黄芪对大鼠心肌梗死后左室胶原的影响

目的观察黄芪对大鼠急性心肌梗死后左室胶原的影响。方法结扎大鼠冠状动脉制成急性心肌梗死模型,随机分组,分别予黄芪,开搏通,黄芪加开搏通,空白治疗,每组又按观察时间分为２周组和６周组,并于观察时间末测血浆血管紧张素Ⅱ和醛固酮及心脏局部血管紧张素Ⅱ的浓度,于观察时间末测左室非梗死区心肌羟脯氨酸含量及心肌Ⅰ型、Ⅲ型胶原蛋白的比值。结果发现黄芪可以降低大鼠心梗６周后血浆和心脏血管紧张素Ⅱ及血浆醛固酮的浓度。结论黄芪可降低左室非梗死区胶原含量,降低Ⅰ型、Ⅲ型胶原蛋白比值     

心肌梗死模型大鼠运动诱导后的缓激肽表达

背景：运动促进冠状动脉侧支循环生成涉及众多的促血管生成相关因子,单纯对一个因子的研究很难明确侧支循环生成的信号通路和传导途径,许多促血管生长因子都与激肽释放酶-激肽系统相关,而运动对该系统的影响目前未见报道。 目的：观察运动诱导对心肌梗死大鼠缓激肽表达的影响。 方法：健康Wistar大鼠30只,随机分为对照组、心肌梗死组及运动组。对照组只开胸,缝扎点穿线,不进行冠状动脉结扎;其余2组制备心肌梗死模型。运动组在成功造模后给予跑台运动,30 min/d,运动4周。实验终点时取血以ELISA法检测大鼠血清缓激肽水平,采用左心房注射微球法取大鼠心肌组织测定相对血流量。 结果与结论：实验结束时运动组缓激肽水平显著高于心肌梗死组（P 〈 0.001）,心肌梗死组缓激肽水平显著高于对照组（P 〈 0.05）。心肌相对血流量实验结束时心肌梗死组、运动组均显著高于同组实验开始前（P 〈 0.05,P 〈 0.001）,实验结束时运动组心肌相对血流量显著高于心肌梗死组（P 〈 0.01）。各组大鼠血清缓激肽含量与心肌相对血流量存在显著相关性。提示运动可以刺激缓激肽表达水平显著升高,使心肌血流量明显增加,说明激肽释放酶激肽系统在运动诱导的血管新生中发挥作用。     

Effects of trimetazidine,a partial inhibitor of fatty acid oxidation,on ventricular function and survival after myocardial infarction and reperfusion in the rat

Trimetazidine (TMZ), a partial inhibitor of fatty acid oxidation, has been effective in treating chronic angina, but its effects on the development of post‐myocardial infarction (MI) left ventricular remodeling are not defined. In this study, we tested whether chronic pre‐MI administration of TMZ would be beneficial during and after acute MI. Two‐hundred male Wistar rats were studied in four groups: sham + TMZ diet (n = 20), sham + control diet (n = 20), MI + TMZ diet (n = 80), and MI + control diet (n = 80) splitted into one short‐term and one long‐term experiments. Sham surgery consisted of a thoracotomy without coronary ligation. MI was induced by coronary occlusion followed by reperfusion. Left ventricle (LV) function and remodeling were assessed by serial echocardiography throughout a 24‐week post‐MI period. LV remodeling was also assessed by quantitative histological analysis of post‐MI scar formation at 24 weeks post‐MI. During the short‐term experiment, 10/80 rats died after MI, with no difference between groups (MI + control = 7/40, MI + TMZ = 3/40, P = 0.3). In the long‐term experiment, the deaths occurred irregularly over the 24 weeks with no difference between groups (MI + control = 16% mortality, MI + TMZ = 17%, P = 0.8). There was no difference between groups as regard to LV ejection fraction (MI + control = 36 ± 13%, MI + TMZ = 35 ± 13%, P = 0.6). In this experimental model, TMZ had no effects on the post‐MI occurrence of LV dysfunction or remodeling. Further investigations are warranted to assess whether the partial inhibition of fatty acid oxidation may limit the ability of the heart to respond to acute severe stress.     

