巴曲酶注射液对大鼠血栓栓塞性脑卒中急性超早期损伤的保护作用

目的 研究巴曲酶注射液对大鼠血栓栓塞性脑卒中急性超早期的保护作用。方法 自体血凝块闭塞左侧大脑中动脉法制备大鼠血栓栓塞性脑卒中模型,32只造模成功大鼠按神经缺陷程度随机分为4组：模型组及巴曲酶注射液低、高剂量（0.3、1.0 BU/kg）组和阿替普酶（rt-PA,9 mg/kg）组,每组8只,另设假手术组8只。造模1 h后尾iv给药,给药后6 h行神经功能评分,采用核磁共振（MIR）技术进行大鼠脑SE-T2WI序列扫描,测量脑病变范围;给药后24 h评分后取脑进行TTC染色,测量脑梗死范围;给药后6、24 h取血浆,测纤维蛋白原（FIB）浓度。结果 与模型组比较,巴曲酶注射液0.3 BU/kg治疗24 h（P<0.05）、1 BU/kg治疗6、24 h（P<0.05、0.01）显著改善大鼠神经功能评分;给药后6 h MRI结果显示,巴曲酶注射液0.3、1.0 BU/kg显著缩小病变范围（P<0.05、0.01）;给药后24 h TTC结果显示,巴曲酶注射液0.3、1.0 BU/kg显著缩小梗死范围（P<0.05）;巴曲酶注射液0.3、1.0 BU/kg于药后6、24 h均可显著降低血浆FIB浓度（P<0.05、0.01、0.001）。结论 巴曲酶注射液能改善大鼠脑缺血急性期受损神经功能、缩小脑病变范围、降低血浆FIB浓度,具脑保护作用。     

临产后剖宫产围术期抗菌药物的预防性应用

目的 探讨临产后剖宫产围术期预防性应用抗菌药物的必要性及最佳用药方案。方法 采用前瞻性随机对照观察方法,选择2014年1月至2014年11月妇产科行子宫下段剖宫产的产妇90例,所有孕妇都进入产程、宫口开2 cm以上、胎膜早破或羊水Ⅲ゜污染。将以上临产后高感染风险剖宫产产妇根据用药时间分为3组,其中A组为临产后使用抗菌药物24 h(29例),B组为临产后使用抗菌药物48 h(30例),C组为临产后使用抗菌药物72 h(31例)。比较3组术后切口感染、术后发热、体温恢复正常时间等,观察临产后产妇围术期24、48及72 h预防性应用抗菌药物的差异。结果 3组产妇术后无一例发生切口感染,3组术后血象异常率比较,差异无统计意义(P > 0.05);术后发热分别为A组10.3% (3/29)、B组13.3%(4/30)、C组16.1%(5/31),3组比较差异无统计学意义(P > 0.05);A组最高体温降到正常所需时间明显小于B、C组,差异有统计学意义(P < 0.05)。结论 临产后剖宫产围术期24 h预防性应用抗菌药物安全有效,无需延长用药时间。     

