温阳通脉方预处理对心肌缺血再灌注大鼠MDA及SOD的影响

目的 观察温阳通脉方预处理对大鼠心肌缺血再灌注损伤（IR）模型丙二醛（MDA）、超氧化物歧化酶（SOD）含量的影响，探讨温阳通脉方对大鼠再灌注心肌的保护机制。方法 采用结扎大鼠冠状动脉左前降支，缺血30min，再灌注120min的方法建立心肌缺血再灌注损伤模型；缺血5min，再灌注5min，反复3次后缺血30min，再灌注120min建立心肌缺血预适应（IP）模型。检测大鼠灌胃14d后温阳通脉方组、心肌缺血预适应组（IP组）、再灌注损伤纽（IR组）、假性处理组血清MDA、SOD含量。结果 温阳通脉方组、IP组MDA含量低于IR组，SOD高于IR组，差异有统计学意义（P〈0．05）。结论 温阳通脉方预处理后，能降低大鼠心肌缺血再灌注损伤模型MDA含量，升高SOD含量，减轻大鼠急性心肌缺血所致心肌损伤，其机制可能是通过模拟心肌缺血预适应参与心肌保护作用。     

心肌缺血/再灌注损伤后的肺组织损伤

目的初步探讨心肌缺血／再灌注损伤对肺组织损伤的可能机制。方法选取雄性成年SD大鼠（4～6月龄）,体重130～160g,建立成年大鼠缺血／再灌注模型。运用CK和MPO试剂盒检测肌酸激酶（CK）和髓过氧化物酶（MPO）的含量,运用双抗体夹心ABC—ELISA法检测细胞间黏附分子-1（ICAM-1）的含量。结果与伪手术组相比,缺血／再灌注大鼠的AN／AAR比值明显增高（P〈0．05）,CK在心肌缺血／再灌注大鼠血清中的含量明显升高（P〈0．05）,MPO与ICAM-1在心肌缺血／再灌注组大鼠血清和肺组织中含量明显升高（P〈0．05）。结论大鼠心肌缺血再灌注损伤后肺组织受到一定的损伤,可能与体循环中炎性介质的作用及肺组织的炎性应激有关。     

脂联素对大鼠心肌缺血-再灌注损伤时心律失常的影响

目的：观察脂联素对大鼠心肌缺血再灌注损伤时心律失常的影响并探讨其可能机制。方法：32只8周龄雄性大鼠被随机分为假手术组、缺血一再灌注（IR）组、地尔硫卓组和脂联素（APN）组,每组8只。①假手术组：只穿线,旷置90min;②IR组：先阻断血流30min,再灌注60min;③地尔硫卓组和APN组：先阻断血流30min,于再灌注开始时,从鼠尾静脉分别注射地尔硫卓（3．5μg／g·min）、APN（60ng／g·min）．再灌注60min。以Medlab生物信号采集处理系统连续监测各组心电图的变化。各模型组于再灌注60min后处死大鼠。测定血清、心肌组织一氧化氮（NO）的含量。结果：（1）与假手术组比较,IR组再灌注60min时段里．8只大鼠均出现再灌注心律失常．再灌注过程中ST段抬高的幅度显著增高（P〈0．001）,心肌组织、血清中NO含量均明显降低（P〈0．001）;（2）与IR组比较．APN组再灌注60min时段里,没有出现再灌注心律失常,再灌注过程中ST段抬高幅度显著下降（P〈0．001）,心肌组织、血清中NO含量均明显升高（P〈0．001）,且优于地尔硫卓组（P〈0．001）。结论：脂联素对缺血一再灌注损伤造成的心律失常有一定的保护作用．其机制可能与脂联素增加心肌组织、血清中NO含量有关。     

