Mason McClatchey P, Wu Fan, Olfert I Mark, Ellis Christopher G, Goldman Daniel, Reusch Jane E B, Frisbee Jefferson C
Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Department of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
J Cardiovasc Transl Res. 2017 Feb;10(1):69-81. doi: 10.1007/s12265-017-9732-6. Epub 2017 Feb 6.
Metabolic syndrome (MS) in obese Zucker rats (OZR) is associated with impaired skeletal muscle performance and blunted hyperemia. Studies suggest that reduced O diffusion capacity is required to explain compromised muscle performance and that heterogeneous microvascular perfusion distribution is critical. We modeled tissue oxygenation during muscle contraction in control and OZR skeletal muscle using physiologically realistic relationships. Using a network model of Krogh cylinders with increasing perfusion asymmetry and increased plasma skimming, we predict increased perfusion heterogeneity and decreased muscle oxygenation in OZR, with partial recovery following therapy. Notably, increasing O delivery had less impact on VO than equivalent decreases in O delivery, providing a mechanism for previous empirical work associating perfusion heterogeneity and impaired O extraction. We demonstrate that increased skeletal muscle perfusion asymmetry is a defining characteristic of MS and must be considered to effectively model and understand blood-tissue O exchange in this model of human disease.
肥胖Zucker大鼠（OZR）中的代谢综合征（MS）与骨骼肌功能受损和充血不足有关。研究表明，需要降低氧扩散能力来解释肌肉功能受损，并且异质性微血管灌注分布至关重要。我们使用生理现实关系对对照和OZR骨骼肌收缩期间的组织氧合进行建模。使用具有增加的灌注不对称性和增加的血浆撇取的克勒氏圆柱网络模型，我们预测OZR中的灌注异质性增加和肌肉氧合减少，治疗后部分恢复。值得注意的是，增加氧输送对VO的影响小于同等程度的氧输送减少，这为先前将灌注异质性与氧提取受损相关联的实证研究提供了一种机制。我们证明，骨骼肌灌注不对称性增加是MS的一个决定性特征，在这个人类疾病模型中，必须考虑这一点才能有效地模拟和理解血液 - 组织氧交换。