罂粟碱联合比伐芦定对急诊PCI术中慢血流/无复流患者血清心肌损伤标志物多指标和近期预后的影响

目的 探讨冠状动脉（以下简称冠脉）内联合应用罂粟碱与比伐芦定对急性ST段抬高型心肌梗死（STEMI）急诊经皮冠状动脉介入治疗（PCI）术中慢血流/无复流患者血清心肌损伤标志物、高迁移率族蛋白B1 （HMGB1）、内皮素-1（ET-1）及转化生长因子-β1（TGF-β1）水平和近期预后的影响。方法 回顾性分析新乡市第一人民医院2018年1月—2021年12月收治的90例急诊STEMI行PCI术中慢血流/无复流STEMI患者的临床资料,根据治疗方案不同分为对照组与试验组,每组各45例。两组均常规行冠脉造影与PCI治疗,经球囊预扩张后植入支架。在发生慢血流/无复流时,对照组于冠脉内注入注射用比伐芦定0.375 mg·kg^-1,试验组在对照组基础上于冠脉内注射盐酸罂粟碱注射液,每次3～5 mg,体质量60 kg以下给予3 mg,体质量60 kg以上给予5 mg,如果无复流,3～5 min重复1次,重复2～3次,总剂量≤20 mg。比较两组术后即刻心肌梗死溶栓实验（TIMI）血流分级3级患者占比、校正的TIMI血流帧数（cTFC）、术后24 h ST段完全回落率。分别于PCI术前和术后24 h、7 d时检测两组患者血清心肌损伤标志物［肌酸激酶同工酶（CK-MB）、肌钙蛋白I（cTnI）］、HMGB1、ET-1及TGF-β1水平。术后1个月内统计两组不良心脑血管事件及临床出血事件发生情况。结果 试验组术后即刻TIMI 3级患者占比、术后24 h ST段完全回落率均显著高于对照组（P<0.05）;术后即刻cTFC显著低于对照组（P<0.05）。两组术后24 h血清CK-MB、cTnI水平均较本组术前显著升高（P<0.05）,术后7 d较术后24 h均显著降低（P<0.05）;且试验组术后24 h、7 d时血清CK-MB、cTnI水平均显著低于同期对照组（P<0.05）。两组术后24 h血清HMGB1、ET-1及TGF-β1水平均较本组术前显著升高（P<0.05）,术后7 d较术后24 h均显著降低（P<0.05）;且试验组术后24 h、7 d时血清HMGB1、ET-1和TGF-β1水平均显著低于同期对照组（P<0.05）。术后1个月内,试验组不良心脑血管事件发生率显著低于对照组（4.44% vs 17.78%,P<0.05）;试验组与对照组临床出血事件发生率对比（15.56% vs 13.33%）,差异无统计学意义（P>0.05）。结论 冠脉内联合应用罂粟碱与比伐芦定治疗急诊PCI术中慢血流/无复流能有效改善患者冠脉血流情况,减轻心肌损伤与内皮损伤,缓解机体炎症反应,改善患者近期预后。     

藏药柳茶挥发油对小鼠急性心肌缺血损伤的干预作用

目的 研究藏药柳茶挥发油对垂体后叶素所致小鼠急性心肌缺血损伤的干预作用。方法 采用垂体后叶素腹腔注射建立小鼠急性心肌缺血损伤模型,给予柳茶挥发油治疗低、中、高剂量组干预后,监测小鼠造模前后心电图Ⅱ导联J点变化,检测血清过氧化氢酶（CAT）、谷胱甘肽转移酶（GSH-Px）、超氧化物歧化酶（SOD）活性以及乳酸（LD）的水平;显微镜下观察心肌缺血损伤的病理学变化及测定心肌梗死面积,并采用RT-PCR法测定组织caspase-3 mRNA的表达差异。结果 与模型组比较,柳茶挥发油中、高剂量组及阳性对照组缺血所致心电图J点的上移均显著降低（P<0.05）;血清CAT、GSH-Px、SOD活力明显增加（P < 0.05或P < 0.01）,LD含量明显降低（P<0.01）,病理学研究发现心肌损害程度减轻,缺血损伤面积明显减少,且高剂量干预组小鼠心肌组织的caspase-3 mRNA表达明显下调（P<0.05）。结论 藏药柳茶挥发油对小鼠急性心肌缺血损伤具有一定的保护作用,且与抑制caspase-3 mRNA的表达有关。     

