MECH OF CONDUCTION SLOWING DURING MYOCARDIAL STRETCH BY VENT VOL LOADING

通气量负荷导致心肌舒张时传导减慢的机制

• 批准号: 8169348
• 负责人: Sanjiv M Narayan
• 金额: $ 2.23万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169348
• 关键词: Computer Retrieval of Information on Scientific Projects Database; Economic Inflation; Electric Capacitance; Funding; Grant; Institution; Membrane; Myocardial; Research; Research Personnel; Resistance; Resources; Source; Stretching; United States National Institutes of Health; Vent; Ventricular

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Passive ventricular loading by volume inflation reversibly slows electrical conduction, but the mechanism behind this slowing remains unclear. We investigates the contributions of stretch-activated channels, altered membrane excitability, and changes in intercellular resistance or effective membrane capacitance during volume loading as the mechanism behind conduction slowing.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 容量膨胀引起的被动心室负荷可逆地减慢电传导，但这种减慢背后的机制仍不清楚。我们研究了拉伸激活通道、改变的膜兴奋性以及体积负荷期间细胞间电阻或有效膜电容的变化作为传导减慢背后的机制的贡献。