CELLULR REMODELING CARDIAC HYPERTROPHY

这项研究计划的主要目标是调查 血流动力学和心肌结构的改变 心脏肥大 使用最可靠的方法 可用的，诱导的肌细胞大小（体积，长度， 和横截面尺寸），形状和数量正在 在各种心脏肥大模型中进行了研究。 修改 在毛细作用和组织含量正在调查 形态计量学 由于心脏肥大可能导致 充血性心力衰竭和更大的死亡率，增加 了解疾病的过程是很重要的。 结构和血流动力学变化将在几个 模型 将从1、5和18中制备分离的肌细胞 月龄自发性高血压（SHR）和Wistar京都 (WKY)大鼠 分离的细胞也将用于研究 大鼠下腔静脉瘘的发展和逆转。 大鼠 将用甲状腺切除术治疗下腔静脉瘘， 努力制造一个心力衰竭模型。 地区差异 （右心室、室间隔和左心室） 心肌内膜、中层和心肌外膜 大小将与左心室和右心室的变化相关 功能（例如，心室峰压最大上升率 收缩压和右压）。 以下肌细胞变化将 测量：体积、长度、横截面积和主要尺寸， 较小的横截面尺寸。核体积-细胞体积 将在单核细胞和双核细胞中检查关系 肌细胞 平均肌细胞体积和肌细胞数量变化30-40% 对于给定的一组相似体重的对照动物， 通常观察心脏重量。 最近的数据显示， 变异是遗传的。 利用选择性育种技术，我们希望 开发两种在心脏功能上有显著差异的大鼠品系， 肌细胞体积和数量。 老鼠的数量增加， 较小的肌细胞将与含有较少但 更大的肌细胞 小细胞系和大细胞系也将被 经受不同类型的心脏超负荷（例如， 甲状腺肥大，下腔静脉瘘），以调查 肌细胞大小对心肌梗死病理过程的影响 心脏肥大 死亡率的变化，左和右 心室功能和心肌细胞尺寸将 比较了两条线的大鼠。

The major goal of this research program is to investigate alterations in hemodynamics and myocardial structure associated with cardiac hypertrophy. Using the most reliable methodology available, induced alterations in myocyte size (volume, length, and cross-sectional dimensions), shape, and number are being studied in various models of cardiac hypertrophy. Modifications in capillarization and tissue content are being investigated morphometrically. Since cardiac hypertrophy may lead to congestive heart failure and greater mortality, increased knowledge of the disease process is important. Structural and hemodynamic changes will be examined in several models. Isolated myocytes will be prepared from 1, 5, and 18 month old Spontaneously Hypertensive (SHR) and Wistar Kyoto (WKY) rats. Isolated cells will also be used to study the development and reversal of aortocaval fistulas in the rat. Rats with aortocaval fistulas will be treated with thyroid hormons in an effort to produce a model of heart failure. Regional differences (right ventricular, interventicular septum, and left ventricular endomyocardium, midmyocardium and epimyocardum) in myocyte size will be correlated with changes in left and right ventricular function (eg. maximum rate of pressure rise, ventricular peak systolic and right pressure). The following myocyte changes will be measured: volume, length, cross-sectional area, and major and minor cross-sectional dimensions. Nuclear volume-cell volume relationships will be examined in mononucleated and binucleated myocytes. A 30-40% variation in mean myocyte volume and myocyte number for a given group of control animlas of similar body weight and heart weight is typically observed. Recent data suggests that this variation is genetic. Using selective breeding techniques, we hope to develop two lines of rats with significant differences in cardiac myocyte volume and number. Rats with an increased number of smaller myocytes will be compared to rats containing fewer but larger myocytes. The small and large cell lines will also be subjected to different types of cardiac overload (eg. hyperthroidism, aortocaval fistulas) to investigate the contribution of myocyte size to the pathological process of cardiac hypertrophy. Changes in mortality, left and right ventricular function, and cardiac myocyte dimensoions will be compared between rats from the two lines.