Effect of Specialization in Sports on the Structural and Functional States of the Left Ventricle of the Heart in Schoolchildren of Different Biological Age

The structural and functional states of the left ventricle of the heart were studied by echocardiography in schoolchildren of three age groups. The first group included 10- to 13-year-old boys without features of sexual maturation. The second group included 13- to 15-year-old adolescents during puberty. The third group included 16- to 18-year-old adolescents with developed secondary sexual characteristics. The children were trained in sports: middle-distance running, swimming, and wrestling. It was found that the posterior wall of the ventricular myocardium in young athletes of all age groups and any specialization in sports was thicker than in untrained children of the same age. Similarly, the trained children were characterized by larger anteroposterior size of the ventricular cavity, larger cavity volume and total volume, greater myocardium mass (both absolute and calculated per kg body weight), more substantial ventricular stroke volume, lower heart rate, lesser ejection fraction, and smaller degree of shortening of the anteroposterior size of the ventricular cavity during systole as compared to untrained children of the same age. The difference between trained and untrained schoolchildren increased with increasing age, duration of the period of training in sports, and level of training in sports (athletic qualification). The training-induced changes in the structural and functional parameters of the left ventricle of the heart in middle-distance runners were larger than in schoolchildren trained in swimming and, particularly, in wrestling.     

Factors influencing left-ventricular stiffness

The aim of the study was to investigate the relative contributions of geometrical and material factors to overall left-ventricular cavity stiffness. Left-ventricular cavity shapes were reconstructed using a computer and the variation of myocardial elastic modulus was calculated, by the finite element method, through the passive phase of diastole when rising volume coincided with rising pressure. Geometric data were obtained from biplane cineangiography, with micromanometer pressure measurements, for ten patients with left ventricular disease. Dimensional analysis was applied to the initial and derived data from which the influences of myocardial compliance, wall thickness-to-long dimension ratio, and aspect ratio (long-to-short axes) were determined. The ratio between the volume elasticity and the myocardial modulus of elasticity, the normalized stiffness ratio (NSR), is proposed as a useful index of left ventricular mechanical behaviour in diastole. The volume elasticity of the chamber is dependent not only upon the myocardium elastic modulus and the wall thickness ratio, but also on the shape of the chambe. Changes in the thickness/radius ratio of the ventricle have less effect upon its distention than those in the long dimension/radius ratio. The left ventricle becomes more spherical in shpae through diastole and hence becomes stiffer by this geometric mechanism.     

Effect of glibenclamide and glimepiride treatment on the development of myocardial infarction in rats

The effect of glibenclamide and glimepiride, two orally active antidiabetic sulphonylurea derivatives, on the development of myocardial infarction has been compared. Permanent coronary artery ligation was induced in rats and the development of infarction was evaluated by a computer-assisted method after nitroblue-terazolium staining. Seven-day coronary ligation produced enlargement of the left ventricular cavity, scar thinning and thickening of the non-infarcted myocardium. Glibenclamide treatment (5 mg/kg b.i.d. intraperitoneally) decreased the infarct volume (29.1 +/- 3.5% vs. 39.1 +/- 3.2% in controls), that occurred primarily as a result of more significant thinning of the scar tissue (1.6 +/- 0.04 mm vs. 2.0 +/- 0.13 mm in controls). Glibenclamide also inhibited the thickening of the non-infarcted ventricular septum (2.1 +/- 0.10 mm vs. 2.9 +/- 0.10 mm in controls). In contrast to the effects of glibenclamide, glimepiride treatment (5 mg/kg b.i.d. intraperitoneally) inhibited the enlargement of the left ventricular cavity (15.2 +/- 1.1% vs. 19.9 +/- 1.2% of the left ventricular volume in controls), it did not precipitate scar thinning and did not influence the development of hypertrophy of the non-infarcted myocardium. These results suggest that glimepiride treatment might inhibit the development of left ventricular dilatation after myocardial infarction. Glibenclamide treatment, however, producing a thinning of the scar tissue may further precipitate morphological changes that can contribute to the development of heart failure.     

