Immediate effects of captopril in acute left ventricular failure secondary to myocardial infarction

Abstract. In eight patients with acute left ventricular failure secondary to myocardial infarction the haemo-dynamic effects of captopril (25 mg), an orally active converting enzyme inhibitor, were measured. Haemo-dynamic modifications were maximal at 60 min and lasted for 2–3 h. Pulmonary wedge pressure fell from 23–5± 4.9(mean ± SD)to 16–8 ± 4.7 mmHg(P<0–01), cardiac output rose from 3–24 ± 1 to 4–05 ± 0–91 1/min (P<001). Systemic vascular resistance decreased from 27–34 ± 3–81 to 17.52 ± 1–65 mmHg min 1^-1 (P<001). Mean arterial pressure fell from 89.6 ± 13.9 to 75.7±0 16.3 mmHg (P<0001) while heart rate was not significantly modified. Six patients who had high pretreatment plasma renin activity values responded by a decrease in ventricular filling pressure and/or an increase in cardiac output. One patient with normal initial plasma renin activity value showed similar haemodynamic effects. These data suggest that in the short term captopril is a vasodilator with both arterial and venous effects and improves cardiac function in acute left ventricular failure secondary to myocardial infarction.     

构建心肌梗死后充血性心力衰竭大鼠模型

背景:结扎大鼠左前降支冠状动脉可造成梗死部位相对一致的心肌梗死,其左室功能和病理生理改变与临床心肌梗死相似.作者的一系列研究均是以该模型为基础.目的:建立和完善大鼠心肌梗死后充血性心力衰竭模型并进行评估.设计、时间及地点:配对样本观察,于2007-01/08主要在美国南加州大学完成.材料:8月龄健康雄性SD大鼠10只,体质量 (500±25)g,分为实验组10只,假手术组8只.方法:实验组大鼠结扎冠状动脉左前降支,造成左心室前壁心肌梗死;假手术组动物只开胸,不结扎左前降支冠状动脉. 主要观察指标:记录大鼠心电图.术后4周超声心动图评估结扎效果,右颈总动脉插管测量血流动力学参数,处死后从左心室根部插管注射蓝色墨水,评价心肌梗死的范围,冰冻切片检查左心室壁的厚度.结果:大鼠术后出现明确的心肌梗死改变,包括心电图的改变、超声心动图测量射血分数下降、血流动力学测定左心室舒张末期压升高,dP/dt40 和-dP/dt下降、蓝色墨水提示的大面积心肌梗死及冰冻切片证实左心室前壁厚度明显变薄. 结论:结扎左前降支冠状动脉后可较理想地得到心肌梗死后充血性心力衰竭的动物模型.     

Baroreflex control of heart rate in rats with heart failure after myocardial infarction: effects of captopril.

Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 micrograms/kg) and nitroprusside (2-50 micrograms/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute myocardial infarction and renal failure following naphtha ingestion

We present a case of a non-Q wave myocardial infarction and acute renal failure following an ingestion of naphtha, a petroleum distillate composed primarily of hydrocarbons. The patient's renal, metabolic, and cardiac status improved over several days with aggressive volume replacement and bicarbonate therapy. Acute cardiotoxic effects of hydrocarbon exposure generally manifest as dysrhythmias, secondary to myocardial sensitization to circulating catecholamines, or, possibly, coronary vasospasm. Ischemia from associated hypotension or direct myocardial toxicity are other potential causes of naphtha-related cardiac injury.     

