QUANTITATIVE MORPHOLOGY OF CARDIAC HYPERTROPHY

心脏肥大的定量形态学

• 批准号: 3340453
• 负责人: THOMAS A MARINO
• 金额: $ 13.77万
• 依托单位: TEMPLE UNIV OF THE COMMONWEALTH
• 依托单位国家: 美国
• 财政年份: 1984
• 资助国家: 美国
• 起止时间: 1984-04-01 至 1993-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3340453
• 关键词: adrenergic receptor; cats; connective tissue development; disease /disorder model; heart circulation; heart contraction; heart failure; hemodynamics; intracardiac pressure; intracardiac volume; vascular resistance; ventricular hypertrophy

In vitro contractile dysfunction is a result of cardiac hypertrophy that is caused by a pressure overload of the ventricular myocardium. This abnormal function occurs whether the pressure overload is from a chronic progressive or an acute overload. In contrast volume overload induced hypertrophy does not result in in vitro contractile dysfunction. In the case of the pressure overload induced hypertrophy, if this process is reversed then the contractile function returns to normal. We have studied an early stage of acute pressure overload right ventricular hypertrophy and found that there is an increase in the connective tissue components of the ventricular myocardium and a change in myocyte size and external sarcolemma surface area/ cell volume ratio. The change in connective tissue associated with pressure overload hypertrophy could contribute directly to compromised contractile performance by altering the elastic properties of the ventricle. The change in myocyte size and shape could contribute indirectly by altering the basic control systems for the contractile apparatus. The SPECIFIC AIM of this proposal is to determine whether these structural effects or other structural modifications that are found in this pathophysiological model are causally related to the impaired contractile function and therefore have etiologic significance for the eventual changes found in this model. Since the chronic progressive pressure overload model does not cause myocardial injury a comparison to the tissue from the acute pressure overload model will determine if the changes seen are a result of the myocardial injury produced by acute pressure overload. Then a comparison of the pressure overload hypertrophied right ventricular myocardium to the volume overload hypertrophied myocardium will identify those structural alterations associated with the abnormal contractile function and those associated with the hypertrophy process in general. Those alterations unique to the myocardium with contractile dysfunction should return to normal when the hypertrophy process is reversed. This will be examined in the reversed chronic progressive pressure overload model. Morphometric ultrastructural studies are used to compare and contrast the right ventricular myocardium under these different hemodynamic conditions. These studies relate to our long-term objectives which are to determine myocardial alterations that result in abnormal function and ultimately heart failure.

体外收缩功能障碍是心脏肥大的结果， 由心室肌压力超负荷引起。 这种不正常 无论压力超负荷是否来自慢性进行性 或急性超负荷。 相反，容量超负荷诱导的肥大 不会导致体外收缩功能障碍。 的情况 压力超负荷引起的肥大，如果这个过程是逆转，那么 收缩功能恢复正常。 我们研究了早期阶段的 急性压力超负荷右心室肥厚，并发现， 是心室的结缔组织成分增加 心肌以及肌细胞大小和肌膜外表面的变化 面积/细胞体积比。 结缔组织的变化与 压力超负荷肥大可能直接导致 收缩性能通过改变弹性性能的 脑室 肌细胞大小和形状的变化可能有助于 间接地通过改变收缩的基本控制系统， 设备. 本提案的具体目的是确定这些 结构效应或其他结构修饰， 病理生理学模型与收缩功能受损有因果关系 因此对最终的变化具有病因学意义 在这个模型中发现。 由于慢性渐进性压力超负荷模型 与急性心肌梗死组织相比， 压力过载模型将确定所看到的变化是否是 急性压力超负荷引起的心肌损伤。 然后 压力超负荷性肥厚右心室 将心肌与体积超负荷肥厚心肌区分开来 这些与异常收缩相关的结构改变 功能和与肥大过程相关的一般。 这些变化是收缩功能障碍心肌所特有的 当肥大过程逆转时应该恢复正常。 这 将在反向慢性渐进性压力超负荷中进行检查 模型 形态学超微结构研究用于比较和 对比不同血流动力学下的右心室心肌 条件 这些研究与我们的长远目标有关， 确定导致功能异常的心肌改变， 最终导致心力衰竭。