超声心动图对心肌致密化不全的诊断及临床意义探讨

目的:探讨超声心动图对心肌致密化不全的诊断及临床意义。方法:应用Vivid7、HP5500彩色多普勒超声诊断仪(探头频率为2～4MHz)对32例左室心肌致密化不全患者进行检查,采用二维、M型、彩色及频谱多普勒观察病变心肌及心内膜改变,重点观察心尖段。常规测量各腔室内径、左室壁正常段心肌厚度及动度,评价心室舒张功能、计算左心室射血分数EF及瓣膜反流等基本信息。结果:①受累的心室内膜面可见多发异常粗大的、呈蜂窝状的肌小梁和交错深陷的隐窝形成网状结构。②病变区域心室壁外层的致密心肌明显变薄,为中低回声,较正常心肌薄2~4mm,其心肌厚度<6mm,而内层心肌疏松增厚为强回声。③病变以近心尖部1/3室壁节段最为明显,很少累及室间隔及基底段室壁。④彩色多普勒可示隐窝间隙之间有低速血流与心腔相通。⑤多数患者以渐进性的心功能不全、呼吸困难、体循环栓塞、心律失常为主要表现,本组患者临床表现为心力衰竭22例,心脏杂音3例,心律失常2例,5例无明显不适症状。结论:超声心动图检查是准确、无创诊断心肌致密化不全的首选方法,能够对房室结构和心功能进行全面评价,有助于明确心力衰竭病因并协助治疗,同时也有助于筛查心肌致密化不全家族,对临床治疗起着很好的指导作用。     

超声心动图对心肌致密化不全的诊断及临床意义探讨

目的：探讨超声心动图对心肌致密化不全的诊断及临床意义。方法：应用Vivid7、HP5500彩色多普勒超声诊断仪（探头频率为2～4MHz）对32例左室心肌致密化不全患者进行检查,采用二维、M型、彩色及频谱多普勒观察病变心肌及心内膜改变,重点观察心尖段。常规测量各腔室内径、左室壁正常段心肌厚度及动度,评价心室舒张功能、计算左心室射血分数EF及瓣膜反流等基本信息。结果：①受累的心室内膜面可见多发异常粗大的、呈蜂窝状的肌小梁和交错深陷的隐窝形成网状结构。②病变区域心室壁外层的致密心肌明显变薄,为中低回声,较正常心肌薄2~4mm,其心肌厚度〈6mm,而内层心肌疏松增厚为强回声。③病变以近心尖部1/3室壁节段最为明显,很少累及室间隔及基底段室壁。④彩色多普勒可示隐窝间隙之间有低速血流与心腔相通。⑤多数患者以渐进性的心功能不全、呼吸困难、体循环栓塞、心律失常为主要表现,本组患者临床表现为心力衰竭22例,心脏杂音3例,心律失常2例,5例无明显不适症状。结论：超声心动图检查是准确、无创诊断心肌致密化不全的首选方法,能够对房室结构和心功能进行全面评价,有助于明确心力衰竭病因并协助治疗,同时也有助于筛查心肌致密化不全家族,对临床治疗起着很好的指导作用。     

Cardiac myocyte hypertrophy and proliferating cell nuclear antigen expression in Wistar rats infected with Trypanosoma cruzi

Chagasic cardiomyopathy is a major life-threatening complication of Trypanosoma cruzi infection in human beings. This study focuses on the hypertrophic and hyperplastic mechanisms underlying the structural changes of the heart during experimental infection. Proliferating cell nuclear antigen (PCNA) expression, transversal diameter, nuclear area, and number of nuclei per unit volume were determined in the ventricular myocytes of T. cruzi-infected Wistar rats. PCNA expression was enhanced throughout the inflamed myocardium and in the spared areas of the left ventricular wall and the septum. Myocyte width increased from 26 to 75% at the inflammation-free myocardium (P < 0.0001), whereas it decreased 25% at the inflamed left ventricular wall areas (P < 0.001). Nuclear size increased in the inflammation-free myocardium of the left ventricle and the septum (> 10-36%, P < 0.01 and >0.2-32%, P < 0.03, respectively) and decreased at the inflamed areas of the left ventricular wall (10-22%. P < 0.02) with respect to the controls. The number of nuclei per unit volume decreased at the inflamed myocardium regardless of topographical location (36-65%) with respect to the controls (P < 0.0001) and in the inflammation-free myocardium of the right ventricle and the septum (<21-37%, P < 0.002 and <8-39%, P < 0.002, respectively). These results show that the heart responds to T. cruzi infection with DNA repair and cell multiplication in the inflamed sites and with hypertrophy of the unaffected myocardium.     