Na+/H+交换器-1反义RNA对大鼠肺动脉平滑肌细胞增殖的影响

目的 :探讨反义 RNA对大鼠肺动脉平滑肌细胞 Na / H 交换器 (NHE) 1表达和活性、细胞内 p H(p Hi)的影响 ,及其与细胞增殖的关系。方法 :构建含 NHE 1反义 RNA序列的 p L XSN反转录病毒重组载体 ,将其转染体外培养的大鼠肺动脉平滑肌细胞 ,G4 18筛选后获取含有重组载体的细胞克隆 ,检测细胞 NHE 1m RNA表达、2 2 Na摄取量、p Hi和 3H Td R掺入量。结果 :与转染 p L XSN空载体的细胞和正常对照组细胞比较 ,转染了重组载体的肺动脉平滑肌细胞中 NHE 1m RNA表达、2 2 Na摄取量明显减少 ,同时伴有 p Hi降低和 3H Td R掺入量减少 ,正常对照组和空载体组间无显著差异。结论 :NHE 1反义 RNA可以减少 NHE 1表达 ,从而诱导细胞酸化 ,抑制肺动脉平滑肌细胞增殖     

依那普利对犬急性右心室心肌梗死心源性休克血流动力学指标的作用

目的观察依那普利、单纯补液对急性右心室心肌梗死(RVMI)心源性休克时血流动力学指标的作用。方法结扎犬冠状动脉造成大面积RVMI并发心源性休克模型。随机分为对照组、补液组、依那普利组。观察各组正常时、梗死后即刻及给药后即刻、1h、1周时点的平均动脉压(MAP)、心排血量(CO)、右心房压力(RAP)、右心室收缩压(RVSP)等血流动力学指标,并评价疗效。结果快速补液后,RAP进一步升高,加重了血流动力学变化。依那普利治疗后RAP降低,CO增加,血流动力学变化得以改善。结论大面积RVMI心源性休克时,快速扩容治疗在RAP≥13mmHg时会进一步损害左、右心室功能,依那普利可降低右心后负荷,增加CO,能有效纠正休克。     

Improved early risk stratification and diagnosis of myocardial infarction, using a novel troponin I assay concept

BACKGROUND: We evaluated the clinical performance of a novel cardiac troponin I (cTnI) assay specifically designed to improve the very early risk stratification in acute coronary syndromes. SUBJECTS AND METHODS: Serum and plasma samples (taken 0, 6-12 h and 24 h after admission) from 531 patients with suspected acute coronary syndrome were studied using a novel investigational cTnI assay, reference cTnI assay and myoglobin. The lowest cTnI concentration giving a total assay imprecision of 10% was used as the positive myocardial infarction (MI) cut-off value. RESULTS: At the time of admission, the investigational assay was positive in 27.9% of the patients, the reference cTnI assay was positive in only 17.5% (P < 0.001) and myoglobin in 24.1% (P = 0.067). Receiver operating characteristic (ROC) curve analysis for the detection of myocardial injury on admission gave area-under-curve (AUC) values of 0.937, 0.775 and 0.762, respectively (P < 0.001). Of those MI patients who presented within 3 h of symptom onset, 50.0% were identified by the investigational assay at the time of presentation, compared with 44.2% by myoglobin (P = 0.791) but only 11.5% by the reference assay (P < 0.001). CONCLUSIONS: The novel cTnI assay considerably improves the performance of cTnI as an early rule-in biomarker for MI.     

双龙丸对实验性心肌梗死形态学和血流动力学的影响

目的探讨活血通络类中药双龙丸对心肌梗死后心脏血流动力学和心肌梗死面积的影响。方法参照Drexler法结扎冠脉左前降支 ,制成急性心肌梗死 (AMI)模型。 66只大鼠分为双龙丸大剂量组 (18只 )、双龙丸小剂量组 (19只 )、正常对照组 (10只 )和心肌梗死对照组 (19只 )。各组半数治疗 2周 ,半数治疗至 4周 ,治疗结束时分别行股动脉和颈总动脉插管 ,应用 8导生理记录仪检测心脏血流动力学参数 ,Masson’s染色测定心肌梗死面积。结果治疗 2周和 4周 ,双龙丸大、小剂量组较同期心肌梗死对照组的左室最大收缩速率增高 (P <0 .0 5或P <0 .0 1) ,且大剂量 2周组较心肌梗死对照组的左室最大舒张速率亦增高 (P <0 .0 5 ) ;大剂量组在 2周和 4周时均较心肌梗死对照组的梗死面积减小 (P <0 .0 5 )。结论双龙丸能提高实验性心肌梗死大鼠的左室最大收缩速率 ,大剂量应用还可改善心肌梗死早期左室舒张功能 ,限制心肌梗死范围的扩展     