心肌梗死后心力衰竭大鼠模型的构建及细胞因子变化

目的 构建大鼠的心力衰竭模型,检测心肌梗死后不同时期血清细胞因子的表达情况,探讨在心力衰竭的发生过程中细胞因子的演变.方法 结扎冠状动脉前降支的方法构建大鼠的心肌梗死后心力衰竭模型,在术前及术后4、16周分别进行心脏超声检查及血流动力学监测,对心功能进行评定,并检测相应血清中TNF-α、IL-6的浓度.结果 ①假手术组应用ELISA法未检测到血清中存在上述两种细胞因子,心力衰竭代偿期TNF-α、IL-6的血清浓度均升高,在心力衰竭失代偿期,尽管仍能检测到TNF-α,但血清水平成明显下降趋势;此时IL-6的血清浓度进一步升高;②在16周时,大鼠的心脏超声与血流动力学检测具有较高的诊断符合率,大鼠心脏超声作为一种无创性的检测手段,可以用于评定大鼠的心脏功能状态.结论 ①细胞因子的持续升高与心肌梗死后心脏功能的恶化有关,不同的细胞因子浓度变化存在不同的时相,TNF-α的升高早于IL-6,呈一过性增高趋势,后者在体内尤其是血清中增高的持续时间较长,表达在心力衰竭的代偿及失代偿期都升高,但失代偿期增高更明显,IL-6的血清细胞因子浓度与心功能损害的关系更大.②在大鼠的心力衰竭模型构建过程中,心脏超声可以替代血流动力学标准用于心力衰竭模型构建过程中的监测.     

Anti-apoptotic and anti-inflammatory effects of hydrogen sulfide in a rat model of regional myocardial I/R

Hydrogen sulfide (H2S) is a novel gaseous mediator produced by cystathionine-beta-synthase and cystathionine-gamma-lyase in the cardiovascular system, including the heart. Using a rat model of regional myocardial ischemia/reperfusion, we investigated the effects of an H2S donor (sodium hydrogen sulfide [NaHS]) on the infarct size and apoptosis caused by ischemia (25 min) and reperfusion (2 h). Furthermore, we investigated the potential mechanism(s) of the cardioprotective effect(s) afforded by NaHS. Specifically, we demonstrate that NaHS (1) attenuates the increase in caspase 9 activity observed in cardiac myocytes isolated from the area at risk (AAR) of hearts subjected in vivo to regional myocardial I/R and (2) ameliorates the decrease in expression of Bcl-2 within the AAR obtained from rat hearts subjected to regional myocardial I/R. The cardioprotective effects of NaHS were abolished by 5-hydroxydeconoate, a putative mitochondrial adenosine triphosphate-sensitive potassium channel blocker. Furthermore, NaHS attenuated the increase in the I/R-induced (1) phosphorylation of p38 mitogen-activated protein kinase and Jun N-terminal kinase, (2) translocation from the cytosol to the nucleus of the p65 subunit of nuclear factor-kappaB, (3) intercellular adhesion molecule 1 expression, (4) polymorphonuclear leukocyte accumulation, (5) myeloperoxidase activity, (6) malondialdehyde levels, and (7) nitrotyrosine staining determined in the AAR obtained from rat hearts subjected to regional myocardial I/R. In conclusion, we demonstrate that the cardioprotective effect of NaHS is secondary to a combination of antiapoptotic and anti-inflammatory effects. The antiapoptotic effect of NaHS may be in part due to the opening of the putative mitochondrial adenosine triphosphate-sensitive potassium channels.     

Improvements in the establishment of a rat myocardial infarction model

Coronary artery ligation is widely used for myocardial infarction (MI) induction in rats but produces a large variation in infarct size--a major determinant of mortality. Accurate control of infarct size is critically important for the establishment of a useful animal model. This study determined the anatomical course of the left anterior descending coronary artery (LAD) by direct visualization in order to locate precisely the position of ligation. MI was induced by conventional methods (control group) or using a detailed anatomical knowledge of the LAD (experimental group). Triphenyltetrazolium chloride (TTC) staining was performed to compare infarct size, and electrocardiogram (ECG) changes were observed. The rate of MI induction was significantly higher in the experimental group than in the control group (89.5% vs 65.6%) and the size of infarction was more consistent in the experimental group. Direct visualization of the rat LAD allowed accurate identification of the ligation site, thereby controlling infarct size and improving the success rate of the rat model.     

