CORONARY MICROVESSEL PERMEABILITY

在心脏内，运动训练会增加冠状动脉的通透性- 表面积乘积，一个交换能力的指数，按未知 机械装置。目前对毛细管交换屏障的看法是 从静态边界之一发展到所涉及的动态结构 在对气体、水和溶质运动的瞬间调节中 在血液和组织之间。由于表面积没有考虑到 观察到培训引起的交流能力的增加，该项目 专注于微血管通透性，并应用专门的 该实验室用于测量微血管传输的技术。从… 这些测量结果揭示了冠脉微血管形成的机制 对运动训练的适应将被阐明。初级阶段 假设运动训练增加冠脉微血管 渗透率(目标1和2)。此外，这些研究旨在 确定培训效果是局部的还是系统性的(目标3)， 运动训练改变血管屏障的动态状态(目的 4)，和/或个别船只的变化是否对 完整心脏的综合反应(AIMS 5)。在抵抗中 久坐动物心脏和肠系膜分离的动脉和小静脉 经过运动训练的猪，已知大小的荧光探针的溶质通量 而变化，将作为灌流压力的函数来测量。从… 这些测量结果表明，扩散溶质的输运系数 渗透率(Pd)和溶剂阻力系数(Lp(1-sigma))将为 计算出来的。将评估微血管的通透性反应 在基础条件下，然后在血管内皮细胞灌流后- 依赖和非依赖的血管扩张剂。渗透率/表面积 产品也将被测量，首先，从久坐不动和 锻炼训练过的猪，第二，锻炼阻力动脉和小静脉 与这些相同的心脏隔绝。关于口述的机制的知识 对单个微血管和完整心脏通透性的控制 为阐明观察到的运动训练诱导提供了依据 冠状动脉交换量的增加。理解的关键 运动训练是否能补偿或逆转所致的功能障碍 冠状动脉疾病也依赖于一种机械的研究方法 在训练中观察到的变化。

Within the heart, exercise training increases coronary permeability- surface area product, an index of exchange capacity, by unknown mechanisms. The current view of the capillary exchange barrier has progressed from one of a static boundary to a dynamic structure involved in moment-to-moment regulation of gas, water, and solute movements between blood and tissue. Since surface area does not account for the observed training-induced increase of exchange capacity, this project focuses on microvessel permeability and applies the specialized techniques of this laboratory to measure microvessel transport. From these measurements the mechanisms responsible for coronary microvessel adaptation to exercise training will be elucidated. The primary hypothesis is that exercise training increases coronary microvessel permeability (Aims 1 & 2). Further, the studies are designed to determine whether training effects are local or systemic (Aim 3), whether exercise training alters the dynamic status of the vascular barrier (Aim 4), and/or whether changes in individual vessels contribute equally to the integrated responses of intact hearts (Aims 5). In resistance arteries and venules isolated from the heart and mesentery of sedentary ad exercise trained pigs, solute flux of fluorescent probes of known size and change, will be measured as a function of perfusion pressure. From these measurements the transport coefficients diffusive solute permeability (Pd) and solvent drag coefficient (Lp(1-sigma)) will be calculated. Permeability responses of the microvessels will be assessed under basal conditions and then following perfusion with endothelium- dependent and -independent vasodilators. Permeability/surface area product will also be measured, first, in whole hearts from sedentary and exercise trained pigs and, second, in resistance arteries and venules isolated from these same hearts. Knowledge of mechanisms that dictate control of permeability in individual microvessels and intact hearts will provide a basis for elucidating observed exercise training-induced increases in coronary exchange capacity. The key to understanding whether exercise training compensates for or reverses dysfunction caused by coronary disease also rests on a mechanistic approach to studying changes observed with training.