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1.
In order to elucidate biosynthesis and secretion of natriuretic peptides in the early phase of acute myocardial infarction (AMI), we measured the plasma level of brain natriuretic peptide (BNP), a novel cardiac hormone secreted from the ventricle, in patients with AMI and compared with that of atrial natriuretic peptide (ANP). The plasma level of BNP increased rapidly (within hours from the onset of AMI) and markedly (greater than 100 times the normal level) as compared to that of ANP. The plasma ANP level correlated with pulmonary capillary wedge pressure (PCWP), whereas the plasma BNP level did not correlate with PCWP but highly correlated inversely with cardiac index. These results indicate that BNP is secreted from the heart much more acutely and prominently than ANP in the early phase of AMI, in association with left ventricular dysfunction.  相似文献   

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目的:实验观察左心室脱血回注循环辅助法对急性心肌梗死血流动力学的改善作用.方法:18只杂种犬分两组制作急性心肌梗死泵衰竭模型,治疗组给予左心室脱血回注循环辅助,对照组不进行治疗.观察比较两组间心律失常、死亡率、外周动脉压、肺动脉毛细血管楔嵌压(PCWP)、左心室舒张末期压(LVEDP)、左心室内径的变化.结果:治疗组室性期外收缩、心室纤颤发生率和死亡率显著低于对照组;对照组的外周动脉收缩压低于80 mmHg以下,治疗组维持在100mmHg以上(P<0.01);治疗组PCWP和LVEDP值在45 min以后的各时段低于对照组(P<0.01);治疗组的左室舒张末期内径小于对照组(P<0.01).结论:左心室脱血回注循环辅助法能够减少急性心肌梗死泵衰竭的心室纤颤发生率和死亡率,有显著改善血流动力学、防止梗死后心肌扩张和有效的左心室辅助作用.  相似文献   

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李文  张鸿举  丁少娟  梁毅  刘孝钧 《生物磁学》2011,(14):2747-2749
目的:探讨急性心肌梗死(AMI)早期脑钠肽(BNP)水平与左室重构及预后的关系。方法:用放射免疫法测定AMI患者早期血浆BNP水平;用超声心动图检查测量左室收缩末容积(ESV)、左室舒张末容积(EDV)、射血分数(EF)并通过计算得左室质量(LVM)。并根据左心室容积指标分组,左心室容积增加率〉20%为左心室重构组,否则为非重构组,比较两组血浆BNP水平。结果:重构组恢复期左心室舒张末期及收缩末期容积指数均高于非重构组(P〈0.01),亦高于急性期左心室容积(P〈0.01)。重构组早期血浆BNP浓度明显高于非重构组(P〈0.01),恢复期也较非重构组高(P〈0.01)。重构组早期BNP浓度与恢复期左心室容积及容积变化量之间呈正相关。结论:AMI早期BNP升高与急性期左室重构密切相关,血浆BNP浓度可以作为溶栓治疗再通的观察指标及预后判断依据。  相似文献   

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目的:观察大鼠急性心肌梗死后不同时间心肌钙敏感受体(CaSR)的表达和心肌细胞凋亡的变化情况。方法:健康Wistar大鼠随机分为假手术组(Sham)和心肌梗死(AMI)组,通过结扎左侧冠状动脉前降支的方法,建立大鼠心肌梗死模型,分别在手术后1、2、4周(每组成功存活n=5)检测心脏形态学和血流动力学的改变,检测心肌组织中CaSRmRNA和蛋白的表达,以及Bax、Bcl-2、caspase-3和caspase-9蛋白的表达,检测血清中乳酸脱氢酶(LDH)、肌酸激酶(CK)活性和肌钙蛋白(cTnT)水平,观察心肌细胞凋亡情况。结果:和Sham组相比,随着心肌梗死的发展,AMI组大鼠心肌组织CaSR的mRNA和蛋白的表达、细胞凋亡指数均明显增加(P<0.05),心肌细胞超微结构损伤严重;左心室收缩压(LVSP)、左心室内压最大上升速率(+dp/dtmax)(mmHg/s)和最大下降速率(-dp/dtmax)(mmHg/s)减少,左心室舒张末期压(LVEDP)明显增大(P<0.05);AMI组血清cTnT水平、CK和LDH活性均升高(P<0.05),随着心肌梗死的发展,cTnT水平和CK活性逐渐降低,LDH变化不明显。心肌组织中促凋亡相关蛋白Bax、caspase-3、caspase-9表达增多,抑制凋亡的相关蛋白(或因子)Bcl-2表达减少(P<0.05)。结论:随着AMI的发展,AMI组大鼠心肌组织中CaSR的mRNA和蛋白的表达增多,细胞凋亡数增加,表明CaSR参与了心肌梗死的发展,其机制可能与促进细胞凋亡有关。  相似文献   