Identification of residual ischemia,infarction, and microvascular impairment in revascularized myocardial infarction using 64‐slice MDCT

This study aimed to assess the potential of 64‐slice MDCT in characterizing revascularized infarcted myocardium at the cellular and microvascular levels. Pigs (n = 7) underwent 2 h left anterior descending coronary artery occlusion/reperfusion. In acute (2–4 h) and subacute (1 week) infarction, first‐pass perfusion (FPP) (1 ml/kg of 300 mg/ml Omnipaque) was performed using a cine (rotation time 60 s/bpm) non‐ECG gated sequence (mAS/kV = 100/120). Delayed contrast enhanced images (DE) (mAS/kV = 650/120) were acquired every 2 min for 10 min to determine the kinetics of Omnipaque and to define infarcted myocardium and microvascular impairment (representing microvascular obstruction and/or no‐ or low‐reflow phenomenon). Maximum upslope, maximum attenuation and time to the peak were measured from FPP plots. 2,3,5‐Triphenyltetrazolium‐chloride (TTC) was used to define true infarction in the excised hearts. Hyperenhanced myocardium on DE was measured and compared with TTC. The contrast media caused minor beam hardening and X‐ray scatter on FPP. The above‐mentioned perfusion parameters significantly differed between remote and acute infarction. Infarcted myocardium showed two patterns of enhancement on DE, hyperenhanced rim representing the perfused infarction and hypoenhanced core representing a microvascular impaired region, with significantly different attenuation. The extent of infarction on DE‐MDCT decreased over the course of 1 week and did not differ from TTC. Post‐processed FPP semi‐quantitative images showed a decline in myocardial blood volume and flow in acute revascularized infarction. In conclusion, modern MDCT has the potential to identify residual ischemia on FPP and microvascular impairment and infarction on DE images. Copyright © 2008 John Wiley & Sons, Ltd.     

脂微球携载前列腺素E1对急性心肌梗死后康复及心功能的影响

探讨脂微球携载前列腺素E1(Lipo-PGE1)在急性心肌梗死后对心功能和血管内皮功能的影响,从而了解其对急性心肌梗死康复的作用。方法:随机将71例住院急性心肌梗死后3―6个月的患者分为两组,治疗组36例在常规治疗基础上,加用Lipo-PGE110μg/天,静脉滴注,共2周;对照组仅接受常规治疗。分别观察两组在治疗前后心功能、内皮功能指标的变化。结果:两组治疗后心功能有不同程度的改善:两组收缩功能的变化无显著差异,而治疗组在治疗后内皮功能指标、左室舒张功能的改善则具有显著差异(P<0.05)。结论:在常规治疗基础上,加用脂微球携载前列腺素E1更能有效地改善心肌梗死康复期患者的血管内皮功能和左室舒张功能。     

缺血后处理对急性心肌梗死患者血清神经生长因子和心肌梗死面积的影响

目的探讨缺血后处理对急性心肌梗死(AMI)患者血清神经生长因子(NGF)和心肌梗死面积的影响及意义。 方法选择2016年1月至2019年12月吉林市中心医院心内科收治的200例发病12 h内的AMI患者,且急诊行经皮冠状动脉介入(PCI)治疗,采用随机数字表法,分为缺血后处理组和对照组,各100例。缺血后处理组采用球囊预扩张反复充盈、回吸的方法,实现梗死相关动脉的缺血再灌注处理,对照组则给予常规PCI术。比较两组患者血清心肌损伤标记物、NGF水平和心肌梗死面积。 结果入院时,缺血后处理组血清肌酸激酶同工酶(CK-MB)[(96.55±4.68)U/L]、心肌肌钙蛋白I(cTnI)[(21.03±2.25)μg/L]和血清NGF水平[(0.13±0.06)ng/L]与对照组[(97.38±5.46)U/L、(21.24±2.36)μg/L、(0.12±0.04)ng/L]比较,均差异无统计学意义(t＝1.15,0.64,1.39;均P>0.05)。入院后3 d,缺血后处理组cTnI水平[ (22.96±2.46)μg/L]低于对照组[(39.85±3.68)μg/L],CK-MB[(101.28±3.46)U/L]、血清NGF水平[(0.22±0.03)ng/L]高于对照组[(93.50±5.68)U/L、(0.14±0.06)ng/L],均差异有统计学意义(t＝38.16,11,70, 11.93 ;均P<0.05)。入院后7 d和14 d,缺血后处理组CK-MB[(13.43±2.35)U/L、(4.23±1.38)U/L]、cTnI[(6.33±1.38)μg/L、(0.78±0.14)μg/L]和血清NGF水平[(0.14±0.04)ng/L、(0.12±0.04)ng/L]均低于对照组[CK-MB(15.48±4.96)U/L、(6.47±1.35)U/L;cTnI(7.75±2.47)μg/L、(1.15±0.39)μg/L;NGF(0.22±0.05)ng/L、(0.19±0.05)ng/L],均差异有统计学意义(t＝3.74,11.60,5.02,8.93,12.49,10.93;均P<0.05)。AMI发病6个月后,两组间不同心肌梗死面积人数比较,差异有统计学意义(χ²＝50.08,P<0.05)。 结论经缺血后处理的AMI患者血清NGF水平呈动态变化,峰值提前,可做为缺血后处理有效及判断预后的指标。缺血后处理可有效减少AMI患者心肌梗死面积。     

