were anesthetized with anesthetic ether, sacrificed and the levels of biochemical observations of the serum and heart tissues were performed. Biochemical assessment of myocardial injury was done by measuring the activities of serum thiobarbituric acid reactive substances and plasma lactate, which were significantly elevated in the rats administered with ISO. Further, our results suggest that prior administration of GSPs significantly maintained the cholesterol, phospholipids, triglycerides, and free fatty acids levels in serum and heart tissue of the ISO-induced myocardial injury in rats. The experiments conclude that GSPs possess cardioprotective and hypolipidemic effect on the treatment of ISO-induced myocardial injury.     

Intermedin1-53 protects the heart against isoproterenol-induced ischemic injury in rats

Intermedin is a novel member of the calcitonin/calcitonin gene-related peptide (CGRP) family peptide, which has vasodilatory and hypotensive actions identical to those of adrenomedullin and CGRP. Cleavage sites located between 2 basic amino acids at Arg93-Arg94 result in the production of prepro-intermedin95-147, namely intermedin1-53. The bioactive action of intermedin1-53 and its physiological significance are unclear. In this work, we aimed to explore the effects of intermedin1-53 on acute myocardial injury induced by isoproterenol. Myocardial ischemia injury in rats was induced by subcutaneous injection of a high dose of isoproterenol, and the therapeutic effect of intermedin1-53 was observed. Plasma lactate dehydrogenase activity, myocardial and plasma malondialdehyde content were higher in the isoproterenol group than that in controls. Isoproterenol-treated rats showed lower maximal rate of increase and decrease of left-ventricle pressure development (+/-left-ventricle dp/dtmax) and higher left-ventricle end-diastolic pressure (all P<0.01), which suggested severe heart failure and myocardial injury. Semi-quantitative RT-PCR analysis showed that the gene expression of calcitonin receptor-like receptor and receptor-activity-modifying protein (RAMP)1, RAMP2 and RAMP3 in ventricular myocardia were up-regulated by 79% (P<0.01), 48% (P<0.01), 31% (P<0.05) and 130% (P<0.01), respectively, compared with controls. In myocardial sarcolemmal membranes, the maximum binding capacity for [125I]-intermedin1-53 was increased by 118% (P<0.01) in the isoproterenol group compared with controls. Rats treated with low dosage intermedin1-53 (5 nmol/kg/day, 2 days) showed 21% (P<0.05) higher myocardial cAMP content, 18% and 31% higher+left-ventricle dp/dtmax and -left-ventricle dp/dtmax respectively, 288% lower left-ventricle end-diastolic pressure (all P<0.01), and attenuated myocardial lactate dehydrogenase leakage and malondialdehyde formation (all P<0.01). Treatment with high dosage intermedin1-53 (20 nmol/kg/day, 2 days) gave better results than that with low dosage intermedin1-53. These results suggest that the intermedin receptor system was up-regulated in isoproterenol-induced myocardial ischemic injury and intermedin1-53 might play a pivotal cardioprotective role in such injury.     

人参皂苷Rh2对高脂膳食大鼠心肌缺血再灌注时内皮祖细胞的影响

目的观察人参皂苷Rh2对高脂膳食大鼠心肌缺血再灌注(IR)时内皮祖细胞数量的影响。方法健康成年雄性SD大鼠,体重180~240 g,高脂饲料喂养24周后,随机分为缺血再灌注组(GIR组)、人参皂苷Rh2组(Rh2组)、假手术组(GS组),另设正常对照组(N组),给予基础饲料喂养24周。每组6只,记录各组大鼠体重。在高脂饲养基础上,采用结扎冠状动脉左前降支30 min,再灌注120 min的方法建立心肌缺血再灌注模型,GS组只穿线不结扎。Rh2组大鼠于缺血再灌注前30 min腹腔注射人参皂苷Rh2 10 mg/kg,GS组、GIR组大鼠于术前30 min腹腔注射等体积生理盐水。于再灌注120 min后处死大鼠,测定血脂水平以及血清血管内皮生长因子(VEGF)水平,流式细胞仪计数大鼠外周血内皮祖细胞(Endothelial progenitor cells,EPCs)的数量。结果喂养24周后,与正常对照组比较,其余组大鼠体重与血脂水平均升高(P<0.05),假手术组大鼠外周血EPCs数量与血清VEGF水平较正常对照组稍有下降,差异有统计学意义(P<0.05);与假手术组比较,缺血再灌注组与人参皂苷Rh2组大鼠外周血内皮祖细胞数量及血清VEGF水平均有升高,且人参皂苷Rh2组升高更为显著(P<0.05)。结论人参皂苷Rh2可增加高脂膳食大鼠心肌缺血再灌注后外周血内皮祖细胞数量,从而减轻心肌缺血再灌注损伤,可能与提高血清VEGF水平相关。     