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The aim of this investigation was to determine the effect of exercise training on the levels of plasma cytokines and acute phase reactants in the early post acute myocardial infarction (AMI) period. Sixty patients were enrolled into this three-week cardiac rehabilitation study. The mean time from AMI was 7.08 +/- 1.60 days, and the patient mean age was 60 +/- 10 years. Subjects were randomly assigned to one of the two groups: the control group treated with standard measures, and the group with additional regular moderate-intensity exercise training. Physical activity was based on the ergospirometry test results. Apart from clinical follow-up and routine laboratory analysis we determined the levels of plasma cytokines: tumor necrosis factor (TNF-alpha), soluble TNF-alpha receptor 1 (TNF-alphaSR1), interleukin (IL)-8, IL-10, and acute phase reactants: high sensitivity C-reactive protein (hsCRP) and fibrinogen. The obtained results confirmed the hypothesis that the early post AMI period is an inflammatory state the intensity of which gradually decreases with standard treatment during the first month after AMI, while including patients into early exercise training improves their inflammatory profile by decreasing the level of acute phase reactant and TNF-alphaSR1.  相似文献   

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目的制备猪急性心肌梗死冠状动脉介入治疗(AMI—PCI)后无复流(no—reflow)动物模型。方法五指山小型猪26头,行左、右冠状动脉造影和左心室造影,记录有创血流动力学参数,通过球囊闭塞、微血栓注入造成左前降支无复流,监测体表和冠脉内心电图变化。结果制模共有21头猪成活,19头达到AMI—PCI后无复流动物模型标准,即TIMI血流≤2级,校正的TIMI血流记帧法(CTFC)≥36.2帧,制模成功率73.1%。无复流模型建立成功后心率增快,血压下降,心肌耗氧量增加,左心室舒张期末压和肺毛细血管楔压升高,较闭塞前均具有统计学差异(P〈0.05)。实验过程中,体表心电图和冠状动脉内心电图均出现类似人AMI再灌注的心电图演变规律。结论选择性冠状动脉前降支急性闭塞、再灌注、微血栓注入制备的无复流小型猪动物模型是可行的。  相似文献   

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目的:观察冠脉介入治疗的急性心肌梗死(AMI)患者的左室重构与血清脂肪特异性丝氨酸蛋白酶抑制剂(vaspin)和白介素-6(IL-6)水平的相关性。方法:入选的研究对象(50例)均来自于2018年9月~2019年6月就诊于同济大学附属普陀人民医院且被诊断为AMI的住院患者,患者均经早期经皮冠脉介入(PCI)治疗,术后规范药物治疗。采用酶联免疫吸附实验(ELISA)测定50例患者发病后1天、7天、30天的血清vaspin和IL-6水平并行超声心动图检查。同时以50例健康体健者作为对照组。比较两组间血清vaspin、IL-6水平的差异,观察AMI后血清vaspin、IL-6水平的变化趋势及其与左室重构的指标包括左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)的相关性。结果:(1)对照组血清vaspin水平为6.03±1.18 ng/mL,AMI组血清vaspin水平4.22±1.37 ng/mL,AMI组血清vaspin水平明显低于对照组(P0.05),且AMI后1月内血清vaspin水平逐渐降低(P0.05);对照组血清IL-6水平为12.04±3.97 ng/mL,AMI组血清IL-6水平为26.72±10.06 ng/mL,AMI组患者血清IL-6水平明显高于对照组(P0.05),且AMI后1月内血清IL-6水平逐渐升高(P0.05);(2)经相关性分析显示:AMI后1天、7天、30天血清vaspin水平与LVEDD、LVESD均呈负相关(P0.05),血清IL-6水平与LVEDD、LVESD均呈正相关(P0.05),血清vaspin水平与IL-6水平均呈负相关(P0.001)。结论:急性心肌梗死后早期,左室重构的进展伴随着血清vaspin的降低与IL-6的升高,临床上应监测两种指标的变化,对左室重构早期干预,预防心力衰竭的发生。  相似文献   