阿司匹林联合氯吡格雷对急性心肌梗死急诊经皮冠脉介入治疗术后心功能影响

目的 探讨阿司匹林联合氯吡格雷对急性心肌梗死急诊经皮冠脉介入治疗（PCI）术后心功能的影响。方法 选择2014年10月-2016年10月,在新疆阿克苏地区第一人民医院急诊科收治的142例急性心肌梗死患者为研究对象,均行PCI术治疗;根据药物治疗方法的不同分为对照组（n=71）和联合组（n=71）;对照组术前术后在常规治疗的基础上给予氯吡格雷;联合组在对照组治疗的基础上给予阿司匹林辅助治疗。持续治疗12个月。比较两组的临床效果,两组术后心功能指标及高敏C蛋白含量变化。结果 两组术后冠脉造影在梗死部位均无血栓影,同时两组1个月内的治疗总有效率分别为90.14%和81.69%,相比差异无统计学意义。两组术后12个月再血栓发生率分别为1.41%和12.68%,联合组明显低于对照组,差异有统计学意义（P<0.05）。联合组治疗后患者心功能明显优于对照组,差异有统计学意义（P<0.05）。两组在治疗后24 h、72 h、7 d血清hs-CRP含量显著低于治疗前,同组治疗前后比较差异有统计学意义（P<0.05）;联合组在治疗后24 h、72 h、7 d血清hs-CRP含量显著低于对照组,差异有统计学意义（P<0.05）。结论 阿司匹林联合氯吡格雷可有效减少PCI术后再血栓的发生,改善急性术后心功能的恢复,降低机体炎性免疫反应。     

药物体外干预改善盐敏感性高血压小鼠内皮祖细胞功能研究

目的 探索改善去氧皮质酮/盐（DOCA-salt）高血压小鼠内皮祖细胞（EPC）功能的药物干预手段。方法 健康的成年C57BL/6小鼠,随机分为模型组和假手术对照组,模型组制备DOCA-salt高血压小鼠模型,用尾动脉测压法测定小鼠血压,提取其EPC并分别用流式细胞仪和荧光显微镜进行鉴定,模型组小鼠EPC分别用四氢生物蝶呤（BH₄）、超氧化物歧化酶-聚乙二醇（PEG-SOD）、N(G)-硝基-L-精氨酸（L-NNA）孵育24 h,检测其功能。结果 与对照组比较,DOCA-salt高血压小鼠的收缩压明显升高（P<0.01）,其EPC的黏附功能和小管形成功能明显受损（P<0.01）,而经BH₄、PEG-SOD、L-NNA孵育24 h后,EPC的黏附功能（P<0.01)和小管形成功能（P<0.05）均显著改善。结论 BH₄、PEG-SOD、L-NNA可有效改善DOCA-salt高血压小鼠EPC受损的功能。     

复方HD对环磷酰胺致免疫抑制小鼠免疫功能的影响

目的 探讨复方HD对环磷酰胺诱导的免疫抑制小鼠的免疫增强作用。方法 ICR小鼠分别以蒸馏水（对照组、模型组）、香菇多糖（200 mg/kg）、复方HD（5、10、20 g/kg）每天1次ig给药,连续10 d;除对照组外,在第4~6天ip环磷酰胺（40 mg/kg）制备免疫抑制小鼠模型（对照组除外）;每天给药前精确称量并记录小鼠体质量。于最后一次给药24 h后,测定小鼠脾指数、胸腺指数;流式细胞术进行全血中T细胞亚群分析;ELISA法检测血浆中IFN-γ和IL-4水平。结果 与模型组比较,复方HD低、中、高剂量组显著提高小鼠的胸腺指数,CD3⁺、CD3⁺CD4⁺细胞数以及CD4⁺/CD8⁺比值（P<0.05）,显著恢复血浆中IFN-γ水平和IFN-γ/IL-4比值（P<0.05）,纠正了Th1/Th2偏移,并呈现出一定的浓度相关性。结论 复方HD能够促进环磷酰胺诱导的免疫抑制小鼠免疫功能的恢复,证明其在预防及治疗免疫功能低下方面具有一定的疗效。     

常规12导心电图与24h动态心电图对起搏器植入术后患者心律失常的诊断比较

目的 对比常规12导心电图与24 h动态心电图(DCG)诊断起搏器植入患者心律失常检出率的差异。方法 选取2011年3月到2014年3月于我院就诊的永久性起搏器置入术后患者共50例,患者均同时采用常规12导心电图和24 h DCG监测和诊断,比较其心律失常阳性检出率差异。结果 24 h DCG检出心律失常患者50例,其检出率为100.0%,常规12导心电图检出心律失常患者22例,检出率为44.0%,检出差异有统计学意义(P <0.05)。24 h DCG在心房早搏、室性早搏等检出率明显高于常规12导心电图,差异有统计学意义(P <0.05)。结论 24 h DCG诊断起搏器植入患者心血管事件心律失常的敏感性和特异性均优于常规12导心电图,能为永久性起搏器植入术后临床随访提供准确的依据。     