Myocardial blood flow regulation relative to left ventricle pressure and volume in anesthetized dogs

The influence of left ventricle pressure and volume changes on coronary blood flow was investigated in eight anesthetized dogs. Coronary artery pressure-flow relationships were determined at two levels of left ventricular pressure and volume. The distribution of blood flow within the myocardium was also determined when these relationships varied. Reducing left ventricle pressures and volumes increased heart rate. Rate-pressure product, diastolic coronary pressure, myocardial O2 consumption, total, subendocardial and subepicardial flow decreased. Hematocrit and blood gas data were unchanged. The pressure-flow relationships were shifted leftward (p = 0.001) but the range of autoregulation was not altered. At low left ventricle pressures and volumes, the lower coronary artery pressure limit was shifted leftward (from 75 to 45 mm Hg (1 mm Hg = 133.3 Pa)), while total, subendocardial, and subepicardial blood flow did not change compared with the control. Below the lower coronary artery pressure limit, subendocardial but not subepicardial flow decreased, resulting in maldistribution of flow across the left ventricular wall. When coronary pressure was reset between control and the lower coronary artery pressure limit, subendocardial flow was restored. These results show that the lower coronary artery pressure limit can be shifted leftward while the distribution of blood flow across the left ventricular wall is preserved.     

Effect of endurance running on cardiac and skeletal muscle in rats

We studied the effect of resistance running on left cardiac ventricle size and rectus femoris muscle fiber composition. Ten male Wistar rats were trained on a treadmill 6 days per week for 12 weeks. Ten rats remained sedentary and served as controls. A higher endurance time (40%) and cardiac hypertrophy in the trained animals were indicators of training efficiency. Morphometric analysis of the left ventricle cross-sectional area, left ventricular wall, and left ventricular cavity were evaluated. The endurance-running group demonstrated a hypertrophy of the ventricular wall (22%) and an increase in the ventricular cavity (25%); (p<0.0001). Semi-quantitative analysis of rectus femoris fiber-type composition and of the oxidative and glycolytic capacity was histochemically performed. Endurance running demonstrated a significant (p<0.01) increase in the relative frequency of Type I (24%), Type IIA (8%) and Type IIX (16%) oxidative fibers, and a decrease in Type IIB (20%) glycolytic fibers. There was a hypertrophy of both oxidative and glycolytic fiber types. The relative cross-sectional area analysis demonstrated an increase in oxidative fibers and a decrease in glycolytic fibers (p<0.0001). Changes were especially evident for Type IIX oxidative-glycolytic fibers. The results of this study indicate that the left ventricle adapts to endurance running by increasing wall thickness and enlargement of the ventricular cavity. Skeletal muscle adapts to training by increasing oxidative fiber Type. This increase may be related to fiber transformation from Type IIB glycolytic to Type IIX oxidative fibers. These results open the possibility for the use of this type of exercise to prevent muscular atrophy associated with age or post-immobilization.     

Myosin types and fiber types in cardiac muscle. I. Ventricular myocardium

Antisera against bovine atrial myosin were raised in rabbits, purified by affinity chromatography, and absorbed with insolubilized ventricular myosin. Specific anti-bovine atrial myosin (anti-bAm) antibodies reacted selectively with atrial myosin heavy chains, as determined by enzyme immunoassay combined with SDS-gel electrophoresis. In direct and indirect immunofluorescence assay, anti-bAm was found to stain all atrial muscle fibers and a minor proportion of ventricular muscle fibers in the right ventricle of the bovine heart. In contrast, almost all muscle fibers in the left ventricle were unreactive. Purkinje fibers showed variable reactivity. In the rabbit heart, all atrial muscle fibers were stained by anti-bAm, whereas ventricular fibers showed a variable response in both the right and left ventricle, with a tendency for reactive fibers to be more numerous in the right ventricle and in subepicardial regions. Diversification of fiber types with respect to anti-bAm reactivity was found to occur during late stages of postnatal development in the rabbit heart and to be influenced by thyroid hormone. All ventricular muscle fibers became strongly reactive after thyroxine treatment, whereas they became unreactive or poorly reactive after propylthiouracil treatment. These findings are consistent with the existence of different ventricular isomyosins whose relative proportions can vary according to the thyroid state. Variations in ventricular isomyosin composition can account for the changes in myosin Ca2+-activated ATPase activity previously observed in cardiac muscle from hyper- and hypothyroid animals and may be responsible for the changes in the velocity of contraction of ventricular myocardium that occur under these conditions. The differential distribution of ventricular isomyosins in the normal heart suggests that fiber types with different contractile properties may coexist in the ventricular myocardium.     

