心肌康颗粒对麻醉开胸犬血流动力学的影响

目的本实验观察心肌康颗粒对正常麻醉开胸犬血流动力学的影响。方法用电磁流量计分别测量冠脉血流量及心输出量,用载波放大器测定左室内压。结果心肌康颗粒可增加心输出量(CO)、冠脉血流量,降低左室舒张末期压(LVEDP)、总外周阻力及冠脉阻力。结论心肌康颗粒可明显降低心肌耗氧量及冠脉阻力,对心脏血流动力学有明显的改善作用。     

冠脉储备的测定及其临床意义

冠脉血流的主要阻力是心肌内小动脉，这些血管的直径从10nm～140nm不等。由于心肌完全依靠有氧代谢，心肌氧耗增加时只能以增加冠脉血流量来满足心肌氧需。而冠脉血流增加主要依靠心肌内小动脉扩张。为了描述冠脉循环最大供血潜力，亦即心肌内阻力血管最大舒张能力。Gxuld等[1]     

冠状动脉搭桥体外循环手术中心肌缺血缺氧性损伤的临床观察

目的以心肌肌钙蛋白(IcTnI)和冠状静脉窦血液氧合参数作为评判指标,观察体外循环(CPB)下接受冠状动脉旁路移植手术患者心肌缺血缺氧性损伤的状况。方法选取择期进行冠状动脉旁路移植手术(CABG)的患者12例,分别于CPB前,主动脉开放后0min、0.5min、1min,1.5min、3min和5min经冠状静脉窦取血,测定血清cTnI浓度,冠状静脉窦血流量和血气值,计算心肌氧输送量、氧耗量及其比值以反映心肌氧代谢状况。结果主动脉开放后,冠状静脉窦内cTnI浓度明显升高(P<0.05),而冠状静脉窦血氧分压和氧饱和度均较高,氧耗量较低(P<0.05),心肌氧输送量/氧耗量比值较高;随着心跳恢复,心肌氧耗增加明显,表现心肌氧输送量/氧耗量比值降低(P<0.01)。结论主动脉阻断期间心肌有一定程度的缺血缺氧性损伤和酸中毒;主动脉开放心跳恢复后,心肌供氧和耗氧状况一般能较快趋于正常,但需注意心肌氧供/氧耗的变化。     

冠心舒对犬实验性心肌缺血及心肌氧代谢的影响

目的 观察中药冠心舒对犬急性缺血性心肌的保护作用.方法 实验犬36只随机分为6组.通过结扎麻醉犬冠状动脉左前降支的方法,造成急性心肌缺血模型.经消化道给药后,测定心率、平均动脉压和冠脉血流量以及动静脉血氧含量,计算心肌耗氧量.免疫组化测定冠心舒对心肌组织中超氧化物歧化酶(SOD)及丙二醛 (MDA)的影响.结果 与模型组相比,中药冠心舒能降低心肌缺血犬的心率,使心肌耗氧量下降,增加其平均动脉压及心肌冠脉血流量,增加血供(P＜0.05,P＜0.01).冠心舒能提高心肌SOD的含量,降低MDA的量(P＜0.05,P＜0.01).结论 冠心舒能增加缺血心肌血供、降低氧耗,并有抗氧化作用.     

红花提取物对急性心肌梗死犬血清微量元素和心肌形态学的影响

目的 观察红花提取物对急性心肌梗死犬血清微量元素和形态学的影响.方法 取杂种犬24只,随机分为4组,每组6只,分别为模型组、阳性药物对照组(地奥心血康胶囊,52.0 mg/kg)、及红花提取物低剂量组(5.5 mg/kg)、红花提取物高剂量组(11.0 mg/kg).结扎犬左冠状动脉前降支,制备急性心肌梗死模型,观察红花提取物对血清微量元素(Cu2+、Zn2+、Ca2+、Mg2+)含量的影响;通过HE染色,观察心肌细胞形态学的变化.结果 与模型组比较,红花提取物各剂量组血清微量元素Cu2+含量降低(P<0.05),Zn2+、Ca2+、Mg2+含量增加(P<0.05,P<0.01),缺血心肌细胞的病理形态学损伤程度减轻.结论 红花提取物对实验性心肌梗死犬的心肌具有明显的保护作用.     