养心氏片防治慢性缺血性心力衰竭及急性心肌缺血再灌注损伤的实验研究

目的 对养心氏片防治慢性缺血性心力衰竭和急性心肌缺血再灌注损伤作用进行实验研究,为其临床应用提供理论依据。方法 采用冠状动脉结扎法构建慢性缺血性心力衰竭大鼠模型及急性心肌缺血再灌注小鼠心梗模型,随机分为假手术组、模型组、阳性药组、以及养心氏片低、中、高剂量组,通过预给药和造模后给药,检测大鼠超声心电图、ACE、ACD及小鼠心肌梗死面积、CK、LDH、SOD、相关因子,并观察心脏病理学切片的形态学变化。结果 与假手术组相比,模型组的生化指标差异具有统计学意义（P<0.001）;与模型组相比,阳性药组、高剂量养心氏片组生化指标差异具有统计学意义（P<0.001,P<0.01,P<0.05）,且能显著减少心肌梗死面积（P<0.01,P<0.05）, 明显改善心肌细胞水肿程度,减少细胞浸润。结论 养心氏片对慢性缺血性心力衰竭、急性心肌缺血再灌注损伤具有明显的预防和治疗作用。     

心电向量检查对心肌缺血及心肌梗死的诊断价值

目的 评价心电向量检查对心肌缺血及心肌梗死的诊断价值。方法 选取2014年12月至2015年2月安徽医科大学第二附属医院就诊的8例心电图QRS波形正常的心肌缺血及心肌梗死患者,同期行心电图、心电向量图及冠状动脉造影检查,3项检查中以冠状动脉造影结果为金标准,与其他2项检查结果比较,对心电图及心电向量图检查的准确性进行评判。结果 8例患者心电图QRS波形正常,1例伴有V1-V3导联ST段上抬,5例伴有不同程度的ST段压低和/或T波变化,2例为正常范围心电图,与冠状动脉造影检查结果不符;8例患者的心电向量检查结果均符合相应部位心肌缺血及心肌梗死的诊断,其中,前壁心肌梗死1例,前壁合并下壁心肌梗死4例,前壁合并后壁心肌梗死1例,下壁合并后壁心肌梗死1例,前壁、下壁合并后壁心肌梗死1例,与冠状动脉造影检查结果相符。结论 心电向量检查对心肌缺血及心肌梗死的诊断价值优于常规心电图。     

Pharmacological evidence that inducible nitric oxide synthase is a mediator of delayed preconditioning

Brief periods of myocardial ischaemia preceding a subsequent more prolonged ischaemic period 24-72 h later confer protection against myocardial infarction ('delayed preconditioning' or the 'second window' of preconditioning). In the present study, we examined the effects of pharmacological modifiers of inducible nitric oxide synthase (iNOS) induction and activity on delayed protection conferred by ischaemic preconditioning 48 h later in an anaesthetized rabbit model of myocardial infarction. Rabbits underwent a myocardial preconditioning protocol (four 5 min coronary artery occlusions) or were sham-operated. Forty-eight hours later they were subjected to a sustained 30 min coronary occlusion and 120 min reperfusion. Infarct size was determined with triphenyltetrazolium staining. In rabbits receiving no pharmacological intervention, the percentage of myocardium infarcted within the risk zone was 43.9+5.0% in sham-operated animals and this was significantly reduced 48 h after ischaemic preconditioning with four 5 min coronary occlusions to 18.5+5.6% (P<0.01). Administration of the iNOS expression inhibitor dexamethasone (4 mg kg(-1) i.v) 60 min before ischaemic preconditioning completely blocked the infarct-limiting effect of ischaemic preconditioning (infarct size 48.6+/-6.1%). Furthermore, administration of aminoguanidine (300 mg kg(-1), s.c.), a relatively selective inhibitor of iNOS activity, 60 min before sustained ischaemia also abolished the delayed protection afforded by ischaemic preconditioning (infarct size 40.0+/-6.0%). Neither aminoguanidine nor dexamethasone per se had significant effect on myocardial infarct size. Myocardial risk zone volume during coronary ligation, a primary determinant of infarct size in this non-collateralized species, was not significantly different between intervention groups. There were no differences in systolic blood pressure, heart rate, arterial blood pH or rectal temperature between groups throughout the experimental period. These data provide pharmacological evidence that the induction of iNOS, following brief periods of coronary occlusion, is associated with increased myocardial tolerance to infarction 48 h later.     