Cardiac hypertrophy in rats after supravalvular aortic constriction. I. Size and number of cardiomyocytes, endothelial and interstitial cells

The ascending aorta of 22 adult male Sprague-Dawley rats was constricted with a silver ring, and 25 animals were subjected to a sham-operation. The hearts, including the main arteries, were fixed by retrograde perfusion 3, 7, 14, 21 and 35 days after the operation. The cross-sectional area of the aorta was reduced by the constriction to an average of 20% of the values found after sham-operation. Twenty-one days after the constriction the weight of the left ventricular myocardium including the septum was increased 1.7-fold compared with controls. No further increase in weight was observed 35 days after the operation. The relative volumes of the tissue components remained largely constant in the subepicardial myocardium. In the subendocardial myocardium, however, the volume fraction of interstitial and, to a lesser extent, of endothelial tissue was significantly increased. Twenty-one days after constriction the estimated total volumes of the different myocardial components per left ventricle were increased 1.7-fold for heart muscle parenchyma, 1.8-fold for endothelial tissue, 2.9-fold for interstitial tissue, and 1.3-fold for capillary lumina compared with controls. At 35 days, only the interstitial tissue showed a further increase to 4.8-fold of control values. The mean cardiomyocyte volume was increased after aortic constriction in proportion to the increase in left ventricular weight, i.e. 1.7-fold over controls at 21 days. After 35 days its value was 29,500 +/- 790 micron 3 in rats subjected to aortic constriction compared with 16,800 +/- 640 micron 3 in controls. At this time the estimated number of cardiomyocytes per left ventricle showed no significant differences between experimental animals (2.9 X 10(7)) and controls (3.1 X 10(7)). Endothelial and interstitial cells were not only increased in average single cell volume (1.3-fold and 2.0-fold, respectively), but also in number per left ventricle (1.4-fold and 2.7-fold, respectively). Two-dimensional parameters indicated that during hypertrophy the capillary supply lagged behind the overall mass increase but achieved control levels on termination of hypertrophic growth at 35 days. These results show that even in pronounced hypertrophy the increase in mass of the myocardial parenchyma in the rat is due exclusively to an enlargement of cardiomyocytes (hypertrophy), whereas in endothelial and interstitial tissues enlargement of cells as well as increase in cell number (hyperplasia) also plays a role.     

Myocardial specificity for initiating endothelial-mesenchymal cell transition in embryonic chick heart correlates with a particulate distribution of fibronectin

The early chick heart tube consists of myocardium and endothelium separated by a myocardially derived basement membrane (MBM). As development proceeds, the endothelium undergoes a transition into mesenchyme in a regionally specific manner; only the atrioventricular (AV) and outflow tract, but not the ventricular endothelium, is transformed into mesenchyme, the progenitor of heart septa and valves. Recent experiments have shown that an EDTA extract of MBM can initiate AV endothelium to form mesenchyme in an in vitro collagen gel culture system. Two-dimensional gel electrophoresis of AV region EDTA extracts showed potentially three isoelectric forms of fibronectin (Fn), while extracts from ventricle contained only two forms. The purpose of the present study was to further investigate the significance of these regional differences by testing of specific myocardial regions (AV vs ventricle) for their ability to induce endothelium to form mesenchyme in vitro, and to immunohistochemically determine if a regionally specific distribution of Fn exists in the MBM that can be correlated with previous electrophoretic data. Embryonic heart regions cultured on three-dimensional collagen gels showed that AV endothelium could only form mesenchyme if cocultured with AV myocardium. Coculture with ventricular myocardial explants did not initiate differentiation of AV endothelium. In contrast, ventricular endothelial cells did not form mesenchyme when cocultured with AV or ventricle myocardium. Immunohistochemical localization of Fn revealed three distinct morphological patterns of distribution in the AV-MBM, i.e., an intense lamina densa staining, diffuse staining in fibrils, and as particles. The Fn localized in particles (0.1 to 0.5 micron in diameter) appeared as a gradient of decreasing concentration extending from the myocardium toward the endothelium. In contrast, no particulate Fn staining was observed in the ventricular region. EDTA extraction selectively depleted the particulate form of Fn. Previous work has shown that this extract, which contains several lower Mr proteins in addition to Fn, is biologically active in initiating mesenchyme formation from AV endothelium in vitro. These results show that a regionally specific interaction of the myocardium with the endothelium is required to initiate the formation of prevalvular mesenchyme. This interaction may be mediated by a multicomponent complex involving Fn and other proteins which appear as a regionally distinct particulate only in areas of endothelial differentiation.     

