血压是否增强了骨陷窝-小管系统中的溶质运输?

Does blood pressure enhance solute transport in the bone lacunar-canalicular system?

机构信息

Graduate Program in Biomechanics and Movement Sciences, University of Delaware, Newark, DE 19716, USA.

出版信息

Bone. 2010 Aug;47(2):353-9. doi: 10.1016/j.bone.2010.05.005. Epub 2010 May 13.

Abstract

Solute transport through bone plays an important role in tissue metabolism and cellular mechanotransduction. Due to limited diffusion within the mineralized bone matrix, both mechanical loading and vascular pressure have been proposed to drive interstitial fluid flow within the lacunar-canalicular system (LCS); thereby augmenting solute diffusion in bone. Although blood supply is critical for bone nutrition, growth, and fracture healing, whether physiological blood pressures can drive significant fluid and solute convection remains controversial within the literature. The goal of this study was to directly test the hypothesis that in vivo blood pressures enhance solute transport in the bone LCS. Using a newly developed imaging approach based on fluorescence recovery after photobleaching (FRAP), we first measured the transport rate of sodium fluorescein (M.W. 376 Da) through the tibial LCS in four anesthetized mice (in the presence of vascular pressure). These data were then compared with the tracer transport rates at the same locations/lacunae after sacrifice (in the absence of vascular pressure). Using paired FRAP experiments we did not detect differences in tracer transport rates between bones from live anesthetized animals versus those in postmortem bodies (p>0.05, N=18). In a separate cohort of four anesthetized mice a mean jugular pulse pressure of approximately 10 mmHg at approximately 10 Hz was measured. Further theoretical analysis showed that for bones from both small and large animal species the blood pressure-driven convection of either small (376 Da) or large (43,000 Da) molecules was at least one order of magnitude smaller than diffusion under either normal or elevated pressure conditions. We conclude that despite the extreme importance of vasculature in bone physiology, vascular pressure itself does not enhance acute solute transport within the bone LCS. Therefore, mechanisms other than the vascular pressure-induced fluid flow such as altered biochemical factors may account for the bone adaptation associated with altered circulation. The present study helped clarify a long-standing controversy regarding vascular pressure-induced bone fluid flow and provided a better understanding of bone adaptation in both physiological and pathological conditions.

摘要

溶质通过骨骼的转运在组织代谢和细胞机械转导中起着重要作用。由于在矿化的骨基质中扩散受到限制,机械加载和血管压力都被认为可以驱动骨的腔隙-小管系统(LCS)中的间质液流动;从而增加骨中的溶质扩散。尽管血液供应对骨营养、生长和骨折愈合至关重要,但在文献中,生理血压是否能驱动显著的液体和溶质对流仍存在争议。本研究的目的是直接检验假设,即在体血压增强骨 LCS 中的溶质转运。使用基于荧光恢复后漂白(FRAP)的新开发的成像方法,我们首先测量了在麻醉小鼠(存在血管压力)的胫骨 LCS 中荧光素钠(MW376Da)的转运速率。然后,将这些数据与在相同位置/腔室中在牺牲后(无血管压力)的示踪剂转运速率进行比较。使用配对 FRAP 实验,我们没有在来自活体麻醉动物的骨骼与死后尸体的骨骼之间检测到示踪剂转运速率的差异(p>0.05,N=18)。在另一组四只麻醉小鼠中,测量到约 10Hz 时约 10mmHg 的颈静脉脉动压力。进一步的理论分析表明,对于来自小动物和大动物物种的骨骼,无论是小分子(376Da)还是大分子(43000Da),血液压力驱动的对流至少比正常或升高压力条件下的扩散小一个数量级。我们得出的结论是,尽管血管在骨骼生理学中极为重要,但血管压力本身并不能增强骨骼 LCS 内的急性溶质转运。因此,除了血管压力诱导的流体流动之外的机制,例如改变的生化因素,可能解释了与循环改变相关的骨骼适应。本研究有助于澄清关于血管压力诱导的骨液流的长期争议,并为生理和病理条件下的骨骼适应提供了更好的理解。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索