A characterization of myocardial infarction induced by thrombotic occlusion and a comparison with mechanical ligation of the rat coronary artery.

In the present study we examined two different methods for inducing myocardial infarction in rats. We previously developed an animal model of coronary artery thrombotic occlusion induced by a photochemical reaction, which occurs when rose bengal (a photosensitizer dye) is injected into the animal and is irradiated with green light. Arterial occlusion is thereby achieved nonmechanically. Using this method, we investigated the effect of thrombolytic intervention on myocardial infarct size. Infarct size was determined 24 h after the induction of myocardial infarction. When tisokinase (3 mg/kg), a native tissue-type plasminogen activator, was administered 3 min after the ST-segment elevation on a lead II electrocardiogram, the infarct size was 20.6 +/- 5.1%, which was significantly smaller than that of control rats (37.3 +/- 4.6%). When tisokinase was administered 10 min after the ST-segment elevation, the infarct size was 27.1 +/- 2.1%, which was not significantly smaller than that of controls. The rat coronary artery thrombosis model incorporates many aspects of coronary thrombosis. It differs from the coronary ligation model in that it lends itself to the study of thrombolytic agents on animal models of myocardial infarction.     

Lidocaine and surgical modification reduces mortality in a rat model of cardiac failure induced by coronary artery ligation

Coronary artery ligation in the rat provides a useful experimental model of cardiac failure; however, this procedure carries with it a high mortality rate (50%). In this study, we used lidocaine (10 mg/kg, i.m.) before coronary artery ligation and 2 h after surgery to minimise the incidence of ventricular fibrillation (VF) that leads to sudden death in this model. We found that coronary artery ligation, using lidocaine in conjunction with a modified surgical procedure, had a mortality rate of 15%, much lower than reported in previous studies using this model. These modifications allow for the production of larger infarcts with 29% of animals having an infarct size > 50% of the epicardial surface. Infarct size in our myocardial infarction (MI) group varied between 5% and 75% of the left ventricular (LV) surface area resulting in a mean infarct size of 41.3 +/- 1.3% for the epicardial surface and 40.0 +/- 1.3% for the endocardial surface.     

Lack of protection of ischemic myocardium by verapamil in conscious dogs

To determine whether coronary dilation and decreased myocardial oxygen requirements resulting from administration of verapamil, a calcium and slow current antagonist, protect ischemic myocardium in conscious dogs, we studied 15 treated and 15 control animals after coronary occlusion. Verapamil (0.2–0.7 mg/kg/h) was given by continoous infusion for 17 h beginning 5 h after the initial plasma creatine kinase (CK) elevation after coronary occlusion. Observed infarct size and infarct size predicted before verapamil were estimated from hourly plasma CK values and infarct size was estimated also from myocardial CK depletion measured directly, 24 h after occlusion. Changes in heart rate, blood pressure, and frequency of premature ventricular complexes (recorded every 30 min) after occlusion were similar in treated and control dogs. Coronary flow after verapamil, measured with radioactively labeled microspheres, did not increase in ischemic zones but increased by 90% in normal myocardium (p < 0.05). The differences between observed and predicted infarct size estimated from plasma CK changes in treated and controls were similar (3.0±2.2 (S.E.) and 2.0±1.4 CK-g-eq), and myocardial CK depletion was also comparable in the two groups (25 ± 2% and 23 ±2%). Thus although verapamil, administered five hours after the initial plasma CK elevation, increased coronary flow in normal myocardium, it did not augment flow in ischemic tissue or limit the extent of infarction.     