急性心肌梗死患者早期血浆脑钠肽水平与左室重构及预后关系的评估

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。     

Regional passive ventricular stress-strain relations during development of altered loads in chick embryo

Mechanical load influences embryonic ventricular growth, morphogenesis, and function. However, little is known about changes in regional passive ventricular properties during the development of altered mechanical loading conditions in the embryo. We tested the hypothesis that regional mechanical loads are a critical determinant of embryonic ventricular passive properties. We measured biaxial passive right and left ventricular (RV and LV, respectively) stress-strain relations in chick embryos at Hamburger-Hamilton stages 21 and 27 after conotruncal banding (CTB) to increase biventricular pressure load or left atrial ligation (LAL) to reduce LV volume load and increase RV volume load. In the RV, wall strains at end-diastolic (ED) pressure normalized whereas ED stresses increased after either CTB or LAL during development. In the left ventricle, both ED strain and stress normalized after CTB, whereas both remained reduced with significantly increased myocardial stiffness after LAL. These results suggest that the embryonic ventricle adapts to chronically altered mechanical loading conditions by changing specific RV and LV passive properties. Thus regional mechanical load has a critical role during cardiogenesis.     

Ultrastructural morphometry of the myocardium of Thunnus alalunga

The common ventricle in the heart of the Thunnus alalunga was studied. The ventricular myocardium consists of an outer compact layer and a thick inner spongy layer. The compact layer has slightly larger cells (4-6 microns diameter) than the spongy layer (2.5-5 microns diameter). Ultrastructurally the myocardium displays normal arrangements of myofibrils and mitochondria. The sarcoplasmic reticulum is poorly developed. The intercalated discs are simple with the fascia adherens being the most frequent junctional type observed; occasionally a desmosome was seen. Nexus type junctions are present but are unassociated with the intercalated discs. There are no t-tubules evident but the plasmalemma exhibits numerous caveolae which rarely form couplings with the sarcoplasmic reticulum. A morphometric analysis of the volume percent of mitochondria and myofibrils showed that the myocardial cells in the spongy layer of the heart have a significantly greater volume percentage of mitochondria than the compact layer. No significant differences were found between myocardial regions when the volume percentages of myofibrils were compared. The physiological studies revealed that the albacore tuna has heart rates (120 bpm) and ventricular blood pressures (100 mmHg) that are among the highest reported for fish.     

Myosin heavy chain isoforms in the myocardium of the atrioventricular junction of Scyliorhinus canicula (Chondrichthyes,Carcharhiniformes)