急性心肌梗死患者脂蛋白（a）与纤维蛋白原及冠脉病变的关系探讨

目的 探讨急性心肌梗死(AMI)患者血浆脂蛋白(a)[Lp(a)]与纤维蛋白原(Fig)及冠脉病变的相关关系.方法 102例AMI患者检测血脂和Fig,并行冠脉造影检查,按血浆Lp(a)浓度分为高Lp(a)组(≥300 mg/L)和低Lp(a)组(<300 mg/L),比较两组血浆Fig及冠脉病变特点的差异.结果 Lp(a)与Fig、冠脉狭窄分数、有明显相关性(P<0.01).高Lp(a)组的Fig水平、冠脉狭窄分数、梗死相关血管的残余狭窄程度、血管闭塞率均明显高于低Lp(a)组(P<0.05),其心肌梗死溶栓治疗试验(TIMI)血流评分明显低于低Lp(a)组(P<0.05).结论 血浆Lp(a)升高的AMI患者,其Fig水平也异常升高,冠状动脉狭窄分数增加,IRA的残余狭窄程度加重,血流速度缓慢,血管闭塞率增加.     

有氧运动对急性心肌梗死患者预后的改善研究

目的探讨12周及24周的有氧运动对急性心肌梗死患者心功能及氧代谢功能的影响。方法选取50例急性ST段抬高型心肌梗死并行急诊PCI的患者,随机分为有氧运动治疗(运动组)及非运动治疗(对照组)各25例,2组患者给予相同药物治疗,于入院后第8天、第12周及24周检查无氧阈值、峰值氧耗量、以及LVEF、N末端B型钠尿肽前体(NT-proBNP)水平。结果与对照组比较,运动组第12周及24周后无氧阈值[(15.05±5.80)ml/(kg·min)vs(14.78±1.50)ml/(kg·min),(15.94±0.86)ml/(kg·min)vs(14.43±1.82)ml/(kg·min),峰值耗氧量[(22.31±2.50)ml/(kg·min)vs(19.50±2.52)ml/(kg·min),(23.06±2.13)ml/(kg·min)vs(19.79±2.89)ml/(kg·min)],LVEF[(55.8±2.8)%vs(53.3±5.1)%,(56.5±2.9)%vs(53.7±5.2)%]明显升高,而NT-proBNP[(2171.4±1014.0)ng/L vs(2922.8±1342.6)ng/L,(1628.2±740.1)ng/L vs(2476.7±964.8)ng/L]明显降低(P<0.05,P<0.01)。与同组第8天比较,2组12、24周后无氧阈值、峰值氧耗量、LVEF明显升高,而NT-proBNP明显降低(P<0.05,P<0.01),运动组24周较12周时NT-proBNP明显降低(P<0.05)结论有氧运动治疗可以明显改善急性心肌梗死患者的心功能及氧代谢指标。     

缩醛基毛冬青提取化合物R4对麻醉犬心功能与血流动力学的影响

目的 研究缩醛基毛冬青提取化合物R4对麻醉犬心功能与血流动力学的影响.方法 采用麻醉犬开胸,测定心脏血流动力学参数,并分离冠状动脉左旋支,放置探头测量冠脉血流量,同步测量心输出量.结果 缩醛基毛冬青提取化合物R4 (0.5 mg/kg、1.0 mg/kg、2.0 mg/kg)可降低麻醉犬的血压,减少心肌耗氧量以及减慢心率,降低左室舒张末期压,左心室内压最大上升和下降速率,同时增加冠脉血流量.结论 缩醛基毛冬青提取化合物R4通过减少心肌耗氧量,降低左室舒张末期压及左心室内压最大上升和下降速率,使冠脉流量增加等环节发挥改善麻醉犬心功能与血流动力学的作用.     

高龄急性心肌梗死患者心脏超声及冠脉造影的临床特征研究

目的:分析心脏超声及冠脉造影诊断高龄急性心肌梗死患者的临床特征.方法:将80例急性心肌梗死患者选择,分为高龄组、对照组,均实施心脏超声及冠脉造影诊断.结果:对比对照组,高龄组冠脉病变支数明显更多、血管狭窄程度在70％及以上占比显著更多、心脏超声诊断结果均明显更高,P<0.05.结论:心脏超声及冠脉造影诊断高龄急性心肌梗...     