蝙蝠葛碱对兔心肌缺血再灌注时血清MDA浓度和SOD活性的影响

目的探讨蝙蝠葛碱（Dau）对兔心肌缺血再灌注（IR）时血清丙二醛（MDA）浓度和超氧化物歧化酶（SOD）活性的影响。方法24只家兔随机分为假手术对照组、缺血再灌注组、缺血再灌注＋蝙蝠葛碱（Dau）干预组各8例。结扎兔左冠状动脉前降支40min造成心肌缺血再灌注模型，观察缺血前后及再灌注不同时相点血清MDA含量和SOD活性的变化。结果家兔心肌缺血40min时血清MDA含量开始明显升高（P〈0．05），SOD活性开始明显下降（P〈0．05）。Dau（剂量3．5mg／kg）能明显降低心肌缺血40min及缺血再灌注后兔血清MDA含量，升高血清SOD活性。结论Dau通过减轻兔心肌脂质过氧化作用所造成的损伤，增强SOD活性，提高氧自由基清除能力，对兔心肌缺血再灌注损伤具有一定保护作用。     

负荷剂量氟伐他汀对心肌缺血再灌注损伤的保护作用——模拟缺血预适应

目的观察负荷剂量氟伐他汀预处理对在体大鼠心肌缺血再灌注损伤的保护作用。方法 84只大鼠随机分为12组,每组7只。其中氟伐他汀组（F-1~F-8组）分别于冠状动脉缺血前1、2、4、6、12、24、48和72 h灌胃氟伐他汀80 mg/kg;假手术组（Sham组）、缺血再灌注组（I/R组）、缺血预适应第一窗口组（IPC-1组）及第二窗口组（IPC-2组）灌胃等量生理盐水。建立大鼠心肌缺血再灌注损伤模型、缺血预适应保护模型及延迟保护模型。记录大鼠心律失常及心肌缺血、心肌梗死情况,测定血清乳酸脱氢酶（LDH）、肌酸激酶同工酶（CK-MB）活性,光学显微镜及透射电镜下观察受损心肌细胞形态。结果氟伐他汀预处理组中,除F-5、F-6组外,其他组心肌梗死面积均较I/R组减小（P〈0.05）;负荷剂量氟伐他汀的保护作用呈现两个窗口,F-3、F-7组分别为其保护作用的最佳组（与I/R组比较,P〈0.05）;与IPC-1组比较,F-3组心肌缺血、心肌梗死程度、血清LDH和CK-MB均显著增高（P〈0.05）,心律失常评分差异无统计学意义（P〉0.05）。与IPC-2组比较,F-7组梗死面积有减少趋势（P〉0.05）,心肌梗死质量显著降低（P〈0.05）,缺血程度显著增高（P〈0.05）。结论负荷量氟伐他汀预处理对在体大鼠心肌缺血再灌注损伤的保护作用存在两个窗口,第一窗口较缺血预适应弱,第二窗口在减轻心肌梗死程度上有强于缺血预适应的趋势。     

牛磺酸对大鼠心肌缺血再灌注损伤细胞凋亡的影响

目的观察牛磺酸对大鼠心肌缺血再灌注损伤后细胞凋亡的影响。方法实验大鼠40只,随机分为5组：假手术组（8只）,再灌注模型组（8只）,牛磺酸低、中、高剂量（30mg／kg、100mg／kg、300mg／kg）组（各8只）。再灌注后观察各组血清SOD、LDH、MDA含量,TUNEL法检测心肌细胞凋亡。结果①牛磺酸对大鼠心肌缺血再灌注后血清SOD、LDH、MDA含量的影响：与假手术组比较,其余各组大鼠血清SOD活性明显降低,LDH、MDA含量明显增高（P〈0．05,P〈0．01）;与模型组比较,牛磺酸中、高剂量组大鼠血清SOD活性明显升高（P〈0．01）,LDH、MDA含量明显降低（P〈0．05,P〈0．01）。②牛磺酸对大鼠心肌缺血再灌注（I／R）损伤后细胞凋亡的影响：I／R后心肌细胞凋亡指数（AI）为（45．6±4．6）,明显高于假手术组的（8．50±1．13）（P〈0．01）,牛磺酸低、中、高组分别为（37．03±3．52）、（30．32±8．23）和（25．62±6．12）,均明显低于I／R（P〈0．01）。结论牛磺酸可降低再灌注损伤大鼠氧自由基值,抑制心肌细胞凋亡。     