p38 alpha mitogen-activated protein kinase inhibition improves cardiac function and reduces myocardial damage in isoproterenol-induced acute myocardial injury in rats

p38 mitogen-activated protein (MAP) kinase is activated during ischemic/hypoxic myocardial injury. However, the role of activated p38 MAP kinase on cardiac function after myocardial injury is not well understood. In the present study, we investigated the cardioprotective effects of p38 MAP kinase inhibition in a rat model of acute myocardial injury, induced by subcutaneous injection of isoproterenol (ISO, 20 mg/kg/d for 3 days). A synthetic p38 alpha MAP kinase inhibitor, SD-282 (40 mg/kg) or vehicle (0.25% Tween 80 in saline) was given intraperitoneally twice a day for 3 days, concomitant with ISO treatment. Cardiac function, systolic blood pressure, gene expression including collagen I and III, fibronectin and COX-2, and the myocardial injury were analyzed. Results showed that administration of SD-282 remarkably improved ISO-induced reduction of cardiac function with increases in ejection fraction (P < 0.001), cardiac output (P < 0.05), stroke volume (P < 0.001), and cardiac index (P < 0.01). SD-282 abolished ISO-induced reduction of systolic blood pressure (106.7 +/- 2.2 versus 123.1 +/- 5.3 mm Hg, P < 0.05). The ISO-induced expression of COX-2, collagen I and III, and fibronectin genes was reduced significantly (P < 0.05 in all cases) by administration of SD-282. The myocardial injury induced by ISO was significantly reduced by the treatment of SD-282 as judged by the reduction of myocardial necrosis. Data suggest that p38 alpha MAP kinase may be involved in the pathogenesis of cardiac dysfunction in ischemic myocardial injury. Inhibition of this enzyme may improve cardiac function and protect myocardium from ischemic/hypoxic injury that occurs during ischemic heart disease.     

异丙肾上腺素导致的心肌损伤大鼠心肌牛磺酸转运障碍和牛磺酸防治作用

目的:观察异丙肾上腺素(ISO)导致心肌损伤大鼠的心肌组织牛磺酸跨膜转运功能及牛磺酸转运体(TAUT)和半胱氨酸亚磺酸脱羧酶(CSD)的改变.方法:用[~3H]标记的牛磺酸测定心肌牛磺酸转运及其与心肌浆膜结合功能;竞争性RT-PCR测定TAUT和CSD mRNA的含量.结果:ISO组与对照组比,心肌[~3H]-牛磺酸摄入减少,释放量增加,心肌浆膜最大结合速率(B_(max))减少,TAUT和CSD mRNA水平减少.牛磺酸治疗组与ISO组比,心肌牛磺酸摄入量明显增加,释放量减少,B_(max)值增加,TAUT和CSDmRNA含量增加,各组间K_d值无明显差异.结论:ISO诱导的心肌损伤存在牛磺酸转运障碍及TAUT和CSD基因的下调,外源性给予牛磺酸对心肌损伤有明显防治作用.     

