Sukhoplyasova Maria, Hamner Jason W, Draghici Adina E
Cardiovascular Research Laboratory, Spaulding Hospital Cambridge, Cambridge, MA 02138, United States.
Schoen Adams Research Institute at Spaulding Rehabilitation, Boston, MA, United States.
J Bone Miner Res. 2025 Mar 15;40(3):404-412. doi: 10.1093/jbmr/zjae204.
Bone vasculature is richly innervated by an extensive network of sympathetic nerves. However, our understanding of bone blood flow regulation and its contribution to human bone health is limited. Here, we further our previous findings by characterizing bone vascular responses in the absence of sympathetic control-studying individuals with spinal cord injury (SCI), a population with known peripheral sympathetic disruption. We assessed tibial vascular responses to isometric handgrip exercise (IHE) in individuals with SCI (n = 12) and controls (n = 12). When sustained to fatigue, IHE increases perfusion pressure and sympathetic vasoconstriction in the nonactive tissues of the legs. During IHE, we measured blood pressure, whole leg blood velocity (LBV) via ultrasound, and tibial perfusion (as hemoglobin content) via near-infrared spectroscopy. Controls demonstrated active sympathetic vasoconstriction in the whole leg (ie, increased vascular resistance [VR], arterial pressure/LBV) and tibia (ie, decreased hemoglobin). In contrast, SCI individuals demonstrated modest whole leg vasoconstriction with lesser increases in VR than controls (p < .04). Tibial vasculature evidenced absent or blunted vasoconstriction compared to controls (p < .01), indicated by increasing tibial hemoglobin until plateauing at higher pressure levels. This suggests that, in the absence of sympathetic control, tibial vascular response may involve other regulatory mechanisms like myogenic vasoconstriction. Lastly, we leveraged existent whole-body DXA scans in a subgroup of 9 individuals with SCI, and we found a strong relationship between leg BMD and tibial hemoglobin at the end of IHE (r2 = 0.67, p < .01). Our findings indicate that in the absence of sympathetic mechanisms, myogenic control may play a compensatory role in regulating blood flow, though to a lesser extent in bone compared to muscle. The close relationship between lesser declines in bone blood content and higher BMD underscores the link between blood flow and bone health.
骨骼血管系统由广泛的交感神经网络丰富地支配。然而,我们对骨血流调节及其对人类骨骼健康的贡献的理解是有限的。在这里,我们通过研究脊髓损伤(SCI)个体(已知外周交感神经中断的人群)在无交感神经控制情况下的骨血管反应,进一步拓展了我们之前的研究结果。我们评估了SCI个体(n = 12)和对照组(n = 12)中胫骨血管对等长握力运动(IHE)的反应。当持续到疲劳时,IHE会增加腿部非活动组织中的灌注压力和交感神经血管收缩。在IHE期间,我们测量了血压、通过超声测量全腿血流速度(LBV)以及通过近红外光谱测量胫骨灌注(作为血红蛋白含量)。对照组在全腿(即血管阻力[VR]增加,动脉压/LBV)和胫骨(即血红蛋白降低)中表现出活跃的交感神经血管收缩。相比之下,SCI个体表现出适度的全腿血管收缩,VR的增加幅度小于对照组(p < 0.04)。与对照组相比,胫骨血管系统显示出血管收缩缺失或减弱(p < 0.01),这表现为胫骨血红蛋白增加,直到在较高压力水平达到平稳。这表明,在没有交感神经控制的情况下,胫骨血管反应可能涉及其他调节机制,如肌源性血管收缩。最后,我们利用了9名SCI个体亚组中现有的全身双能X线吸收法(DXA)扫描,并且我们发现在IHE结束时腿部骨密度(BMD)与胫骨血红蛋白之间存在很强的关系(r2 = 0.67,p < 0.01)。我们的研究结果表明,在没有交感神经机制的情况下,肌源性控制可能在调节血流中发挥补偿作用,尽管在骨骼中与肌肉相比程度较小。骨血含量下降较少与较高BMD之间的密切关系强调了血流与骨骼健康之间的联系。