参连复脉颗粒对大鼠再灌注心律失常的影响及机制研究

目的:探讨参连复脉颗粒对大鼠再灌注心律失常的影响及机制研究。方法:将SD大鼠随机分为模型组、假手术组、美西律组、参连复脉颗粒低剂量组、参连复脉颗粒中剂量组、参连复脉颗粒高剂量组。干预完成后,除假手术组外其余各组大鼠建立心肌缺血再灌注模型;观察各组大鼠心肌缺血再灌注后室性期前收缩(PVC)总个数和心室颤动(VF)+室性心动过速(VT)总时程。进一步检索参连复脉颗粒药物成分,预测成分靶点,同时检索再灌注心律失常靶点,获取药物与再灌注心律失常的交集靶点并筛选核心靶点,借助Metascape平台分析其作用的信号通路。结果:与模型组比较,参连复脉颗粒中、高剂量组PVC总个数和VF+VT总时程均明显下降(P<0.05或P<0.01);与美西律组比较,参连复脉颗粒高、中剂量组VT+VF总时程升高(P<0.05或P<0.01),而参连复脉颗粒高、中剂量组PVC总个数与美西律组比较差异无统计学意义(P>0.05)。筛选得到参连复脉颗粒与再灌注心律失常交集靶点共136个,进一步筛选其核心靶点主要为蛋白激酶B1(AKT1)、肿瘤坏死因子(TNF)、白介素6(IL6)、白介素1β...     

温阳通脉方预适应对心肌再灌注损伤大鼠一氧化氮的影响

目的探讨温阳通脉方保护心肌缺血的机制是否通过模拟心肌缺血预适应（IP）而增加血浆一氧化氮（NO）的含量发挥作用。方法采用结扎大鼠冠状动脉左前降支，缺血30min，再灌注120min的方法建立缺血再灌注（IR）损伤模型，检测温阳通脉方组、IP组、IR组、假性颓处理组灌胃14d造模后血清NO含量，观察温阳通脉方对其的影响。结果温阳通脉方预处理组、IP组NO含量高于IR组（P〈0.05），温阳通骧方预处理组与IP组间比较无统计学意义。结论温阳通脉方预处理后，能增强大鼠心肌缺血再灌注损伤模型NO的含量，可能存在预适应样作用。     

川芎嗪后处理对大鼠心肌缺血再灌注损伤的保护作用

目的：观察川芎嗪后处理对大鼠心肌缺血再灌注损伤的保护作用及探讨其可能的作用机制。方法：采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注损伤模型,记录各组心律失常发生情况,测定肌酸激酶（CK）、超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）、一氧化氮合酶（NOS）含量,HE染色光镜下观察心肌组织形态学改变并秤重检测心肌梗死面积。结果：川芎嗪组的心律失常发生率明显降低,心肌细胞肿胀明显减轻,血中SoD、NO、NOS含量增加,MDA,CK的生成减少。（P〈0．05）。结论：川芎嗪后处理能降低心律失常发生、减少坏死面积,其作用可能与提高sOD、NO、NOs含量,减少MDA生成有关。     

川芎嗪后处理对大鼠心肌缺血再灌注损伤的保护作用

目的：观察川芎嗪后处理对大鼠心肌缺血再灌注损伤的保护作用及探讨其可能的作用机制。方法：采用结扎大鼠左冠状动脉前降支方法制备心肌缺血再灌注损伤模型,记录各组心律失常发生情况,测定肌酸激酶（CK）、超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）、一氧化氮合酶（NOS）含量,HE染色光镜下观察心肌组织形态学改变并秤重检测心肌梗死面积。结果：川芎嗪组的心律失常发生率明显降低,心肌细胞肿胀明显减轻,血中SoD、NO、NOS含量增加,MDA,CK的生成减少。（P〈0．05）。结论：川芎嗪后处理能降低心律失常发生、减少坏死面积,其作用可能与提高sOD、NO、NOs含量,减少MDA生成有关。     