人参皂苷Rg1对大鼠肠缺血/再灌注损伤的影响

目的观察人参皂苷Rg1(ginsenoside Rg1)对大鼠肠缺血/再灌注后肠组织损伤的影响,并探讨其机制。方法制备SD大鼠肠缺血/再灌注损伤模型。实验分为3组(n=10):假手术组、缺血/再灌注组(对照组)、人参皂苷Rg1干预组(治疗组)。比较各组大鼠肠黏膜肿瘤坏死因子α(TNF-α)水平、白细胞介素6(IL-6)水平、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性的变化;用Chiu氏评分法观察肠黏膜的损伤情况。结果与假手术组相比,对照组TNF-α、IL-6水平明显升高,MDA含量明显增高,SOD活性明显降低,小肠损伤评分明显升高;与对照组相比,治疗组TNF-α、IL-6水平明显降低,MDA含量明显降低,SOD活性明显升高,小肠损伤评分明显降低。结论人参皂苷Rg1对大鼠肠缺血/再灌注后的肠道有保护作用,该保护作用可能与减少TNF-α、IL-6、MDA含量,提高SOD活性有关。     

Efficacy of sesamol on plasma and tissue lipids in isoproterenol-induced cardiotoxicity in wistar rats

Myocardial infarction is the leading cause of death all over the world. Sesamol is a potent phenolic antioxidant contained only in processed sesame oil and possesses potent chemopreventive, antimutagenic, antihepatotoxic and antioxidation properties. This study was undertaken to investigate the effect of sesamol on plasma and tissue lipid profiles in isoproterenol (ISO) - induced rats. Myocardial infarction was induced in adult male albino rats of the Wistar strain, weighing 180-200 g, by administration of isoproterenol (85 mg/kg of body weight), subcutaneously for 2 consecutive days. Sesamol dissolved in saline (0.9% NaCl) was administered intraperitoneally once in a day in the morning for 7 days. Increased levels of total cholesterol, phospholipids, triglycerides and free fatty acids in the plasma and the decreased levels of phospholipids in tissues were observed in ISO-induced rats. Very low density lipoprotein cholesterol (VLDL-C) and low density lipoprotein cholesterol (LDL-C) increased while high density lipoprotein cholesterol (HDL-C) decreased in the plasma of ISO-induced rats. Administration of sesamol (50, 100 and 200 mg/kg of body weight) improved the above changes and brought towards normal level. The protective role of sesamol against isoproterenol-induced myocardial infarction was further confirmed by histopathological examination. These results suggest that sesamol has antihyperlipidaemic effect against cardiotoxicity.     

地高辛抗血清对大鼠心肌缺氧复氧损伤心功能的影响及机制研究

目的研究内洋地黄素特异性拮抗剂地高辛抗血清对大鼠心肌缺氧复氧损伤心功能的影响及其作用机制。方法制备离体大鼠心肌缺氧复氧损伤模型,60只SD大鼠随机分为6组,每组10只。对照组,缺氧复氧组,维拉帕米组,小剂量、中剂量、高剂量地高辛抗血清组。连续纪录各组ECG、HR、LVDP、±dp/dtmax。各组于复氧结束后测定心肌组织中内洋地黄素水平、线粒体内Ca2+含量和冠脉流出液中NO含量。电镜观察心肌线粒体及血管内皮细胞结构的变化。结果缺氧复氧组心肌组织内洋地黄素水平升高,线粒体内Ca2+含量升高,NO含量降低,心肌线粒体及内皮细胞明显损伤,心功能明显受抑制。中、高剂量地高辛抗血清能降低心肌组织内洋地黄素水平和线粒体内Ca2+含量,升高NO含量,减轻缺氧复氧所致的心肌线粒体及内皮细胞的损伤,改善心肌收缩和舒张功能。结论地高辛抗血清抑制心肌缺氧复氧损伤所致的心功能减弱,其机制可能与拮抗内洋地黄素,减轻线粒体内Ca2+超载,升高NO浓度,保护了线粒体及内皮细胞功能有关。     

呋塞米对心衰大鼠心功能及心肌纤维化的影响

目的探讨呋塞米对心肌梗死后心力衰竭大鼠心功能及心肌纤维化的影响。方法采用结扎冠状动脉左前降支构建心肌梗死后心力衰竭大鼠模型。术后2周将34只大鼠随机分为3组:假手术组(10只,生理盐水)、心衰对照组(12只,生理盐水)及呋塞米组[12只,20 mg/(kg·d)]。药物干预4周后分别行超声心动图、血流动力学、心肌Masson染色,测定胶原容积分数(CVF)、血浆血管紧张素Ⅱ(AngⅡ)、醛固酮以及心肌转化生长因子β1(TGF-β1)和胶原纤维Ⅲ(CollagenⅢ)mRNA的表达。结果与心衰对照组比较,呋塞米组的左室舒张末期压(LVEDP)明显升高(P<0.05),而射血分数(EF)升高不明显。呋塞米组的AngⅡ、醛固酮、CVF及TGF-β_1和Collagen Ⅲ mRNA的表达均显著升高(P<0.05)。结论呋塞米能进一步激活心衰大鼠的肾素-血管紧张素-醛固酮系统(RAAS),进而升高TGF-β水平,促进心肌纤维化重构,最终加剧心功能的恶化。     

