Low-flow vascular remodeling in the metabolic syndrome X.
Low-flow vascular remodeling in the metabolic syndrome X.
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DOI：
10.1152/ajpheart.00836.2003
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发表时间：
2004-03
期刊：
影响因子：
--
通讯作者：
D. Stepp;D. Pollock;J. Frisbee
中科院分区：
文献类型：
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作者：
D. Stepp;D. Pollock;J. Frisbee
外周微血管功能障碍是代谢综合征X患者的常见症状。以前的研究已经描述了一些血管损伤的血管控制在人类患者和动物模型的X综合征，但这些损伤的微血管结构的净效应尚未检查。本研究的目的是检验X综合征减少肌肉灌注并诱导血管重塑的假设。以肥胖Zucker大鼠作为X综合征模型，检测后肢和脑微循环。肥胖Zucker大鼠肥胖、高血脂、高胰岛素血症和高血糖。相对于瘦大鼠，肥胖大鼠的后肢血流量减少了59%。肥胖大鼠后肢微循环的骨骼肌阻力动脉壁薄，管腔小，扩张性降低。来自肥胖大鼠的后肢微血管也表现出血管平滑肌细胞标志物表达的减少。这些特征中的每一个都与低流量重塑一致。与此相反，脑微循环，其中流量是积极的自动调节，显示没有血管重塑，也没有微血管平滑肌标志物表达的变化。无论是体力活动还是肌肉质量都没有显着差异瘦和肥胖大鼠。总之，这些发现表明，X综合征通过减少后肢血流量，诱导微循环显著重塑，有利于更小，更少扩张的血管。这种重构可能导致最大灌注容量的结构限制，并且可能是外周微血管疾病进展中的重要适应不良。
Peripheral microvascular dysfunction is a common affliction in patients with the metabolic syndrome X. Previous studies have described a number of vascular impairments in vasomotor control in both human patients and animal models of syndrome X, but the net effect of these impairments on microvascular structure has not been examined. The goal of the current study was to test the hypothesis that syndrome X reduces muscle perfusion and induces vascular remodeling. The obese Zucker rat was used as a model of syndrome X, and the microcirculation of the hindlimb and brain were examined. Obese Zucker rats were obese, hyperlipidemic, hyperinsulinemic, and hyperglycemic. Blood flow to the hindlimb was reduced by 59% in obese rats relative to lean rats. Skeletal muscle resistance arteries of the hindlimb microcirculation of obese rats had thinner walls, smaller lumens, and reduced distensibility. Hindlimb microvessels from obese rats also demonstrated reduced expression of vascular smooth muscle cell markers. Each of these traits is consistent with low-flow remodeling. In contrast, the cerebral microcirculation, where flow is vigorously autoregulated, showed no vascular remodeling nor were there changes in microvascular smooth muscle marker expression. Neither physical activity nor muscle mass were significantly different between lean and obese rats. Taken together, these findings suggest that syndrome X, by reducing hindlimb blood flow, induces a marked remodeling of microcirculation to favor smaller, less distensible vessels. This remodeling may result in an architectural limitation of maximum perfusion capacity and may be an important maladaption in the progression of peripheral microvascular disease.