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目的:脑利钠肽后处理对兔急性心肌梗死的保护作用及可能机制。方法:30 只兔随机分为3 组,每组10 只,左冠状动脉的左 室支缺血30 分钟,再灌注120 分钟。AMI(急性心肌梗死)组:再灌注期间静脉滴注生理盐水;BNP(脑利钠肽)组:再灌注期间静脉 滴注rhBNP(重组人脑利钠肽);BNP+GLY(脑利钠肽+格列苯脲)组:再灌注期间静脉滴注rhBNP,同时舌下静脉注射GLY 。连续 监测心电变化,统计再灌注120 min 室性心动过速(VT)、心室颤动(VF)的发生率。心肌再灌注120 min 后,分别测定SOD(超氧化 物歧化酶)、MDA(丙二醛)、cTnI(肌钙蛋白I)、CK-MB(肌酸激酶同工酶)。各组随机抽取2 只兔,分别于再灌注1 小时和2 小时末 取心尖组织,HE 染色。结果:(1)再灌注心律失常:BNP 组与AMI组比较,VT 和VF发生率均明显升高(均为P<0.01);BNP+GLY 组与BNP 组比较,VT 和VF 发生率均明显升高(均为P<0.01)。(2)SOD、MDA、cTnI 和CK-MB 水平:BNP 组与AMI 组比较, MDA、cTnI 和CK-MB 均明显降低(均为P<0.01),而SOD 明显升高(P<0.01);BNP+GLY 组与BNP 组比较,MDA、cTnI 和 CK-MB 均明显升高(分别为P<0.01,P<0.05和P<0.01),而SOD明显降低(P<0.01)。(3)心肌HE 染色:AMI组和BNP+GLY 组心 肌损伤明显,BNP 组心肌损伤轻微。结论:脑利钠肽后处理对兔急性心肌梗死(缺血- 再灌注损伤)具有保护作用,可能与KATP 通道相关。  相似文献   

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目的:研究曲美他嗪(TMZ)联合麝香保心丸(HMP)治疗急性心肌梗死的效果。方法:采用40只雄性C57BL/6J小鼠构建急性心肌梗死模型,随机分成4组,每组10只:(1)假手术组;(2)心肌梗死组;(3)心肌梗死+TMZ组(TMZ 20 mg/Kg灌胃,3次/天);(4)心肌梗死+TMZ+HMP组(HMP 14 mg/Kg灌胃,3次/天)。2周后行心脏超声检查采集心功能参数左室舒张末内径、左室收缩末内径、室间隔厚度、舒张末期左室后壁厚度及射血分数。同时,对心脏标本行形态学分析。结果:TMZ+HMP组左室舒张末内径、左室收缩末内径、舒张末期左室后壁厚度及射血分数均优于于TMZ组(均为P0.05)。心肌组织HE及PSR染色显示TMZ+HMP组心肌细胞坏死及纤维化程度较其余组低。结论:曲美他嗪联合麝香保心丸治疗急性心肌梗死的效果较单用曲美他嗪更加显著。  相似文献   

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No in vivo data exist about the relationship of circulating granulocyte-macrophage colony stimulating factor (GM-CSF) and soluble adhesion molecules ICAM-1 and VCAM-1 (sICAM-1 and sVCAM-1) to the severity of acute myocardial infarction (AMI) and the pathophysiological events of post-infarction left ventricular dysfunction. We investigated the kinetics of these inflammatory mediators in the plasma of patients with AMI, and correlated the findings with the clinical severity of the disease during the first week of hospitalization as well as the degree of left ventricular dysfunction one month after the AMI. Plasma levels of inflammatory markers were determined in 41 AMI patients (all received thrombolytic treatment) by ELISA assays, serially during the first week of hospitalization and one month after hospital admission. Patients (n = 20) with uncomplicated AMI (Killip class I) were classified as group A, patients (n = 21) with AMI complicated by heart failure manifestations (Killip classes II and III) were classified as group B, while 20 age- and sex-matched volunteers were used as healthy controls. A sustained increase in GM-CSF, sICAM-1 and sVCAM-1 plasma concentrations was observed only in group B during the first week of the study. Patients from group B exhibited significantly higher levels of GM-CSF (P < 0.01), sICAM-1 (P < 0.05) and sVCAM-1 (P < 0.01) than patients from group A and the healthy controls (P < 0.001). In group B patients, significant correlations were observed between the peak of GM-CSF levels and the peak of serum creatine kinase-MB (r = 0.42; P < 0.05), white blood cell counts (r = 0.67; P < 0.001) and LVEF (r =- 0.51; P < 0.01). At one month follow-up, patients (n = 17) with severe post-infarction left ventricular dysfunction (LVEF 35%). Significant correlations were observed between GM-CSF levels and left ventricular end-diastolic volume index (r = 0.55; P < 0.001) or left ventricular end-systolic volume index (r = 0.49; P = 0.001). We have found a significant elevation of plasma GM-CSF and soluble adhesion molecules during the course of AMI, with the highest values in patients with AMI complicated by heart failure manifestations and severe left ventricular dysfunction. These monocyte-related inflammatory mediators may actively contribute to the pathophysiology of the disease and post-infarction cardiac dysfunction.  相似文献   

