Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type.
Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type.
复制标题
大鼠慢性心力衰竭对相反纤维类型肌肉收缩后微血管 PO2 恢复的影响。
DOI：
10.1113/expphysiol.2004.027367
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发表时间：
2004
期刊：
影响因子：
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通讯作者：
Poole,DavidC
中科院分区：
文献类型：
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作者：
McDonough,Paul;Behnke,BradJ;Musch,TimothyI;Poole,DavidC
慢性心力衰竭 (CHF) 会损害肌肉 O2 输送 (Q̇O2)，并且在给定的 O2 摄取 (V̇O2) 下，会降低微血管 O2 压力（PmvO2：由 Q̇O2 与 V̇O2 比率确定），这可能会损害运动后高能磷酸盐的恢复。由于 CHF 优先减少慢肌的 Q̇O2，我们假设 CHF 大鼠比目鱼肌（SOL：～84% I 型纤维）的恢复 PmvO2 动力学比腓骨（PER：～14% I 型纤维）的恢复 PmvO2 动力学减慢程度更大。PmvO2 动力学在对照肌肉（CON：n = 6；左心室）中测定。 停止电刺激（180 秒；1 Hz）后出现舒张末压，LVEDP：～3 mmHg）、中度 CHF（MOD：n= 7；LVEDP：～11 mmHg）和重度 CHF（SEV：n= 4；LVEDP：～25 mmHg）。在 PER 中，CHF 不会改变恢复 PmvO2 值和平均响应时间（MRT；达到总体响应 63% 的时间的加权平均值）（CON：66.8 ± 8.0，MOD：72.4 ± 11.8，SEV：69.1 ± 9.5 s）。与此形成鲜明对比的是，SEV 组恢复开始时的 SOLPmvO2 显着降低（∼6 Torr），并且随着 CHF 严重程度的增加，PmvO2MRT 减慢（CON：45.1 ± 5.3，MOD：63.2 ± 9.4，SEV：82.6 ± 12.3 s；P < 0.05 CONvs.MOD 和 SEV）。这些数据表明，CHF 会减慢收缩后的 PmvO2 恢复，并降低慢肌 SOL 中毛细血管 O2 驱动压力，但不会降低快肌 PER 肌肉中的毛细血管 O2 驱动压力。这些结果可以部分解释CHF患者肌肉运动后恢复动力学减慢（磷酸肌酸和V̇O2）和明显疲劳。
Chronic heart failure (CHF) impairs muscle O2delivery (Q̇O2) and, at a given O2uptake (V̇O2), lowers microvascular O2pressures (PmvO2: determined by theQ̇O2‐to‐V̇O2ratio), which may impair recovery of high‐energy phosphates following exercise. Because CHF preferentially decreasesQ̇O2to slow‐twitch muscles, we hypothesized that recoveryPmvO2kinetics would be slowed to a greater extent in soleus (SOL: ∼84% type I fibres) than in peroneal (PER: ∼14% type I) muscles of CHF rats.PmvO2dynamics were determined in SOL and PER muscles of control (CON:n= 6; left ventricular end‐diastolic pressure, LVEDP: ∼3 mmHg), moderate CHF (MOD:n= 7; LVEDP: ∼11 mmHg) and severe CHF (SEV:n= 4; LVEDP: ∼25 mmHg) following cessation of electrical stimulation (180 s; 1 Hz). In PER, neither the recoveryPmvO2values nor the mean response time (MRT; a weighted average of the time to 63% of the overall response) were altered by CHF (CON: 66.8 ± 8.0, MOD: 72.4 ± 11.8, SEV: 69.1 ± 9.5 s). In marked contrast, SOLPmvO2, at recovery onset, was reduced significantly in the SEV group (∼6 Torr) andPmvO2MRT was slowed with increased severity of CHF (CON: 45.1 ± 5.3, MOD: 63.2 ± 9.4, SEV: 82.6 ± 12.3 s;P< 0.05 CONvs.MOD and SEV). These data indicate that CHF slowsPmvO2recovery following contractions and lowers capillary O2driving pressure in slow‐twitch SOL, but not in fast‐twitch PER muscle. These results may explain, in part, the slowed recovery kinetics (phosphocreatine andV̇O2) and pronounced fatigue following muscular work in CHF patients.