Circulatory effects of intravenous and oral acebutolol in acute myocardial infarction

The hemodynamic dose-response effects of intravenous (25 and 50 mg) and oral (200 and 400 mg) acebutolol were compared in a randomized between-group study in men within 17 hours of an acute uncomplicated myocardial infarction. Six subjects were evaluated in each of the four groups. After a 1-hour control period, hemodynamic variables and plasma drug concentrations were determined at 15 (intravenous therapy only), 30, 60, 90, 120, and 240 minutes after dosing. At the doses studied, hemodynamic dose-response effects were not evident after either intravenous or oral acebutolol. In all groups acebutolol reduced systolic and mean systemic arterial pressure, heart rate, cardiac output, and stroke volume. Pulmonary artery occluded pressure and systemic vascular resistance were transiently increased. Maximum changes developed between 15 and 30 minutes after intravenous dosing and between 1 and 2 hours after oral dosing. However, there were substantial reductions in cardiac output (-0.7 L/min/m2; P less than 0.05) by 30 minutes after oral dosing. Effects lasted for 2 hours after intravenous dosing and for 4 hours after oral dosing. Our data confirm the hemodynamic safety of acebutolol after acute myocardial infarction. The relevance of the time-dependent hemodynamic differences between intravenous and oral initiation of beta-blockade to the overall goal of reducing myocardial oxygen requirements after acute coronary artery occlusion merits closer examination.     

Acute myocardial infarction after administration of low-dose intravenous epinephrine for anaphylaxis

This case describes a 29-year-old woman who presented with an acute severe anaphylactic reaction to penicillin. In addition to other medications administered in the emergency department, she received 0.1 mg intravenously of 1:10 000 epinephrine, after which she immediately developed severe chest pain. Her ECG showed ST elevations consistent with an anterior myocardial infarction, and her serum troponin level was elevated. A CT angiogram showed no signs of coronary artery disease or abnormal anatomy. This case is an example of vasospasm-induced myocardial injury and illustrates a potential danger of intravenous epinephrine use. The authors were able to identify only 2 other case reports where therapeutic doses of epinephrine have been reported to cause this phenomenon.     

制备心肌梗死大鼠模型方法的改进

背景：心肌梗死动物模型对于研究人类冠心病的发病机制、病理生理改变以及对治疗方法的评估具有重大意义，提高存活率及制模成功率是许多研究者追求的目标。 目的：对大鼠心肌梗死模型制备方法进行改进。 方法：选取Wistar大鼠100只，分为模型组（n=80）和假手术组（n=20）。3%戊巴比妥钠腹腔麻醉，气管切开，小动物呼吸机辅助呼吸，左侧胸部开胸，第4肋间入胸，结扎左冠状动脉前降支。假手术组大鼠只穿线不结扎。逐层关胸，撤除呼吸机，拔除气管插管。为防止窒息，不缝合气管及颈部切口。 结果与结论：通过观察心脏形态及苏木精-伊红染色鉴定证实心肌梗死模型制作成功率为98.6%。模型组术后3周成活率为88.75%，共死亡9只，其中术中及术后24 h内死亡7只，后期死亡2例，假手术组存活率为100%。通过对大鼠心肌梗死模型制作方法的改进，如麻醉方法、气管切开时采用纵行切口、术后不缝合气管切口，开关胸方法的改进等，提高了手术成功率及大鼠存活率。     

Acute myocardial infarction in a child with myocardial bridge

BACKGROUND:

Myocardial infarction (MI) is rare in children, and Kawasaki disease is now recognized as the main cause for MI. In this report, we present a child with MI caused by myocardial bridge (MB).

METHODS:

A 7.5-year-old boy was admitted to Weifang People’s Hospital on September 16, 2008 for heart disease. By electrocardiogram, coronary CT angiography, emission computed tomography, and other examinations, he was initially diagnosed as having (1) acute inferior myocardial infarction and extensive anterior myocardial infarction; (2) fulminant myocarditis; or (3) coronary myocardial bridge. He was treated with oxygen, thrombolysis, myocardial nutrition, vitamin C (4.0 g per time), dexamethasone (7.5 mg per time), a large dose of gamma globulin, and interferon.

RESULTS:

Myocardial enzymes, liver function, C-reactive protein, and troponin-I returned to normal at 21 days after treatment. At 29 days, electrocardiogram indicated that II, III, aVF, V4 - V6 leads had abnormal Q wave, and ST-T changed. The patient was discharged.