Prognostic significance of postprocedural sustained ventricular tachycardia or fibrillation in patients undergoing primary percutaneous coronary intervention (from the HORIZONS-AMI Trial)

The prognostic significance of postprocedure sustained ventricular tachycardia or ventricular fibrillation (VT/VF) in patients undergoing primary percutaneous coronary intervention (PPCI) for ST-segment elevation myocardial infarction (STEMI) has rarely been studied, although a previous study has suggested that its occurrence portends decreased survival. We examined outcomes from the prospective large-scale multicenter randomized HORIZONS-AMI trial to evaluate the incidence, clinical correlates, and outcomes of in-hospital sustained VT/VF after PPCI. Of 3,485 patients undergoing PPCI in whom VT/VF did not occur before or during the procedure, 181 patients (5.2%) developed VT/VF after PPCI. Most postprocedural VT/VF episodes (85%) occurred in the first 48 hours. Patients with postprocedural VT/VF were more likely men with Killip class > I on presentation but had a lower prevalence of hypertension and diabetes. Patients with postprocedural VT/VF were also less frequently taking β blockers and angiotensin-converting enzyme inhibitors/angiotensin receptor blockers at admission. Mean door-to-balloon time was shorter and Thrombolysis In Myocardial Infarction grade 0 flow before PPCI was more common in patients with VT/VF, although Thrombolysis In Myocardial Infarction grade 3 flow rates after PPCI did not vary. There were no significant differences in adjusted 3-year rates of mortality (hazard ratio 0.73, 95% confidence interval 0.30 to 1.79) or composite major adverse clinical events (death, myocardial infarction, target vessel revascularization, or stroke; hazard ratio 0.71, 95% confidence interval 0.44 to 1.15) in patients with versus without postprocedural sustained VT/VF. In conclusion, sustained VT/VF after PPCI in the HORIZONS-AMI trial was not significantly associated with 3-year mortality or major adverse clinical events. Further studies are required to address the prognostic significance of VT/VF in patients with STEMI undergoing PPCI.     

Cardiac troponin T and cardiac enzymes after external transthoracic cardioversion of ventricular arrhythmias in patients with coronary artery disease

BACKGROUND: Serum levels of cardiac troponins after external cardioversion (ECV) for atrial fibrillation and atrial flutter are widely investigated, and no increases in cardiac troponin T (cTnT) levels have been reported. However, the effect of ECV on cardiac enzyme release may depend on the type of arrhythmias. Furthermore, ventricular tachycardia (VT) or ventricular fibrillation (VF) could cause release of cardiac enzymes after ECV due to underlying myocardial ischemia, myocardial dysfunction, or more pronounced hemodynamic deterioration during arrhythmia. AIM: The purpose of this study was to determine whether direct current (DC) shock may increase cardiac enzyme levels in patients with coronary artery disease undergoing ECV for VT or VF, so that diagnosis of acute myocardial infarction, which initially presents with VT or VF, can be excluded. METHOD AND RESULTS: We obtained measurement of cTnT, total creatine kinase (CK), and CK MB isoenzyme (CK-MB) activity before and after ECV in 27 patients (mean +/- SD age, 62 +/- 13 years) with induced VT or VF (22 patients) who required ECV during provocative electrophysiologic testing and who underwent ECV due to VT (5 patients) in the cardiology department. Blood samples were drawn before, and 4 h, 8 h, and 24 h after ECV. The total energy used was 630 +/- 375 J (range, 200 to 1,280 J). CK levels rose to the upper limit of reference range in seven patients (26%), and CK-MB activity was higher than the normal reference range in five patients (19%) after ECV. In contrast, cTnT concentrations remained within the normal range (< 0.1 micro g/L) in all patients. Peak CK and CK-MB activity levels strongly correlated with the total energy delivered. CONCLUSION: Elevation of cTnT level after an urgent DC shock strongly indicates the diagnosis of acute myocardial infarction presented with life-threatening arrhythmias, rather than myocardial damage caused by ECV.     