8周不同运动干预对心肌梗死大鼠心功能的影响

目的:探究8周高强度间歇性运动(high intensity interval training,HIIT)、中等强度持续运动(continuous moderateintensity training,CMT)、静息(sedentary,SED)干预对心肌梗死(myocardial infarction,MI)后心脏功能的影响及其分子机制。方法:24只大鼠随机分为对照组(CON)、心梗静息组(MI-SED)、心梗CMT组(MI-CMT)、心梗HIIT组(MI-HIIT),分别进行8周干预,观察实验终点时左心室射血分数(left ventricular ejection fraction,LVEF)、心肌梗死面积比及过氧化物酶体增殖物激活受体γ辅激活因子1α(peroxisome proliferator-activated receptor gamma coactivator 1-alpha,PGC1-α)表达。结果:干预8周后,①与MI-SED组比较,MI-CMT、MI-HIIT组梗死面积比均显著降低(14.93±1.934%,PMI-CMT=0.000;16.72±1.125%,...     

运动训练对心肌梗死后心室重构及MMP-2,MMP-9表达的影响

目的:观察大鼠心肌梗死(MI)后早期运动训练对左心室(LV)重构、心室功能、心肌间质胶原、基质金属蛋白酶(MMPs)的影响。方法:SD大鼠随机分为假手术组(Sham组)、MI对照组(AMI-Sed组)和MI+运动训练组(AMI-Ex组),结扎前降支建立MI模型。手术后1周Ex组进行8周跑台训练(运动强度相当于45%VO2max),术后第9周测量各组大鼠左心室重量、血液动力学参数,处死大鼠,用Masson染色检测左心室非梗死区心肌胶原容积分数(CVF),RT-PCR检测Ⅰ、Ⅲ型胶原纤维mRNA表达,Westernblot检测非梗死区心肌基质金属蛋白酶-2(MMP-2)及基质金属蛋白酶-9(MMP-9)蛋白表达。结果:与Sham组比较,AMI-Sed、AMI-Ex组左心室重量指数(LVWI)和左心室长轴径(LVLA)均显著增加(P0.05),运动训练对LVWI和LVLA无明显影响;与AMI-Ex组比较,AMI-Sed组RVWI、肺含水率显著增高,左心室压峰值(LVSP)和左心室压力变化最大值(+dp/dtmax)显著降低,左心室压力负最大值(LVEDP)显著升高(P均0.05);与AMI-Sed组比较,AMI-Ex组大鼠左心室非梗死区CVF降低,Ⅰ、Ⅲ型胶原纤维mRNA表达量均降低(P0.05),以Ⅰ型胶原纤维表达降低为著;与Sham组比较,AMI-Sed、AMI-Ex组MMP-2表达均显著升高(P0.05),MMP-9无显著变化;AMI-Ex组MMP-2蛋白表达显著低于AMI-Sed组(P0.05)。结论:AMI后早期运动训练可抑制非梗死区心肌纤维化、改善左心室重构及左心室功能,机制可能与抑制胶原纤维合成有关,MMP-2表达变化对此可能发挥一定作用。     