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目的:探讨急性心肌梗死(AMI)早期脑钠肽(BNP)水平与左室重构及预后的关系.方法:用放射免疫法测定AMI患者早期血浆BNP水平;用超声心动图检查测量左室收缩末容积(ESV)、左室舒张末容积(EDV)、射血分数(EF)并通过计算得左室质量(LVM).并根据左心室容积指标分组,左心室容积增加率>20%为左心室重构组,否则为非重构组,比较两组血浆BNP水平.结果:重构组恢复期左心室舒张末期及收缩末期容积指数均高于非重构组(P<0.01),亦高于急性期左心室容积(P<0.01).重构组早期血浆BNP浓度明显高于非重构组(P<0.01),恢复期也较非重构组高(P<0.01).重构组早期BNP浓度与恢复期左心室容积及容积变化量之间呈正相关.结论:AMI早期BNP升高与急性期左室重构密切相关,血浆BNP浓度可以作为溶栓治疗再通的观察指标及预后判断依据.  相似文献   

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Experimental data suggest that atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) act locally as antifibrotic factors in heart. We investigated the interrelationships of natriuretic peptides and collagen markers in 93 patients receiving thrombolytic treatment for their first acute myocardial infarction (AMI). Collagen formation following AMI, evaluated as serum levels of amino terminal propeptide of type III procollagen, correlated with NH(2)-terminal proANP (r = 0.45, P < 0.001), BNP (r = 0.55, P < 0.001) and NH(2)-terminal proBNP (r = 0.50, P < 0.01) on day 4 after thrombolysis. Levels of intact amino terminal propeptide of type I procollagen decreased by 34% (P < 0.001), and levels of carboxy terminal cross-linked telopeptide of type I collagen (ICTP) increased by 65% (P < 0.001). ICTP levels correlated with NH(2)-terminal proBNP (r = 0.25, P < 0.05) and BNP (r = 0.28, P < 0.05) on day 4. Our results suggest that ANP and BNP may act as regulators of collagen scar formation and left ventricular remodeling after AMI in humans. Furthermore, degradation of type I collagen is increased after AMI and may be regulated by BNP.  相似文献   

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Serum levels of atrial natriuretic peptide (ANP) are elevated in chronic heart failure presumably due to dilatation of the left atrium resulting from increases in intracardiac pressures. To define the time course of changes in serum ANP levels and to determine the relationship to left ventricular end-diastolic pressure, rats were subjected to coronary artery ligation to produce myocardial infarction and left ventricular failure. Atrial natriuretic peptide levels were measured weekly for four weeks thereafter. In rats with myocardial infarction and elevation of left ventricular end-diastolic pressure there was no change in ANP levels at 7 and 14 days. However, at day 21 and 28, ANP levels were elevated more than 3 fold. There was a correlation between ANP levels and left ventricular end-diastolic pressures. There was no correlation between ANP levels and right atrial pressures or serum sodium concentrations. We conclude that the chronic elevation of left ventricular end-diastolic pressure is required to produce an increase in ANP after myocardial infarction which results in chronic heart failure.  相似文献   

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目的建立一种稳定可重复的大鼠急性心肌梗死动物模型。方法SD大鼠经口气管插管,呼吸机辅助呼吸,开胸结扎冠脉左前降支。术后28 d行心脏超声,血流动力学及组织病理学检查。结果大鼠术后存活率60%;手术组LVEF较假手术组显著降低(P〈0.01);与假手术组比,手术组的LVSP明显下降(P〈0.05),±dp/dt显著降低(P〈0.01),而LVEDP明显升高(P〈0.01);病理组织学检查可见瘢痕形成,纤维组织增生。结论本文建立心肌梗死动物模型的方法操作简便、重复性好。  相似文献   

17.
We have previously reported the marked increase in plasma levels of endothelin-1 in patients with acute myocardial infarction (AMI). To investigate the effects of severe myocardial ischemia on the production of endothelin-1, plasma concentrations of endothelin-1 were measured by a sandwich-type enzyme immunoassay that we developed recently in both the coronary sinus and the aorta of dogs with artificially induced AMI. Dogs were anesthetized and chests were opened. The proximal left anterior descending coronary artery was completely occluded by ligation for 1 h and then was reperfused for 1 h. Throughout the experiment (at the end of occlusion for 1 h, at the beginning of reperfusion, at the end of reperfusion for 1 h), plasma endothelin-1 levels were not significantly altered either in the coronary sinus or in the aorta. The present findings indicate that severe myocardial ischemia itself does not affect the production of endothelin-1 in the coronary circulation of dogs.  相似文献   