What is the best predictor of spontaneous ventricular tachycardia and sudden death after myocardial infarction?

BACKGROUND. Death during the first year after myocardial infarction is most commonly due to spontaneous ventricular tachycardia (VT) or fibrillation (VF). The purpose of this study was to compare, in a single cohort of patients, the values of inducible VT, delayed ventricular activation, low left ventricular ejection fraction, high-grade ventricular ectopy, and ST segment displacement on exercise in predicting electrical events (witnessed instantaneous death and spontaneous VT or VF) during the first year after myocardial infarction. METHODS AND RESULTS. Three hundred sixty one patients aged less than 71 years underwent electrophysiological study, signal-averaged electrocardiogram, gated blood-pool scan, 24 hour ambulatory electrocardiographic monitoring, and exercise testing 1-2 weeks after myocardial infarction and were then followed up for at least 1 year. There were 34 deaths (eight witnessed instantaneous, 26 other), and nine patients survived one or more episodes of spontaneous VF or VT. Patients with inducible VT were 15.2 times more likely to suffer electrical events than patients without inducible VT. No proportional-hazards model excluding inducible VT was as good a predictor of electrical events as was inducible VT alone. CONCLUSIONS. Inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden death after myocardial infarction.     

Predictors of new malignant ventricular arrhythmias after coronary surgery: a case-control study

OBJECTIVES: We sought to investigate the relationship between perioperative factors and the occurrence of ventricular tachycardia (VT) and ventricular fibrillation (VF), as well as the impact of VT/VF on early and late mortality. BACKGROUND: Both VT and VF are rare but serious complications after coronary artery bypass graft surgery (CABG), and their etiology and implications remain uncertain. METHODS: Data on 4,411 consecutive patients undergoing CABG (1,154 [25.8%] had off-pump surgery) between April 1996 and September 2001 were extracted from a prospective database and analyzed. Odds ratios (ORs) describing associations between possible risk factors and VT/VF were estimated separately. Factors observed to be significantly associated with VT/VF were further investigated using multivariate logistic regression. RESULTS: Sixty-nine patients suffered VT/VF (1.6%). There were 61 (1.4%) in-hospital/30-day deaths, 15 among patients who had postoperative VT/VF (21.7%). Patient factors independently associated with an increase in the odds of VT/VF included age <65 years, female gender, body mass index <25 kg/m(2), unstable angina, moderate or poor ejection fraction, and the need for inotropes and an intra-aortic balloon pump (OR 1.72 to 4.47, p < 0.05). After adjustment, off-pump surgery was associated with a substantial but nonsignificant protective effect against VT/VF (OR 0.53, 95% confidence interval [CI] 0.25 to 1.13; p = 0.10). Actuarial survival at two years was 98.2% among patients who had VT/VF and who survived to discharge/30 days, compared with 97.0% for the control group (adjusted hazard ratio 0.96 (95% CI 0.40 to 2.31, p = 0.92). CONCLUSIONS: The incidence of VT/VF is low in patients undergoing coronary surgery but is associated with high in-hospital mortality. The late survival of the discharged VT/VF patients compares favorably with that of controls.     

Identification of patients at high risk for recurrence of sustained ventricular tachycardia after healing of acute myocardial infarction.