Effects of glucose-insulin-potassium on baroreflex sensitivity,left ventricular function and ventricular arrhythmia in the subacute phase of myocardial infarction in rats

Glucose-insulin-potassium (GIK) is clinically used for reducing mortality in acute myocardial infarction (MI). It is known that ventricular arrhythmia, left ventricular dysfunction and impaired baroreflex sensitivity (BRS) are the three major determinants for predicting the mortality after acute MI. The present work was designed to study the effects of GIK on BRS, ventricular arrhythmia, and left ventricular function in rats with coronary artery ligature. Sprague-Dawley rats were used and the myocardial infarction was produced by ligature of the left anterior descending artery. Five weeks after coronary artery ligation, BRS was measured in conscious state with a computerized blood pressure monitoring system and left ventricular function and electrocardiogram were determined in the anaesthetized state in the subacute phase of myocardial infarction. It was found that GIK did not affect the blood pressure and heart period in both conscious and anaesthetized rats. GIK did not enhance BRS, but reduced ventricular arrhythmia and improved left ventricular function by reducing left ventricular end diastolic pressure in anaesthetized rats with MI. It is proposed that reducing ventricular arrhythmia and improving left ventricular function contribute to the effect of GIK on reducing the mortality after MI.     

瑞舒伐他汀钙对高脂血症大鼠心肌梗死后神经重构及心室颤动阈值的影响

目的：探讨瑞舒伐他汀钙对高脂血症大鼠心肌梗死(MI)后神经重构及心室颤动阈值的影响。方法将MI 模型制作成功的20只高脂血症大鼠随机分为2组：B 组(MI 组);C 组(MI+瑞舒伐他汀钙组),每组各10只;另设A 组(假手术组,n =10)。1月后行心脏电生理及 M 型超声心动图检测,应用免疫组化法检测梗死周边区酪氨酸羟化酶(TH)及生长相关蛋白43(GAP-43)阳性神经纤维分布及密度,并采用实时定量 RT-PCR 法对 MI 后神经生长因子(NGF)的变化进行检测。结果与 A 组比较,阳性神经纤维密度以及 NGF mRNA 表达在 B、C 组明显增加(P 均<0.05),心室颤动阈值明显降低(P <0.05)。C 组阳性神经纤维密度和 NGF mRNA 表达均较 B 组显著减少(P 均<0.05),心室颤动阈值明显升高(P <0.05)。结论瑞舒伐他汀钙通过改善高脂血症大鼠 MI 后神经重构以及提高心室颤动阈值而起到预防室性心律失常的作用,其机制可能与 NGF 表达下调有关。     

早期短期给予caspase抑制剂对于急性心肌梗死大鼠心功能影响的实验研究

目的评价早期、短期给予caspase抑制剂对于急性心肌梗死大鼠心功能的影响,并探讨其机制。方法将Wistar大鼠随机分为3组心肌梗死组、治疗组、假手术组。应用超声心动图评价心功能;caspase-3活性检测试剂盒测定caspase-3活性;TUNEL法检测心肌细胞凋亡情况。结果治疗组较心肌梗死组左室舒张末期直径(LVEDd)、左室收缩末期直径(LVESd)明显降低,而射血分数(EF)、左室短轴缩短率(FS)明显升高。治疗组较心肌梗死组caspase-3活性及凋亡指数(AI)明显降低。结论早期、短期给予caspase抑制剂可以有效改善心肌梗死大鼠心功能。抑制心肌细胞凋亡和改善心室重构是其主要作用机制。     

