Constance C G, Sabini G, Turi G K, Hines G L
Department of Surgery, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey.
Cardiovasc Surg. 1993 Jun;1(3):291-5.
The effect of descending thoracic aortomyoplasty using conditioned latissimus dorsi muscle on cardiac output in five mongrel dogs with pharmacologically induced congestive heart failure was evaluated. A neurovascular left latissimus dorsi flap was lifted and through a left thoracotomy placed around the proximal descending thoracic aorta. The flap was conditioned for 4-6 weeks with a neurostimulator using the following parameters: amplitude 0.5 V, pulse width 210 microseconds and frequency 2 Hz. The neurostimulator was then removed and a cardiomyostimulator inserted and programmed to burst-stimulate the muscle during diastole. Baseline measurements of central venous pressure, heart rate, mean arterial blood pressure, pulmonary capillary wedge pressure, and cardiac output were obtained with the cardiomyostimulator off and on (study 1). Heart failure was induced with a combination of propranolol and verapamil, and measurements again taken with the stimulator off and on. The neurostimulator was reimplanted to continue stimulation of the latissimus dorsi muscle, and another set of measurements taken at 6 weeks with the cardiomyostimulator off and on (study 2). Counterpulsation in control conditions (before cardiac failure) in both studies demonstrated no significant increase in cardiac output. However, mean(s.d.) cardiac output was significantly (P < 0.1) increased by muscle stimulation in dogs with heart failure (study 1: from 2.39(1.10) to 3.14(1.41)l/min; study 2: from 1.89(0.64) to 2.38(0.57)l/min). There was no significant difference in the increase in cardiac output associated with muscle stimulation between studies 1 and 2. The results indicate that the model can increase cardiac output in heart failure and that this improvement is constant over a 4-6 week period, suggesting that muscle fatigue may not occur.
评估了在五只经药物诱导出现充血性心力衰竭的杂种犬中，使用经预处理的背阔肌进行降胸主动脉成形术对心输出量的影响。掀起带神经血管蒂的左背阔肌皮瓣，经左胸切口将其置于降胸主动脉近端周围。使用神经刺激器对皮瓣进行4至6周的预处理，参数如下：幅度0.5伏、脉宽210微秒、频率2赫兹。然后移除神经刺激器，插入心肌刺激器并进行编程，使其在舒张期对肌肉进行爆发式刺激。在心肌刺激器关闭和开启的情况下，分别获取中心静脉压、心率、平均动脉血压、肺毛细血管楔压和心输出量的基线测量值（研究1）。用普萘洛尔和维拉帕米联合诱导心力衰竭，再次在刺激器关闭和开启的情况下进行测量。重新植入神经刺激器以继续刺激背阔肌，并在6周时再次在心肌刺激器关闭和开启的情况下进行另一组测量（研究2）。两项研究中，对照条件下（心力衰竭前）的反搏均未显示心输出量有显著增加。然而，心力衰竭犬在肌肉刺激后，平均（标准差）心输出量显著增加（P<0.1）（研究1：从2.39（1.10）升/分钟增至3.14（1.41）升/分钟；研究2：从1.89（0.64）升/分钟增至2.38（0.57）升/分钟）。研究1和研究2中，与肌肉刺激相关的心输出量增加无显著差异。结果表明，该模型可增加心力衰竭时的心输出量，且这种改善在4至6周内持续存在，提示可能未发生肌肉疲劳。