A prognostic index for nonfatal recurrences of ventricular tachycardia (VT) was developed using a retrospective analysis of a group of 206 patients with sustained monomorphic VT or ventricular fibrillation (VF) after healing of acute myocardial infarction. 74 patients (36%) (64 with VT and 10 with VF) had recurrences of sustained monomorphic VT during 3.4 +/- 9 years of follow-up. Three clinical variables were selected and weighted by stepwise logistic discriminant analysis of the study group. They were coded as follows: interval of myocardial infarction to arrhythmia (less than 2 months = 1; 2 to 6 months = 2; greater than 6 months = 3), drug therapy with or without sotalol (with = 1, without = 2), and VT or VF as the presenting arrhythmia (VT = 1, VF = 2). The prognostic index was: 3.41 - (0.56 x interval) - (1.94 x therapy) + (0.86 x arrhythmia). This index was validated prospectively in a test group of 158 consecutive patients with VT or VF after healing of acute myocardial infarction. Patients were allocated into different classes with decreasing prognostic index values associated with increasing risk for recurrences of VT. In the test group, 27 of 158 (17%) patients (22 with VT and 5 with VF) had recurrences of VT (follow-up of 2 +/- 2 years). Two risk classes of patients were identified: high risk for recurrences of VT (61%) corresponding to patients with a negative index; and low risk (4%) consisting of those with a positive index. Thus, using O as the cutoff point, the sensitivity, specificity, and positive and negative predictive values were 81, 89, 62 and 96%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

A new protocol of programmed stimulation for assessment of predisposition to spontaneous ventricular arrhythmias

We have devised a simple method for identifying predispositionto spontaneous sustained ventricular fibrillation (VF) and tachycardia(VT). A standardized protocol of programmed stimulation wasapplied to 111 control subjects without ventricular diseaseand with no history of VF or VT (Group I) and to 27 patientswith previous myocardial infarction and documented spontaneous(in the absence of evidence of further acute myocardial ischaemia)VF or VT (Group II). The stimulation protocol consisted of singleand paired ventricular extrastimuli introduced during ventriculardrive at the right ventricular apex and ouflow tract, at twicediastolic threshold current intensity and at 20 mA. None ofthe Group I subjects exhibited VF or sustained (more than 10s) VT. In contrast sustained arrhythmias were induced in 24(89%) of Group II patients. We conclude: In our study population,initiation of a sustained ventricular tachyarrhythmia at programmedstimulation was both a sensitive (89%) and specific (100%) indicatorfor predisposition to spontaneous VF and VT.     

Determinants of induced sustained arrhythmias in survivors of out-of-hospital ventricular fibrillation

We prospectively studied 196 consecutive survivors of out-of-hospital ventricular fibrillation (VF) not associated with acute myocardial infarction and 46 consecutive, control patients without prior ventricular arrhythmias. Programmed stimulation included two extrastimuli (S3 protocol) in all patients and three extrastimuli (S4 protocol) in the last 140 study patients and in all control patients. Sustained ventricular tachycardia (VT) or VF was not induced in any control patient. In study patients, logistic regression identified two independent predictors of induced, sustained VT for both S3 and S4 protocols: prior spontaneous, sustained VT (37 patients; p less than or equal to .001) and prior myocardial infarction (113 patients; p = .005). With the S3 protocol, sustained VT was induced in 54% of patients with both prior myocardial infarction and prior sustained VT vs 4% without either; with the S4 protocol, sustained VT was induced in 91% vs 13%, respectively. Eighty-three percent of induced VT episodes had a cycle length less than 300 msec, and all required termination by cardioversion or pacing. VF was induced only in survivors of out-of-hospital VF without prior, spontaneous, sustained VT (S3 protocol, 9%; S4 protocol, 24%) but not in study patients with prior sustained VT (S3, p = .10; S4, p = .05) or control patients (S3, p = .06; S4, p = .01). The mean coupling intervals of extrastimuli that induced VF were not significantly different from the intervals that induced sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Detection of prior myocardial infarction patients prone to malignant ventricular arrhythmias using wavelet transform analysis

Ventricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death remains responsible for significant mortality in patients with prior myocardial infarction (MI). The study population consisted of 50 normal controls and 50 patients with prior MI. The MI subjects were divided into 3 groups: VT/VF (-) group; 25 patients without ventricular tachyarrhythmia, VT group; 13 patients with sustained VT, and VF group; 12 patients with resuscitated VF. The parameters on the signal-averaged ECG and the frequency components recorded from the wavelet-transformed ECG were compared. The high-frequency components (HFC; 80-150 Hz) were developed in the MI group to a greater extent than those in the control group. Among the MI patients, the HFC were more developed in the VT and VF groups than in the VT/VF (-) group. In the VF group, the positive rate of LP was 50%. Meanwhile, when the peak power value at 150 Hz > 300 was defined as abnormal, the HFC was detected in 13 (100%) patients in the VT group and 12 (91.7%) in the VF group. The sensitivity of the abnormal HFC in identifying patients with VT/VF was higher than that of SAECG (96% versus 72%), although the specificity remained similar (68.5% versus 64.3%). Abnormal HFC recorded from the wavelet-transformed ECG may be a novel factor in detecting patients who are prone to VT/VF.     

米诺环素预处理对大鼠缺血性室性心律失常的影响

目的观察米诺环素(MC)预处理对大鼠心肌缺血性室性心律失常的影响并探讨其可能机制。方法采用冠状动脉左前降支结扎法建立大鼠心肌梗死(MI)模型。将60只雄性SD大鼠随机分成6组:MI组,MI+MC组,MI+LY294002(LY)组,MI+5-羟基癸酸(5-HD)组,MI+MC+LY组及MI+MC+5-HD组。各组在制作MI模型前分别给予生理盐水、MC、LY、5-HD、MC+LY、MC+5-HD预处理。持续心电监护,观察缺血30 min内各组室性心动过速(VT)和心室颤动(VF)发生率、以及VT+VF持续时间、发生次数和室性心律失常的严重程度。缺血30min后迅速摘取心脏,用TTC法测心肌梗死面积。结果与MI组比较,MI+MC组的VT发生率无明显变化(P0.05),但VF发生率显著降低,VT+VF持续时间、发生次数和严重程度以及心肌梗死面积显著减少(P均0.05);而MI+MC+LY组及MI+MC+5-HD组上述指标与MI组无差异。结论 MC预处理可以减轻大鼠MI诱导的室性心律失常,这种作用可能与3-磷酸肌醇激酶/Akt信号通路和线粒体ATP敏感性钾离子通道的激活有关。     

Endocardial excitation and conduction during reperfusion arrhythmias

In order to clarify the role of Purkinje fibers in the occurrence of reperfusion arrhythmias, endocardial mapping was performed on perfused canine hearts by attaching 42 close bipolar electrodes to the endocardial surface of the left ventricular septum. Reperfusion with oxygenated Krebs-Ringer solution following 30 min of coronary occulusion induced ventricular tachycardia (VT) in 14 out of 23 preparations. These VT degenerated into ventricular fibrillation (VF) within 1 min after the reperfusion in all but 3 cases. Endocardial mapping revealed that the excitations during VT were always initiated by the Purkinje activities and that myocardial excitations were expanded in a centrifugal manner through Purkinje-muscle junctional area. Furthermore, this excitation pattern was preserved, in the early phase of VT, even though the propagation pattern was distorted. VF was always induced by reperfusion following 30 min of ischemic condition, that is, coronary perfusion with a hyperkalemic (K = 10 mM), acidic (pH = 6.8) and hypoxic (PO2 = 20-40 mmHg) solution (4/4 cases). Elimination of hyperkalemia from the ischemic condition markedly prevented occurrence of VF (1/6 cases) during reperfusion but it did not affect occurrence of VT (4/6 cases); this implies that hyperkalemia causes the onset of VF but has less effect on the occurrence of VT. It has been separately confirmed by micro-electrode experiment, using the dissected papillary muscle of the canine right ventricle, that abnormal impulse formation during re-oxygenation was triggered in Purkinje fibers around Purkinje-muscle junction.