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骨骼结构对机械使用的适应性(SATMU):4. 机械因素对完整纤维组织的影响。

Skeletal structural adaptations to mechanical usage (SATMU): 4. Mechanical influences on intact fibrous tissues.

作者信息

Frost H M

机构信息

Department of Orthopaedic Surgery, Southern Colorado Clinic, P.C., Pueblo 81004.

出版信息

Anat Rec. 1990 Apr;226(4):433-9. doi: 10.1002/ar.1092260405.

Abstract

This paper proposes that the growth in length of living fibrous tissue structures (tendon, ligament, fascia) responds primarily to circulating systemic rather than mechanical factors. However, growth of the thickness of those structures responds primarily to their mechanical tension loads in the special sense that, when the tissue's typical peak mechanical strains exceed a threshold value, its cells begin to add new collagen to increase its thickness, strength, and tension stiffness. When subsequent peak strains reduce to the threshold value, then further additions of collagen stop. That process defines mechanically controlled modeling of fibrous tissues. The collagen in these tissues can also develop mechanical microdamage (MDx) under repeated tension load-deload cycles. Special maintenance mechanisms normally repair that MDx to prevent accumulations that would threaten structural integrity. As a result, spontaneous complete ruptures of these structures can happen when MDx production exceeds its repair. These maintenance mechanisms also prevent gradual stretching under continuous tension loads, a process the author suggests calling creep compensation. When the creep compensation mechanism becomes incompetent, structures can stretch under continuous loads; when it becomes overactive, contractures can occur. The above meld of fact and inference provides the kernel of a general theory for the responses of the architecture and mechanical competence of intact fibrous tissues to mechanical usage.

摘要

本文提出,活体纤维组织结构(肌腱、韧带、筋膜)长度的增长主要响应循环系统因素而非机械因素。然而,这些结构厚度的增长主要响应其机械张力负荷,具体而言,当组织典型的峰值机械应变超过阈值时,其细胞开始添加新的胶原蛋白以增加其厚度、强度和张力刚度。当随后的峰值应变降至阈值时,胶原蛋白的进一步添加停止。该过程定义了纤维组织的机械控制建模。这些组织中的胶原蛋白在反复的张力加载-卸载循环下也会产生机械微损伤(MDx)。特殊的维持机制通常会修复这种MDx,以防止可能威胁结构完整性的累积。因此,当MDx产生超过其修复能力时,这些结构可能会发生自发性完全断裂。这些维持机制还可防止在持续张力负荷下逐渐拉伸,作者建议将此过程称为蠕变补偿。当蠕变补偿机制失效时,结构会在持续负荷下拉伸;当它过度活跃时,可能会发生挛缩。上述事实与推断的融合为完整纤维组织的结构和机械性能对机械使用的响应提供了一个通用理论的核心。

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