HOST FACTORS RELATING TO HIV INFECTIONS

多条证据表明，心脏的收缩性能 心肌组织受肌节之间的密切关系支配 长度和钙-肌丝激活(LDA)构成了 弗兰克-斯塔林机制。相反，放松是由 钙化肌丝失活与外力的竞争 与肌肉力量和负荷相关的恢复力。为了 消除大块组织的机械和电学不均匀，优先 已经在完整的单个心肌细胞中进行了收缩能力的研究， 尽管处于松弛长度(因为没有令人满意的方法来改变 此模式下的长度/负载，或化学蒙皮单元中的长度/负载。要检查 力量对单人抽动收缩和松弛的影响 具有完整肌膜的心肌细胞，我们开发了一种新的技术 能够在高达15%-18%的休止单元长度中实现可逆分级。 我们的初步结果表明：(1)沐浴钙对 增大缩短率随细胞长度的变化与 肌丝-钙激活是长度/负荷依赖的概念。 静息细胞长度的延长会增加抽动幅度并加速 松弛不改变细胞内钙瞬变。因此，一个 细胞内钙依赖松弛的松弛长度可以是 被与拉伸相关的外部恢复力覆盖， 与松弛的长度/载荷相关的概念相一致 大块心肌，此外，伸展运动是一种主要的 组织中钙-肌丝失活松弛的决定因素 保持“正常”的钙稳态。

Multiple lines of evidence has established that contractile performance of cardiac tissue is governed by the intimate relationship between sarcomere length and calcium-myofilament activation (LDA) forming the basis of the Frank-Starling mechanism. In contrast, relaxation is governed by the competition between calcium-myofilament inactivation and the external restoring force associated with muscle strength and loading. In order to eliminate mechanical and electrical inhomogeneity of bulk tissue, prior studies of contractility have been performed in intact single myocytes, albeit at slack length (as no satisfactory method exists to alter length/load in this mode , or in chemically-skinned cells. To examine the effect of strength on the twitch contraction and relaxation of single ventricular myocytes with intact sarcolemma, we developed a novel technique enabling reversible gradation in the resting cell length of up to 15-18%. Our initial results show (1) that the relative effect of bathing calcium to augment shortening velocity varied with the cell length is consistent with the concept that myofilament-calcium activation is length/load-dependent. A stretch of resting cell length increases twitch amplitude and accelerates relaxation without changing the cytosolic calcium transient. Thus, a cytosolic calcium-dependence of relaxation at slack length can be overridden by the external restoring force associated with stretch, consistent with the concept of a length/load-dependence of relaxation in bulk cardiac muscle, and, moreover, stretch represents a principal determinant of relaxation over calcium-myofilament inactivation in tissue with "normal" calcium homeostasis.