CONCLUSION:

Myocardial bridge may be one of the causes of MI in children.KEY WORDS: Myocardial bridge, Electrocardiogram, Acute myocardial infarction     

新型心肌梗死大鼠模型制备方法的建立和模型鉴定

目的建立可用于制备心肌梗死大鼠模型的新方法。方法异氟醚气体麻醉Sprague-Dawley大鼠后,钝性分离肋间肌,结扎左冠状动脉前降支,制备心肌梗死大鼠模型。以仅穿刺不结扎左冠状动脉前降支的方法制备假手术大鼠模型。术后采用小动物心电图仪、血流动力学分析仪、2,3,5-氯化三苯基四氮唑(TTC)染色及苏木素-伊红(HE)染色鉴定心肌梗死大鼠模型。结果心肌梗死大鼠模型及假手术大鼠模型存活率均为80.0%。心肌梗死模型组大鼠术后第2、7天心电图检查可见ST段明显抬高。血流动力学检测结果显示,心肌梗死模型组大鼠颈总动脉收缩压和舒张压,左心室收缩压,以及左心室压力上升和下降最大速率均较假手术模型组均明显降低,心率和左心室舒张末压则明显增加(P0.05)。TTC染色显示梗死心肌与正常心肌色差明显,坏死心肌呈白色。HE染色显示梗死心肌细胞肿胀、排列紊乱,出现空泡,甚至断裂,部分断裂心肌细胞间隙见炎症细胞浸润。结论建立的方法效果理想且操作简单,适用于心肌梗死大鼠模型的制备。     

代谢综合征/心肌梗死大鼠模型的建立

背景：代谢综合征合并急性心肌梗死是目前临床研究的热点问题之一,但现今有关代谢综合征合并急性心肌梗死动物模型的报告罕见报道。目的：建立代谢综合征/左前降支心肌梗死大鼠模型。方法：将雄性SD大鼠给予高果糖饮食,喂养时间8周,建立代谢综合征模型。再将此模型大鼠结扎左冠状动脉前降支深部建立代谢综合征/心肌梗死大鼠模型。结果与结论：采用高果糖喂养后的大鼠出现了高血压、高三酰甘油以及胰岛素抵抗现象（P〈0.05）。代谢综合征/心肌梗死大鼠模型建模成功率为70%;组织切片可见大量心肌细胞坏死,瘢痕形成;超声心动图显示代谢综合征/心肌梗死模型大鼠左室舒张末内径和收缩末内径显著增加（P〈0.05）,射血分数和缩短分数显著减少（P〈0.05）,有创血流动力学检查提示代谢综合征/心肌梗死大鼠左室收缩压、左心室压最大上升速率和左心室压最大下降速率均下降（P〈0.05）,而左室舒张末期压和心率升高（P〈0.05）。结果证实,采用高果糖喂养可以制作可靠的大鼠代谢综合征模型;采用结扎左前降支方法能成功建立代谢综合征大鼠的心肌梗死模型。     

代谢综合征/心肌梗死大鼠模型的建立

背景:代谢综合征合并急性心肌梗死是目前临床研究的热点问题之一,但现今有关代谢综合征合并急性心肌梗死动物模型的报告罕见报道.目的:建立代谢综合征/左前降支心肌梗死大鼠模型.方法:将雄性SD大鼠给予高果糖饮食,喂养时间8周,建立代谢综合征模型.再将此模型大鼠结扎左冠状动脉前降支深部建立代谢综合征/心肌梗死大鼠模型.结果与结论:采用高果糖喂养后的大鼠出现了高血压、高三酰甘油以及胰岛素抵抗现象(P < 0.05).代谢综合征/心肌梗死大鼠模型建模成功率为70%;组织切片可见大量心肌细胞坏死,瘢痕形成;超声心动图显示代谢综合征/心肌梗死模型大鼠左室舒张末内径和收缩末内径显著增加(P < 0.05),射血分数和缩短分数显著减少(P < 0.05),有创血流动力学检查提示代谢综合征/心肌梗死大鼠左室收缩压、左心室压最大上升速率和左心室压最大下降速率均下降(P < 0.05),而左室舒张末期压和心率升高(P < 0.05).结果证实,采用高果糖喂养可以制作可靠的大鼠代谢综合征模型;采用结扎左前降支方法能成功建立代谢综合征大鼠的心肌梗死模型.     