The atrioventricular junction of the fish heart, namely the segment interposed between the single atrium and the single ventricle, has been studied anatomically and histologically in several chondrichthyan and teleost species. Nonetheless, knowledge about myosin heavy chain (MyHC) in the atrioventricular myocardium remains scarce. The present report is the first one to provide data on the MyHC isoform distribution in the myocardium of the atrioventricular junction in chondrichthyans, specifically in the lesser spotted dogfish, Scyliorhinus canicula, a shark species whose heart reflects the primitive cardiac anatomical design in gnathostomes. Hearts from five dogfish were examined using histochemical and immunohistochemical techniques. The anti-MyHC A4.1025 antibody was used to detect differences in the occurrence of MyHC isoforms in the dogfish, as the fast-twitch isoforms MYH2 and MYH6 have a higher affinity for this antibody than the slow-twitch isoforms MYH7 and MYH7B. The histochemical findings show that myocardium of the atrioventricular junction connects the trabeculated myocardium of the atrium with the trabeculated layer of the ventricular myocardium. The immunohistochemical results indicate that the distribution of MyHC isoforms in the atrioventricular junction is not homogeneous. The atrial portion of the atrioventricular myocardium shows a positive reactivity against the A4.1025 antibody similar to that of the atrial myocardium. In contrast, the ventricular portion of the atrioventricular junction is not labelled, as is the case with the ventricular myocardium. This dual condition suggests that the myocardium of the atrioventricular junction has two contraction patterns: the myocardium of the atrial portion contracts in line with the atrial myocardium, whereas that of the ventricular portion follows the contraction pattern of the ventricular myocardium. Thus, the transition of the contraction wave from the atrium to the ventricle may be established in the atrioventricular segment because of its heterogeneous MyHC isoform distribution. The findings support the hypothesis that a distinct MyHC isoform distribution in the atrioventricular myocardium enables a synchronous contraction of inflow and outflow cardiac segments in vertebrates lacking a specialized cardiac conduction system.     

Morphological and functional differences in cardiac parameters between power and endurance athletes: a magnetic resonance imaging study

The present study compared morphological and functional parameters of the left ventricle by magnetic resonance imaging (MRI) in competitive athletes engaged in endurance and power activities and sedentary control subjects. Twenty male subjects, 7 endurance-trained athletes (ETA) (age 23.8+/-3.5 yr), 7 strength-trained athletes (STA) (age 22.8+/-4.0 yr), and 6 sedentary controls (age 24.1+/-2.2 yr) were studied by MRI. In the ETA group body size related left ventricular mass (rel.LVM) was significantly higher than that in the STA group (71.0+/-9.2 vs 57.4+/-15.7 g/m3). The difference between their size related left ventricular wall thickness (rel.LVWT) values (9.37+/-1.0 vs 8.37+/-1.8 mm/m) was near to the level of significance (p=0.057). Relative left ventricular internal diameter (rel.LVID) was significantly higher in the ETA group compared to the STA group (42.3+/-1.0 vs 40.1+/-2.5 mm/m, p<0.05). The muscular quotient (MQ=LVWT/LVID) of the ETA group was not significantly higher compared to the strength athletes. Relative left ventricular end-diastolic volume (LVEDV) was also higher in the ETA group than in the STA group (69.5+/-6.7 vs 59.9+/-8.2 ml/m3, p<0.05) and the controls (53.6+/-3.7, p<0.001). Significantly higher relative stroke volume (SV) was measured in the ETA group compared to the STA group and the controls (41.0+/-5.7; 32.6+/-6.9; 32.0+/-3.2 ml/m3). According to the present data, the strongest impact on LV cavity size and wall thickness is caused by long-term high intensity endurance training. Intense strength training does not necessarily induce wall thickening.     

鬼笔环肽对心肌梗死大鼠离体心脏牵张所致电生理学改变的影响

本文旨在探讨肌动蛋白稳定剂--鬼笔环肽(phalloidin)对心肌梗死(myocardial infarction,MI)大鼠离体心脏牵张所致电生理学改变的影响.将32只Wistar大鼠随机分为正常对照组(n=9)、鬼笔环肽组(n=7)、MI组(n=9)、MI 鬼笔环肽组(n=7).离体心脏经Langendorff灌流后,通过改变水囊容积,以△V=0.1、0.2、0.3 mL对心室牵张5 S,观察牵张后效应30 s,记录左心室内压力变化[左心室收缩压(left ventricular systolic pressure,LVSP)、左心室舒张末压(left ventricular end-diastolic pressure,LVEDP)、室内压最大上升,下降速率(±dp/dt max)]、单相动作电位复极90%的时程(monophasic action po-tential duration at 90%repolarization,MAPD 90)、室性期前收缩(premature ventricular beats,PVB)及室性心动过速(ventriculartachycardia,VT)发生率.结果显示,牵张使正常对照组及MI组大鼠MAPD 90明显延长(P<0.05,P<0.01),MI组大鼠MAPD 90延长更显著(P<0.05,P<0.01).鬼笔环肽(1 μmol/L)对正常及MI心肌基础状态下的MAPD 90无影响,但使MI心肌牵张后已延长的MAPD90缩短(△V=0.3 mL时,P<0.05).牵张后MI组大鼠PVB、VT的发生率明显高于正常对照组(均P<0.01).鬼笔环肽对正常大鼠心肌牵张后PVB、VT的发生率无显著影响,但使MI心肌PVB、VT的发生率明显下降(均P<0.01).MI组大鼠LVSP及 ap/dt max 较正常对照组显著降低(P<0.01);鬼笔环肽可使MI心肌LVSP轻度回升,但无统计学意义.结果表明,MI后牵张加重恶性心律失常的发生和持续,鬼笔环肽可以明显抑制其发生.     