Effects of zoledronate in the repair of chronically infarcted rat myocardium

Zoledronate (Zol), one of the class of bisphophonate drugs, is commonly used to treat postmenopausal osteoporosis. Treatment of liposomal bisphosphonates has been shown to worsen myocardial infarct repair in an experimental model. The purpose of this study was to investigate the effect of Zol in the repair of chronically infarcted myocardium without liposomal encapsulation to mimic the clinical setting. Zol (20 μg/kg, a dose known to treat experimental osteoporosis in rats, n = 15) was administered subcutaneously to female Sprague-Dawley rats 1 day before coronary artery ligation. Rats receiving phosphate-buffered saline (n = 12) were used as controls. Left ventricular function, infarct size, and remodeling were studied at 4 weeks postinfarction. Zol pretreatment did not affect left ventricular ejection fraction in hearts with myocardial infarction (49.5 ± 1.4% in Zol; 50.6 ± 2.1% in phosphate-buffered saline). Infarct size was similar in Zol versus untreated hearts (34.2% ± 2.9% in Zol; 33.4% ± 2.9% in phosphate-buffered saline). Left ventricular cavity volume and circumference, infarct thickness, and expansion index were comparable between the groups. To investigate a potential effect of Zol on tissue macrophage infiltration after myocardial infarction, heart specimens were harvested 48 hours postinfarction and sections were immunostained with CD68 antibody, a macrophage-specific marker. Results of macrophage immunostaining revealed that the level of tissue macrophage infiltration was similar between groups. In conclusion, administration of Zol before myocardial infarction had no adverse effects on cardiac contractile function, infarct size, or remodeling. These results suggest that treatment of Zol given before the onset of myocardial infarction does not cause worsening of infarct repair.     

Reperfusion duration paradox with late myocardial preconditioning in rabbits

In this study, pharmacological late preconditioning was induced in 53 rabbits with an adenosine A(1) receptor agonist (2-chloro-N(6)-cyclopentyladenosine, CCPA, 100 microg/kg), or a NO-donor (S-nitroso-N-acetyl-penicillamine, SNAP, 2.5 microg/kg/min; 75 min) vs. saline as control. Later, after 24 h, rabbits underwent a 30-min coronary occlusion and subsequent reperfusion. After 3 h of coronary artery reperfusion, infarct size was reduced with CCPA (43+/-4%) and SNAP (27+/-4%) vs. saline (56+/-4%). However, after 72 h of coronary artery reperfusion, infarct sizes were similar in all groups, demonstrating an only transient effect of late preconditioning against myocardial infarction. Combined administration of CCPA and SNAP failed to induce sustained cardioprotection.     

葛花异黄酮对急性心肌梗死小鼠心肌的保护作用

目的通过小鼠急性心肌梗死模型观察葛花异黄酮对缺血心肌的影响,并探讨其作用机制。方法开胸结扎左冠状动脉前降支建立小鼠急性心肌梗死模型,以丹参注射液为阳性对照,观察葛花总黄酮低、高剂量组对心肌梗死面积、血清心肌酶、血清SOD和MDA含量的影响;并通过RT-PCR的方法,检测葛花总黄酮对缺血心肌β-肾上腺受体激酶1(β-adrenergic receptor kinase,β-ARK1)表达的影响。结果葛花总黄酮可明显缩小小鼠心肌梗死面积,降低血清心肌酶和MDA含量,下调心肌β-ARK1 mRNA的表达,并随着剂量的增加其作用加强。结论葛花总黄酮对急性心肌梗死小鼠心肌有明显的保护作用,其作用机制与其抗氧化损伤及下调心肌β-ARK1mRNA的表达有关。     

