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首页> 外文期刊>American Journal of Physiology >Low-flow vascular remodeling in the metabolic syndrome X.
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Low-flow vascular remodeling in the metabolic syndrome X.

机译：代谢综合征X中的低流量血管重塑

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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.
机译：周围微血管功能障碍是代谢综合征X患者的常见疾病。先前的研究已经描述了人类患者和X综合征动物模型的血管舒缩控制中的许多血管损伤，但是这些损伤对微血管结构的净影响尚不明确。经过检查。本研究的目的是检验X综合征减少肌肉灌注并引起血管重塑的假设。肥胖的Zucker大鼠被用作X综合征的模型，并检查了后肢和大脑的微循环。肥胖Zucker大鼠为肥胖，高脂血症，高胰岛素血症和高血糖症。与瘦大鼠相比，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较薄，管腔较小，并且扩张性降低。肥胖大鼠的后肢微血管还显示出血管平滑肌细胞标志物的表达减少。这些特征中的每一个都与低流量重塑一致。相比之下，大脑微循环中的血流被强烈地自动调节，因此没有血管重塑，微血管平滑肌标志物的表达也没有变化。瘦和肥胖大鼠之间的体育活动和肌肉质量均无显着差异。综上所述，这些发现表明综合症X通过减少后肢的血流量，引起微循环的显着重塑，从而有利于较小，难以扩张的血管。这种重塑可能会导致最大灌注能力的结构限制，并且可能是外周微血管疾病进展中的重要障碍。

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