Cardiomyogenic differentiation-independent improvement of cardiac function by human cardiomyocyte progenitor cell injection in ischaemic mouse hearts

We previously showed that human cardiomyocyte progenitor cells (hCMPCs) injected after myocardial infarction (MI) had differentiated into cardiomyocytes in vivo 3 months after MI. Here, we investigated the short-term (2 weeks) effects of hCMPCs on the infarcted mouse myocardium. MI was induced in immunocompromised (NOD/scid) mice, immediately followed by intramyocardial injection of hCMPCs labelled with enhanced green fluorescent protein (hCMPC group) or vehicle only (control group). Sham-operated mice served as reference. Cardiac performance was measured 2 and 14 days after MI by magnetic resonance imaging at 9.4 T. Left ventricular (LV) pressure-volume measurements were performed at day 15 followed by extensive immunohistological analysis. Animals injected with hCMPCs demonstrated a higher LV ejection fraction, lower LV end-systolic volume and smaller relaxation time constant than control animals 14 days after MI. hCMPCs engrafted in the infarcted myocardium, did not differentiate into cardiomyocytes, but increased vascular density and proliferation rate in the infarcted and border zone area of the hCMPC group. Injected hCMPCs engraft into murine infarcted myocardium where they improve LV systolic function and attenuate the ventricular remodelling process 2 weeks after MI. Since no cardiac differentiation of hCMPCs was evident after 2 weeks, the observed beneficial effects were most likely mediated by paracrine factors, targeting amongst others vascular homeostasis. These results demonstrate that hCMPCs can be applied to repair infarcted myocardium without the need to undergo differentiation into cardiomyocytes.     

Maturation of end-systolic stress-strain relations in chick embryonic myocardium

The embryonic myocardium increases functional performance geometrically during cardiac morphogenesis. We investigated developmental changes in the in vivo end-systolic stress-strain relations of embryonic chick myocardium in stage 17, 21, and 24 white Leghorn chick embryos (n = 10 for each stage). End-systolic stress-strain relations were linear in all developmental stages. End-systolic strain decreased from 0.50 +/- 0.02 to 0.31 +/- 0.01 (mean +/- SE, P < 0.05), while average end-systolic wall stress was similar at 3.29 +/- 0.34 to 4.19 +/- 0.43 mmHg (P = 0.14) from stage 17 to 24. Normalized end-systolic myocardial stiffness, a load-independent index of ventricular contractility, increased from 2.98 +/- 0.19 to 6.03 +/- 0.39 mmHg from stage 17 to 24 (P < 0.05). Zero-stress midwall volume increased from 0.024 +/- 0.002 to 0.124 +/- 0.004 microl from stage 17 to 24 (P < 0.05). These results suggest that the embryonic ventricle increases normalized ventricular "contractility" while maintaining average end-systolic wall stress over a relatively narrow range during cardiovascular morphogenesis.     

Active and passive stresses in the myocardium

A mathematical approach that can be used to calculate the passive stress in the ventricular wall is presented. The active fiber stress (force/unit area) generated by the muscular fibers in the ventricular wall is expressed by means of body force (force/unit volume of the myocardium). It is shown that the total intramyocardial passive stress induced in the passive medium of the myocardium can be expressed as the sum of a passive stress induced by the left ventricular pressure and a passive stress induced by the active fiber stress. Applications to experimental data published in the literature are given. New results are presented that show the relation among those two components of the intramyocardial passive stress. New relations between the intramyocardial passive stress, the slope (elastance) of the pressure-volume relation, and the residual volume are also derived. The results obtained give a better understanding of some aspects of the mechanics of cardiac contraction and can provide a more detailed interpretation of clinical conditions.