尼可地尔对猪急性心肌梗死再灌注后无再流的影响

目的评价尼可地尔防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪24只,随机分成对照组、尼可地尔组和假手术组,每组8只。结扎冠状动脉(冠脉)3h、松解1h制备AMI再灌注模型。AMI前后和再灌注后均行血流动力学测定和心肌声学造影(MCE)检查,最终行病理学分析。结果1与AMI前相比,对照组AMI后3h左室收缩压(LVSP)、心排血量(CO)和左室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0.05或P<0.01),左室舒张末压(LVEDP)显著升高(P<0.01);再灌注后1h仅LVSP显著恢复(P<0.05),±dp/dtmax继续显著下降(P均<0.05)。尼可地尔组AMI后3h各项指标变化与对照组相同;但再灌注后1hLVSP、LVEDP、±dp/dtmax和CO均恢复,差异有显著性(P<0.05),且比对照组更显著(P均<0.05)。2对照组MCE和病理染色所测冠脉结扎区心肌范围(LA%)高度一致(P>0.05),再灌注后无再流范围(ANR%)分别为(78.50±4.35)%和(82.30±1.90)%,心肌坏死范围(NA%)为(98.50±1.35)%。尼可地尔组LA%虽与对照组相当(P均>0.05),但两方法所测ANR%和NA%均显著小于对照组(P<0.05或P<0.01)。3对照组再灌注即刻和再灌注后1h冠脉血流量(CBV)仅占AMI前的50.6%和45.8%(P均<0.01);尼可地尔组CBV分别提高到69.4%和67.9%,均比对照组显著增加(P均<0.01)。结论尼可地尔能有效防治AMI再灌注后无再流,改善其心功能,缩小梗死面积。     

hVEGF165腺相关病毒对心肌梗死大鼠心功能的影响

目的探讨直接心肌注射基因重组hVEGF165腺相关病毒（rAAV—hVEGF165）对急性心肌梗死大鼠心功能的影响。方法取81只雄性Sprague—Dawley大鼠,制备急性,0．／肌梗死大鼠模型。将心肌梗死大鼠模型随机分成4组：假手术组15只;心肌梗死组25只;生理盐水纽25只;VEGF组16只。生理盐水组和VEGF组分别接受生理盐水或rAAV—hVEGF165100μ1分3点注射于梗死交界处心肌内。于注射4周后测定心肌组织VEGF含量、超声心动图参数、梗死范围、微血管数量、心钠素（atrial natriuretic peptide,ANP）水平。结果假手术组中3只大鼠、心肌梗死组中13只大鼠、生理盐水组中15只大鼠、VEGF组中7只大鼠死亡,43只大鼠进入研究。VEGF组心肌梗死范围较心肌梗死组和生理盐水组明显减小（38．6±3．0）％VS（42．5±3．8）％、（42．5±2．6）％（P〈0．05）。VEGF组的左心室射血分数显著高于心肌梗死组和生理盐水组（61．11±8．37）％VS（44．17±5．31）％、（39．40±5．48）（P〈0．01）。VEGF纽心肌组织中VEGF含量较心肌梗死组和生理盐水组有所增加。血管计数显示,VEGF组有更多的新生血管形成（522．38±82．14）mm2vs（419．99±32．17）mm2、（420．86±16．50）mm2（P〈0．01）。结论梗死区交界处心肌内直接注射rAAV-hVEGF165能够显著改善急性心肌梗死大鼠的心功能,缩小梗死范围,促进心肌内新生血管的形成。     

吗啡对急性心肌梗死再灌注损伤保护效应的实验研究

目的　通过测定急性心肌梗死再灌注损伤模型大鼠的血浆降钙素基因相关肽 (CGRP)、内皮素(ET 1)浓度及心肌梗死面积的变化 ,探索吗啡对急性心肌损伤的保护机制。方法　将 4 0只 SD大鼠随机分为单纯缺血再灌注模型组、吗啡预处理组、吗啡 纳洛酮组和手术对照组 ,每组各 10只。采用戊巴比妥钠(40 m g/ kg)腹腔注射麻醉大鼠 ,采用穿线结扎左冠状动脉前降支制备大鼠心肌缺血再灌注模型。用放射免疫法测定血浆 CGRP和 ET 1浓度 ,同时测定血清中肌酸磷酸激酶同工酶 (CK MB)含量 ;用氯化三苯四唑(TTC)法染色和数码照相计算机图像分析系统计算心肌梗死面积。结果　大鼠左冠状动脉前降支结扎 10 m in时血浆 ET 1和 CGRP浓度较手术对照组显著增高 (P均 <0 .0 1) ;再灌注 4 .5 h时吗啡预处理组血浆 ET 1及 CK MB浓度较结扎 10 m in时显著降低 ,心肌梗死面积也显著缩小 (P均 <0 .0 1) ;而血浆 CGRP浓度则显著增高 (P<0 .0 1) ;吗啡预处理组以上变化较吗啡 纳洛酮组差异有统计学意义 (P均 <0 .0 1)。结论　吗啡预处理可通过显著降低 ET 1而增加 CGRP血浆浓度、缩小心肌梗死面积 ,对急性心肌梗死后再灌注心肌产生保护效应。