目的:先前在慢性肾脏病(CKD)中的研究表明,随着CKD严重程度的恶化,不同循环床的血管功能障碍逐渐恶化。这项研究评估了静息时的肌肉氧合和微血管反应性,在闭塞再灌注操作期间,以及在不同阶段的CKD患者与对照组的运动过程中。
方法:观察性对照研究。
方法:90名参与者(每个CKD阶段2,3a,3b,4和18个控件)。
方法:CKD阶段。
结果:主要,休息时的肌肉氧合;继发性,闭塞再灌注和运动过程中的肌肉氧合,和肌肉微血管反应性(充血反应)。
方法:在休息时使用近红外光谱法连续测量肌肉氧合[组织饱和指数(TSI%)],在闭塞-再灌注期间,并且在3分钟的握力练习中(最大自愿收缩的35%)。还记录了主动脉脉搏波速度(PWV)和颈动脉内膜中层厚度(cIMT)。
结果:静息肌肉氧合在研究组之间没有差异(对照组:64.3±2.9-2阶段:63.8±4.2阶段-3a:64.1±4.1阶段-3b:62.3±3.3阶段-4:62.7±4.3%;p=0.6)。在闭塞期间,在TSIocl量值和闭塞斜率方面,组间没有检测到显著差异.然而,再灌注期间,与对照组相比,CKD分期更晚期的患者组的TSImax和充血反应显著更低(对照:11.2±3.7分期-2:8.3±4.6分期-3:7.8±5.5分期-3b:7.3±4.4分期-4:7.2±3.3;p=0.04).在手握练习期间,CKD患者的肌肉氧合(TSI平均下降)略低于对照组,但CKD各阶段未检测到显著差异.
结论:样本量适中,横截面评估。
结论:虽然静息或闭塞时的肌肉氧合没有差异,再灌注过程中的微血管充血反应在CKD中显著受损,在更晚期的CKD中最为明显.微脉管系统对刺激的反应能力受损可能是CKD患者不良血管分布的关键组成部分,并可能导致运动不耐受。
Previous studies in chronic kidney disease (CKD) showed that vascular dysfunction in different circulatory beds progressively deteriorates with worsening CKD severity. This
study evaluated muscle oxygenation and microvascular reactivity at rest, during an occlusion-reperfusion maneuver, and during exercise in patients with different stages of CKD versus controls.
Observational controlled
study.
90 participants (18 per CKD stage 2, 3a, 3b, and 4, as well as 18 controls).
CKD stage.
The primary outcome was muscle oxygenation at rest. Secondary outcomes were muscle oxygenation during occlusion-reperfusion and exercise, and muscle microvascular reactivity (hyperemic response).
Continuous measurement of muscle oxygenation [tissue saturation index (TSI)] using near-infrared spectroscopy at rest, during occlusion-reperfusion, and during a 3-minute handgrip exercise (at 35% of maximal voluntary contraction). Aortic pulse wave velocity and carotid intima-media thickness were also recorded.
Resting muscle oxygenation did not differ across the
study groups (controls: 64.3% ± 2.9%; CKD stage 2: 63.8% ± 4.2%; CKD stage 3a: 64.1% ± 4.1%; CKD stage 3b: 62.3% ± 3.3%; CKD stage 4: 62.7% ± 4.3%; P=0.6). During occlusion, no significant differences among groups were detected in the TSI occlusion magnitude and TSI occlusion slope. However, during reperfusion the maximum TSI value was significantly lower in groups of patients with more advanced CKD stages compared with controls, as was the hyperemic response (controls: 11.2%±3.7%; CKD stage 2: 8.3%±4.6%; CKD stage 3: 7.8%±5.5%; CKD stage 3b: 7.3%±4.4%; CKD stage 4: 7.2%±3.3%; P=0.04). During the handgrip exercise, the average decline in TSI was marginally lower in patients with CKD than controls, but no significant differences were detected across CKD stages.
Moderate sample size, cross-sectional evaluation.
Although no differences were observed in muscle oxygenation at rest or during occlusion, the microvascular hyperemic response during reperfusion was significantly impaired in CKD and was most prominent in more advanced CKD stages. This impaired ability of microvasculature to respond to stimuli may be a crucial component of the adverse vascular profile of patients with CKD and may contribute to exercise intolerance.
Previous studies in chronic kidney disease (CKD) have shown that vascular dysfunction in different circulatory beds progressively deteriorates with CKD severity. This
study evaluated muscle oxygenation and microvascular reactivity at rest, during an occlusion-reperfusion maneuver, and during exercise in patients with nondialysis CKD versus controls, as well as across different CKD stages. It showed that the microvascular hyperemic response after an arterial occlusion was significantly impaired in CKD and was worst in patients with more advanced CKD. No significant differences were detected in skeletal muscle oxygenation or muscle oxidative capacity at rest or during the handgrip exercise when comparing patients with CKD with controls or comparing across CKD stages. The impaired ability of microvasculature to respond to stimuli may be a component of the adverse vascular profile of patients with CKD and may contribute to exercise intolerance.