静脉溶栓治疗急性心肌梗死对血小板功能的激活

目的 急性心肌梗死（AMI）是心血管急症这一，链激酶（SK）、尿激酶（UK）同属第一代溶栓剂，在我国AMI临床治疗中应用广泛。本研究的目的在于比较SK与UK静脉溶栓对血小板、内皮细胞功能、肾素活性的影响及其临床意义。方法 选择符合1979年WHO诊断标准的AMI患者45例，其中16例使用SK治疗（SK组），14例使用UK溶栓治疗（UK组），15例接受常规治疗作为对照组。所有患者于入院即刻及发病后24h、第7天分别采卧位静脉血5ml，测定血栓素B2（TXB2）、6-酮-前列腺素F1a(6-keto-PGF1a)、血浆肾素活性（PRA）、血管紧张素Ⅱ（AngⅡ）的水平。结果 TXB2在SK组治疗前后及对照组各点均有升高，二者比较，差异无显著意义，UK组治疗后（即发病后24h、7thd)较对照组、SK组明显升高；6-keto-PGF1a在3组无变化；二者比值TXB2/6-keto-PGF1a(T/P)在UK组也明显升高；PRA、AngⅡ在3组呈升高趋势，但差异无显著意义。结论 心梗后及SK、UK溶栓后血小板活性均有增强，UK和SK相比，前者使血小板活化作用更强。这种作用可能会限制溶栓的效果，故溶栓治疗中尤其UK溶栓时更应加强抗血小板治疗，包括加大阿司匹林剂量或加用其他更有效的抗血小板制剂。     

解剖M型超声、定量组织多普勒检测心肌梗死大鼠左室局部收缩功能

目的大鼠心肌梗死模型上,探讨急性心肌缺血、梗死及其演变过程中解剖M型超声(AME)、定量组织多普勒速度成像(QTVI)变化规律及特征,比较它们在检测局部心肌收缩功能变化中的相对价值。方法31只SD大鼠分成MI组(n=22)和对照组(n=9)。MI组大鼠在开胸手术下结扎左冠状动脉前降支(LAD),随后复苏饲养4周。对照组动物仅行假手术。应用超声显像仪分别同步记录术前、术后即刻、2周及4周的AME、QTVI图像或曲线,以AME观察左室壁局部收缩期与舒张期厚度(WTs、WTd)及局部室壁增厚率(WTF)、QTVI观察局部心肌内膜下、外膜下及全层室壁组织速度(SPVendo、SPVepi、SPV)。结果与术前基线及对照组对应阶段比较:术后即刻WTd、WTs及WTF呈降低趋势,术后2周及4周WTd、WTs和WTF均呈显著性降低。术后即刻SPVepi及SPV呈降低趋势,而SPVendo则呈显著性降低;术后2周及4周SPVendo、SPVepi及SPV均呈显著性降低。与术前基线及对照组对应阶段比较:大面积MI组WTF在术后即刻即显著降低,而中小面积MI组WTF在术后2周或以上才显著降低;无论大或中小面积MI组,术后即刻SPV即显著降低。AME确定的与组织学确定的心肌梗死的范围无显著性差异(0.28±0.14和0.35±0.13,P>0.05),且两者具有高度相关性(r=0.73,SEE=0.14,P<0.01)。结论AME和QTVI均能对缺血或梗死心肌进行局部心功能定量分析;心肌缺血或梗死面积大小影响AME、但可不影响QTVI对局部心功能异常的早期检测;AME可较好地确定缺血或梗死心肌的受累范围,而QTVI通过检测从心内膜下至心外膜下层心肌的速度梯度变化可区别不同层次的心肌功能。