Zelis R, Nellis S H, Longhurst J, Lee G, Mason D T
Prog Cardiovasc Dis. 1975 Nov-Dec;18(3):181-99. doi: 10.1016/0033-0620(75)90010-9.
In congestive heart failure, patients appear to have alimited ability to dilate their resistance vessels in skeletal muscle in response to a metabolic stimulus. This is true whether the metabolic stimulus is ischemia, dynamic, or static exercise. The mechanism for this limited arteriolar capacity is at least twofold; an increased sodium content of the vessels as well as an increased tissue pressure which is seen in edematous states. This can be considered a positive compensatory mechanism in that it helps to maintain systemic arterial pressure during exercise when the cardiac output fails to increase normally. If the resistance vessels were to dilate normally, then in the face of a limited cardiac output, exercise syncope would be expected to occur...
在充血性心力衰竭中,患者似乎在面对代谢刺激时扩张骨骼肌阻力血管的能力有限。无论代谢刺激是缺血、动态运动还是静态运动,都是如此。这种有限的小动脉扩张能力的机制至少有两方面;血管钠含量增加以及在水肿状态下出现的组织压力增加。这可以被认为是一种积极的代偿机制,因为当心输出量不能正常增加时,它有助于在运动期间维持体循环动脉压。如果阻力血管正常扩张,那么在面对有限的心输出量时,预计会发生运动性晕厥……