三七总皂苷对大鼠心肌缺血的保护作用

目的探讨三七总皂苷(PNS)预处理对急性心肌缺血的作用。方法 SD大鼠ig给予PNS 25～800 mg·kg-1,每天2次连续7次,末次给药30 min后,结扎冠状动脉前降支缺血24 h。氯化三苯基四氮唑染色法测定心肌梗死面积,颈总动脉插管测定左心室内血流动力学变化,自动生化分析仪检测心肌酶谱。结果与急性心肌缺血模型组相比,PNS 50,100,200和400 mg·kg-1能显著降低心肌缺血大鼠的心肌梗死面积(P<0.05),降低心肌缺血后左心室舒张末压,提高左心室收缩压,增强等容收缩期左心室内压最大上升速率和等容舒张期左心室内压最大下降速率;显著降低血清中乳酸脱氢酶和肌酸激酶活性,降低α-羟丁酸脱氢酶和天冬氨酸氨基转移酶活性。结论 PNS在50～400 mg·kg-1剂量范围内能显著降低心肌缺血大鼠的心肌梗死面积,提高左心室舒张和收缩功能,明显抑制急性心肌缺血大鼠心肌酶的释放,具有改善心肌缺血的作用。     

Beneficial effects of a new prostacyclin analogue, KP-10614, on acute myocardial infarction in rats.

The potential therapeutic value of a new prostacyclin analogue, (4z, 16s)-4,5,18,18,19,19-hexadehydro-16,20-dimethyl-delta 6(9a)- 9-(O)-methano-PGI1 (KP-10614), was studied in acute myocardial infarction in rats. Myocardial infarction was induced by ligation of the left coronary artery and ischemic injury was followed up to 4 h. The infarct size, evaluated by the area unstained by 2,3,5-triphenyltetrazolium chloride, reached 41.1 +/- 1.4% of the left ventricle at 4 h. KP-10614 (3 ng/kg/min x 4 h) reduced the infarct size at 4 h significantly (26.5 +/- 2.9%). At the same dose, KP-10614 inhibited ADP-induced ex vivo platelet aggregation significantly (21.5 +/- 4.0% of the control aggregation), but did not alter the arterial blood pressure or heart rate. To assess the role of platelets in myocardial infarction, circulating platelets were reduced by about 95% with rabbit antiserum to rat platelets. In platelet-depleted rats, the infarct size decreased significantly to 24.1 +/- 4.6% of the left ventricle at 4 h. These results suggest that platelets play an important role in expression of myocardial ischemic injury resulting from coronary artery occlusion in rats, and the ability of KP-10614 to decrease the infarct size appeared to be attributable, at least in part, to the inhibition of platelet aggregation or cellular metabolic effects produced by platelets at the site of tissue injury.     

Cardioprotective activity of alcoholic extract of Tinospora cordifolia in ischemia-reperfusion induced myocardial infarction in rats

It has been suggested that the beneficial effects of reperfusing the myocardium might be in part reversed by the occurrence of reperfusion injury. Oxidative stress was suggested to be implicating in the pathogenesis of ischemia-reperfusion (I/R) injury. Many antioxidative plants were shown to be cardioprotective in experimental models of myocardial ischemia-reperfusion (I/R) injury. The present study was designed to investigate the effects of pretreatment with alcoholic extract of Tinospora cordifolia in an in vivo rat model. The model adopted was that of surgically-induced myocardial ischemia, performed by means of left anterior descending coronary artery occlusion (LAD) for 30 min followed by reperfusion for another 4 h. Infarct size was measured by using the staining agent TTC (2,3,5-triphenyl tetrazolium chloride). Lipid peroxide levels in serum and in heart tissue were estimated spectrophotometrically by the methods developed by Yagi and Ohkawa et al. respectively. A lead II electrocardiogram was monitored at various intervals throughout the experiment. A dose dependent reduction in infarct size and in lipid peroxide levels of serum and heart tissue were observed with the prior treatment of T. cordifolia with various doses for 7 d compared to control animals. Hence, the present study suggests the cardioprotective activity of T. cordifolia in limiting ischemia-reperfusion induced myocardial infarction.