Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506-5802, USA.
Am J Physiol Heart Circ Physiol. 2010 Dec;299(6):H1755-61. doi: 10.1152/ajpheart.00590.2010. Epub 2010 Sep 3.
Chronic heart failure (CHF) induces muscle fiber-type specific alterations in skeletal muscle O(2) delivery and utilization during metabolic transitions. As a result, the recovery of microvascular Po(2) (Pmv(O(2))) is prolonged in slow-twitch skeletal muscle but not fast-twitch skeletal muscle in rats with CHF. We tested the hypothesis that CHF slows Pmv(O(2)) recovery in rat skeletal muscle of a mixed fiber-type analogous to human locomotory muscles and that the degree of slowing correlates with central indexes of heart failure. Healthy control [n = 6, left ventricular end-diastolic pressure (LVEDP): 10 ± 1 mmHg], moderate CHF (n = 6, LVEDP: 18 ± 2 mmHg), and severe CHF (n = 4, LVEDP: 34 ± 2 mmHg) female Sprague-Dawley rats had their right spinotrapezius muscles (41% type I, 7% type IIa, and 52% type IIb and d/x) exposed, and Pmv(O(2)) was measured via phosphorescence quenching during 180 s of recovery from 180 s of electrically induced twitch contractions (1 Hz, 4-6 V). CHF progressively slowed the mean response time (MRT; the time to reach 63% of the overall dynamic response) of Pmv(O(2)) recovery (MRT(off); control: 60.2 ± 6.9, moderate CHF: 72.8 ± 6.6, and severe CHF: 109.8 ± 6.6 s, P < 0.05 for all). MRT(off) correlated positively with central hemodynamic (LVEDP: r = 0.76, P < 0.01) and morphological (right ventricle-to-body weight ratio: r = 0.74, P < 0.01; and lung weight-to-body weight ratio: r = 0.79, P < 0.01) indexes of heart failure. The present investigation suggests that slowed Pmv(O(2)) kinetics during recovery in CHF constitutes a mechanistic link between impaired circulatory and metabolic recovery after contractions in CHF.
慢性心力衰竭（CHF）会导致骨骼肌中氧气输送和利用在代谢转换期间发生纤维类型特异性改变。因此，在 CHF 大鼠的慢肌中，微血管氧分压（Pmv（O2））的恢复时间延长，但在快肌中则不会。我们假设 CHF 会使大鼠混合纤维型骨骼肌的 Pmv（O2）恢复速度减慢，并且这种减慢的程度与心力衰竭的中心指标相关。健康对照组[n = 6，左心室舒张末期压（LVEDP）：10 ± 1 mmHg]、中度 CHF 组（n = 6，LVEDP：18 ± 2 mmHg）和重度 CHF 组（n = 4，LVEDP：34 ± 2 mmHg）的雌性 Sprague-Dawley 大鼠右斜方肌（41% I 型、7% IIa 型、52% IIb 和 d/x 型）暴露，通过磷光猝灭法测量 180 s 电诱导抽搐收缩（1 Hz，4-6 V）后 180 s 的 Pmv（O2）恢复过程中的平均响应时间（MRT；达到整体动态响应的 63%所需的时间）。CHF 逐渐减慢 Pmv（O2）恢复的平均响应时间（MRT（off）；对照组：60.2 ± 6.9，中度 CHF：72.8 ± 6.6，重度 CHF：109.8 ± 6.6 s，所有 P < 0.05）。MRT（off）与中心血流动力学（LVEDP：r = 0.76，P < 0.01）和形态学（右心室/体重比：r = 0.74，P < 0.01；和肺重/体重比：r = 0.79，P < 0.01）指标呈正相关。本研究表明，CHF 中恢复期间 Pmv（O2）动力学的减慢是 CHF 后收缩时循环和代谢恢复受损的机制联系。