心肌缺血的病理生理学

心肌缺血是冠状动脉功能不全的主要后果,也是临床对冠心病处理的中心问题。急性缺血更是对患者健康以至生命的严重威胁。心肌缺血的基本发病原因是:(1)冠脉供血不足。常由冠脉阻塞引起,其次见于舒张压过低或舒张期过短的疾病。(2)心肌耗氧过高。多因心肌负荷过重使其代谢增强所致。影响冠脉血流的因素器官血流量是指单位时间内流经该器官的血量。冠脉血流量(CBF)约为85.0 ml分/100g心肌。在一定范围内其流量可通过机体的自我调节而保持相对的稳定。CBF主要受以下几     

Coronary flow velocity immediately after reperfusion reflects myocardial microcirculation in canine models of acute myocardial infarction

Recent reports indicate that the coronary microcirculation is sometimes injured, despite successful reperfusion in acute myocardial infarction (AMI). However, it is difficult to evaluate the coronary microcirculation immediately after reperfusion by using only angiography. The purpose of this study was to examine the relationship between the pattern of coronary blood flow velocity and myocardial microcirculatory injury immediately after reperfusion in AMI. The authors recorded the left circumflex coronary flow velocity by using the Doppler guide wire method 10 minutes after reperfusion in a canine model of AMI. In addition, myocardial contrast echocardiography was performed with the injection of contrast medium into the left circumflex coronary artery before clamping of the coronary artery and 15 minutes after release of the clamp. From these images, the ratio of the normalized gray-level postreperfusion to preclamping in the contrast-enhanced area was determined. It was compared with coronary flow velocity variables. In the 10 dogs with a diastolic-to-systolic velocity ratio (DSVR) < 4.0, this velocity ratio 10 minutes after reperfusion correlated positively (r = 0.75, p < 0.01) with the normalized gray-level ratio. However, the remaining three dogs with a DSVR > or = 4.0 markedly deviated from this pattern. Coronary flow velocities in the three dogs were characterized by a greater decrease in systolic flow velocity and occurrence of early systolic retrograde flow. Myocardial contrast echocardiographic images in these three dogs demonstrated a lower normalized gray-level ratio. In conclusion, the coronary flow velocity pattern immediately after reperfusion may reflect myocardial microcirculatory injury.     

Myocardial contractility, haemodynamics, and metabolism in acute myocardial infarction. Experimental and clinical study

In order to investigate the systemic and central haemodynamics, blood perfusion, and metabolism of the myocardium in acute myocardial infarction (AMI), experiments were carried out in 80 mongrel dogs with experimental AMI, induced by ligation of the descending branch of the left coronary artery, and 183 patients with transmural AMI were clinically followed-up. It was found that after coronary artery ligation the blood flow in the intact myocardial parts increased, whereas in the infarcted zone it decreased. These shifts persisted fairly long after the induction of AMI. Simultaneously the cardiac output markedly tended to decrease in all animals, and this tendency also persisted for the next two days. It was proved that the haemodynamic shifts in question were associated with a decrease in the myocardial biosynthesis of individual fractions of RNA after the coronary artery ligation. The clinical observations confirmed that AMI was accompanied by a decrease in myocardial contractility. The degree of the decrease was directly proportional to the infarct size. The dependence of the changes on the localization of AMI was less marked.     