Synergistic effect of nicorandil and amlodipine on mitochondrial function during isoproterenol-induced myocardial infarction in rats

The synergistic effects of nicorandil (KATP-channel opener) and amlodipine (calcium-channel blocker) on heart mitochondrial enzymes and the mitochondrial antioxidant defence system was examined on isoproterenol-induced myocardial infarction in rats. The rats given isoproterenol (150 mg kg(-1) daily, i.p.) for two days showed significant changes in marker enzymes, mitochondrial enzymes and the mitochondrial defence system. Pre-co-treatment with nicorandil (2.5 mg kg(-1) daily, p.o.) and amlodipine (5.0 mg kg(-1) daily, p.o.) for 3 days significantly prevented these alterations and restored enzyme activity to near normal. These findings demonstrate the protective and synergistic effect of nicorandil and amlodipine in combination against isoproterenol-induced cardiac damage.     

Seabuckthorn attenuates cardiac dysfunction and oxidative stress in isoproterenol-induced cardiotoxicity in rats

We investigated the effects of seabuckthorn (SBT) oil in isoproterenol (ISO)-induced cardiotoxicity with reference to hemodynamic, antioxidant, histopathological, and ultrastructural parameters. Rats were administered SBT oil (5, 10, and 20 mL/kg per d) or vehicle orally for 30 days along with ISO (85 mg/kg, subcutaneously, at 24-hour interval) on 29th and 30th day. On 31st day, ISO control rats showed cardiac dysfunction, increased lipid peroxidation, depletion of cardiac injury marker enzymes, and antioxidant activities. Myocardial necrosis, edema, and inflammation were evident from the light microscopic and ultrastructural changes. Seabuckthorn oil at the dose of 20 mL/kg per d significantly modulates hemodynamic and antioxidant derangements. The preventive role of SBT oil on ISO-induced cardiotoxicity was reconfirmed by histopathological and ultrastructural examinations. Thus, the present study reveals that SBT oil mitigates myocardial damage in ISO-induced cardiac injury in rats by maintaining hemodynamic, biochemical, histopathological, and ultrastructural perturbations owing to its free radical scavenging and antioxidant activities.     

Andrographis paniculata extract protect against isoproterenol-induced myocardial injury by mitigating cardiac dysfunction and oxidative injury in rats

Present study evaluated the cardioprotective effect of Andrographis paniculata (100, 200 or 400 mg/kg) against isoproterenol (85 mg/kg, b.w.)-induced cardiotoxicity referred as myocardial infarction in rats. Isoproterenol significantly (p < 0.05) decreased mean arterial pressure, heart rate, contractility and relaxation and increased left ventricular end diastolic pressure. Isoproterenol also significantly (p < 0.05) decreased antioxidants, superoxide dismutase, catalase, glutathione peroxidase, glutathione and increased leakage of cardiac injury markers; creatine phosphokinase-MB isoenzyme, lactate dehydrogenase concomitant to increased lipid peroxidation and histopathological perturbations. However, pretreatment with A. paniculata favorably restored hemodynamic parameters and left ventricular function and significantly (p < 0.05) prevented the depletion of endogenous antioxidants and myocyte marker enzymes as well as inhibited lipid peroxidation. Significant (p < 0.05) reversal of almost all the hemodynamic, biochemical and histopathological parameters by A. paniculata pretreatment in isoproterenol-induced cardiotoxicity depicted the cardioprotective effect of A. paniculata. Results showed that A. paniculata protected heart against cardiotoxic effects of isoproterenol by boosting endogenous antioxidant network, restoring ventricular function and maintaining structural integrity of heart.