18.
Catestatin is a peptide which is a potent inhibitor of catecholamine secretion and played essential functions in the cardiovascular system. Previous research found that dramatic changes of catestatin were associated with hemodynamics in acute myocardial infarction (AMI) during the first week after the AMI symptoms onset, but whether catestatin is also involved in the pathophysiological progression after AMI and then a predictor for outcomes is not clear. The aim of this study is to determine the correlation of plasma catestatin levels at different time points and the prognosis of AMI. 100 participants recruited were all patients with AMI, all of who received successful primary percutaneous coronary intervention (PCI) within 12h from the AMI symptom onset in our center; the concentrations of plasma catestatin were evaluated from blood samples of those 100 participants. Subsequent 65 months'' follow-up was performed after discharging to evaluate cardiac adverse events and the association between catestatin levels and prognosis of AMI was examined. We confirmed the dramatic change of catestatin concentrations in the first week of AMI, and the levels of catestatin on D3 were much higher in adverse events group than those in non-adverse events group (p<0.0001), but the ratio of D7/D3 was significantly lower. In addition, the Kaplan-Meier analysis showed that the groups in which the levels on D3 were higher (p<0.0001) and the ratios of D7/D3 were lower (p<0.0001), patients trended to be more susceptive to adverse events after AMI. Furthermore, according to the analysis, we surmised catestatin level on D3 as an appropriate predictor for outcomes in patients with AMI with good specificity as well as sensitivity. All of the evidence confirmed that catestatin plays an important role in the progress of AMI, and may act as a promising target for prognostic prediction.  相似文献   

19.
目的:观察急性心肌梗死(AMI)患者围手术期血浆apelin的表达变化,分析AMI合并2型糖尿病(T2DM)患者血浆apelin的表达与预后的相关性,探讨apelin在冠脉介入治疗(PCI)中的心脏保护作用。方法:72例于2012年2月~8月在我院心内科接受冠状动脉造影确诊为AMI并成功完成PCI的冠心病患者,分别在术前、术后0小时、术后4小时、术后24小时收集血清,酶联免疫吸附法测定血浆apelin-13水平;进一步对糖尿病及非糖尿病AMI患者(每组各20例)进行亚组分析,随访两组患者在术后6个月时主要不良心脑血管事件(MACCE)。结果:AMI患者术后0 h组apelin水平与术前基线水平明显降低(31.54±5.48 vs35.15±6.48 ng/L,P0.05);术后4小时及24小时组apelin水平较术前明显升高(39.65±5.48 vs 35.15±6.48 ng/L,43.93±5.37 vs35.15±6.48 ng/L,P0.05)。糖尿病与非糖尿病组apelin水平术前无明显差异;糖尿病组在术后各时间点的apelin水平均明显高于非糖尿病组(31.12±5.50 vs 29.21±6.53 ng/L,40.57±5.37 vs 33.49±3.89 ng/L,43.50±7.41 vs 34.54±3.52 ng/L,P0.05)。两组术后6个月随访T2DM组LVEF值改善明显高于NT2DM组,但MACCE事件无明显差异。结论:AMI患者PCI术后存在血浆apelin表达的升高,其中糖尿病患者在术后血浆apelin表达较非糖尿病患者明显增高,提示PCI冠脉血运重建可促进糖尿病患者apelin分泌,调节胰岛素抵抗改善预后。  相似文献   

20.
目的:观察急性心肌梗死伴新发左、右束支传导阻滞的临床特点,评价束支阻滞对急性心肌梗死预后的影响。方法:对上海交通大学附属第一人民医院心内科重症监护室2010年1月1日到12月31日收治的197例急性心肌梗死患者的病历资料进行回顾性分析,根据束支传导阻滞有无及类型分为左束支传导阻滞组(12例),右束支传导阻滞组(19例)和对照组(无束支传导阻滞的急性心梗,166例)。分析和比较三组患者的基线资料,心梗部位、Killip分级、恶性室性心律失常、左室射血分数LVEF、病变血管数量、梗死相关冠脉、住院天数及病死率、实验室检查(BNP,心肌损伤标志物峰值)。结果:LBBB组AMI患者的恶性心律失常发生率明显高于对照组(P=0.007),LVEF明显低于RBBB组和对照组(P值分别为0.020、0.045),梗死相关动脉以LAD多见。结论:急性心梗伴束支传导阻滞往往提示病情严重,预后不良,急性心梗合并左束支阻滞较合并右束支阻滞病情更严重。  相似文献   

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