Relation between the transmural extent of acute myocardial infarction and associated myocardial contractility two weeks after infarction

To characterize the relation between the transmural extent of acute myocardial infarction (AMI) and associated regional contractility after recovery from ischemia, 11 mongrel dogs underwent occlusion of the proximal left anterior descending coronary artery and were evaluated 2 weeks after infarction. Occlusion was permanent in 5 dogs, and reperfusion was allowed after 2 hours of occlusion in 6 dogs. All dogs had computer-assisted quantitative wall-thickening analysis by 2-dimensional echocardiography and infarct localization by the triphenyl-tetrazolium chloride technique. Percent systolic wall thickening was correlated with the transmural extent of AMI in 40 regions of interest, each measuring approximately 60 arc degrees in circumference. In 11 non-infarct-containing regions, the mean wall thickening was 59 +/- 16% (+/- standard deviation). In 29 infarct-containing segments (with transmural extent of infarction 11 to 100%) systolic wall thickening ranged from -4% to 47%. Wall thickening and transmural extent of AMI were inversely related. Least-squares regression analysis found the relation to be best described by the logarithmic function, percent wall thickening = 61 - 26 log (percent transmural extent of infarction +1), r = -0.87. The nature of this relation between structure and function suggests that salvage of small amounts of myocardium (transmural extent less than 30 to 40%) by coronary reperfusion or other means may have little effect on systolic myocardial function when compared with the function of transmural infarcts. Alternatively, salvage of more than 40% of the jeopardized myocardium should be expected to appreciably augment myocardial function.     

快速洋地黄类药对犬实验性急性心肌梗死早期血流动力学、梗死面积的影响

探讨洋地黄类药物对急性心肌梗死早期血流动力学、梗死面积的影响。方法３０只健康种状随机分为对照组及哇巴因组,结扎左冠状动脉前降支,造成实验性ＡＭＩ模型,通过心内导管及主动脉电磁流量计测量结扎前后、用药前后两组血流动力学,冠状动脉流量。心肌Ｎ－ＢＴ染色测量两组梗死面积。     

Nifedipine in acute myocardial infarction

Preliminary experimental and clinical data suggest that nifedipine can abort early acute myocardial infarction (AMI) or decrease infarct size by reversal of coronary artery spasm, improved coronary flow to the ischemic zone, reduction in myocardial oxygen demand or protection of ischemic cells. The first large clinical trial testing the ability of nifedipine to reduce infarct size, the Nifedipine Angina Myocardial Infarction Study, was recently reported. Nifedipine treatment failed to prevent progression of threatened infarction to AMI or to reduce infarct size in patients with AMI. The study suggested an increased early mortality rate in patients with AMI treated with nifedipine, but this finding should be interpreted with caution pending the results of similar trials now in progress.     

急性心肌梗死患者血B-型尿钠肽水平的变化特点

目的观察急性心肌梗死(AMI)后血B-型尿钠肽(BNP)水平升高的特点,探讨AMI后BNP水平升高的意义。方法连续入选住院AMI患者230例及正常对照111例进行BNP测定。按照首次或再发AMI后ST段抬高型或非ST段抬高型AMI(STEMI或NSTEMI)、不同部位AMI、不同冠状动脉病变、不同梗死相关血管(IRA)、IRA不同TIMI血流和是否急诊经皮冠状动脉介入治疗(PCI)进行分组,采用Student-t检验和ANOVA分析对比各组间BNP水平和心功能相关指标的差异。结果AMI后2~7天,患者BNP水平显著升高(P<0.01),平均为(553.7±735.1)ng/L,是对照组的21倍;与首次AMI组对比,再发组左室射血分数(LVEF)显著降低(P<0.01),左室舒张末径(LVEDd)、BNP水平和LnBNP均显著升高(P均<0.01);与无显著狭窄病变AMI患者对比,单支、三支血管狭窄组的BNP水平显著为高(P均<0.05);IRA的TIMI血流0~1、2级组BNP水平均显著高于TIMI血流3级组(P均<0.01);与未急诊PCI组对比,急诊PCI组血肌酸激酶同工酶(CK-MB)、肌钙蛋白T(TnT)虽显著升高(P<0.05~0.01),然BNP水平显著降低(P<0.05)。结论AMI后,血BNP水平显著升高。以再发AMI、未行急诊PCI治疗和IRA血流TIMI0~2级者更高。急诊PCI可出现心肌酶升高,而BNP降低的矛盾现象。     

New theory on the pathogenesis of acute myocardial infarction

Autopsy studies of hearts from 140 patients who had suffered acute myocardial infarction (AMI) and 26 cases of sudden coronary death revealed two distinct types of myocardial cell death: "kinetic cell death" (KD) and "static cell death" (SD). In KD, the predominant type of cell death in AMI-myofibrils disintegrated through alternating overcontraction and overextension. KD was found not only in patients having died after some time had elapsed from the onset of AMI, but also in cases of sudden coronary death. Muscle fibers in SD, which by contrast began to appear at least seven hours after the onset of AMI, characteristically preserved cross striations, while their nuclei were pyknotic or had already disappeared. Such fibers were observed only in territories peripheral to occlusive coronary thrombus, a secondary rather than a primary event that takes place during the course of AMI. As a result of the above observations, we were able to produce a new experimental model of AMI using mongrel dogs. As a preparatory procedure we first injected them intravenously with 2% calcium chloride at a constant rate for 90 or 120 minutes, and then with a sudden injection of caffeine, calcium chloride and catecholamine in order to induce KD. In contrast, ligation of the intraventricular coronary artery near its origin caused SD of myocardial fibers in the dependent territories. Overall results led us to conclude that AMI is initiated by instantaneous overcontraction of myocardial fibers, resulting in their KD, a phenomenon that could be called "myocardial self-destruction."     

急性心肌梗塞冠脉内溶栓与支架术疗效的比较

目的：观察急性心肌梗塞患者冠脉内溶栓及急诊置人支架术的效果。方法：根据冠状动脉造影资料，50例病人中，33例成功支架植入为支架组；17例不适合或支架失败者为冠脉内溶栓组，经导管注入50万单位尿激酶至梗塞相关血管，术中监测TIMI血流，再灌注性心律失常，心电图及心肌酶和心功能。结果：血管开通率，支架组达到97％，冠脉内溶栓组只达到59％，两组差异有显著性（P〈0．05）。结论：植入支架是急性心肌梗塞患者恢复心肌血流灌注的最好方法。对于不适合植入支架者，冠脉内溶栓也是一种值得应用的方法。     

Influence of frequency of atrial contraction on coronary blood flow and ventricular performance in the conscious dog with myocardial infarction.

The effects of alterations in the frequency of contraction on coronary blood flow and ventricular performance were studied in 12 conscious, unsedated dogs with established myocardial infarction. Total and regional coronary blood flow was measured using radioactive microspheres. The peak increase in flow to the right ventricle was 71% to the infarcted area of the left ventricle was 72% to the non-infarcted area of the left ventricle was 90% and to the ventricular septum was 104%. Despite the generalized increases in regional myocardial blood flow, flow tended to decrease to the subendocardial portion of the infarcted area of the left ventricle. The peak increases in coronary flow and the reduction in flow to the subendocardial portion of the infarcted area occurred at a heart rate of approximately 200/min provided by atrial pacing. Myocardial contractility, as evidenced by peak increases of 16% in maximum LV dP/dt and 12% in dP/dtP, was only enhanced with abrupt incremental changes in heart rate and not with continuous atrial pacing over 15-min periods. Despite the generalized increases in coronary perfusion coronary sinus oxygen content decreased with a widening of the coronary arteriovenous oxygen difference indicating increased myocardial oxygen usage. Thus increasing frequency of contraction in myocardial infarction results in a slight initial but not sustained inotropic effect, a moderate and generalized increase in regional myocardial blood flow, increased myocardial oxygen consumption, and the potential for subendocardial extension of the area of myocardial damage within the infarcted area.     

非ST段抬高型与ST段抬高型急性心肌梗塞冠脉造影病变的对比

目的：比较非ST段抬高型与ST段抬高型急性心肌梗塞（AMI）病人冠状动脉血管造影结果。方法：回顾分析我院接受冠脉造影的268例AMI患者的资料,患者被分为A、B两组：A组为非ST段抬高型AMI（NSTEMI）。共148例,B组为ST段抬高型AMI（STEMI）,共120例。结果：非ST段抬高型AMI组冠脉造影病变的血管数及血管狭窄程度明显高于ST段抬高型AMI组的（P〈0．01）。4年随访中NSTEMI组死亡19例（12．8％）。STEMI组死亡9例（7．5％）,NSTEMI组死亡率显著高于STEMI组（P〈0．01）。结论：非ST段抬高型AMI的病情较ST段抬高型AMI更重。