Thomas G A, Isoda S, Hammond R L, Lu H, Nakajima H, Nakajima H O, Greer K, Gilroy S J, Salmons S, Stephenson L W
Department of Surgery, Wayne State University, Detroit, Michigan 48201, USA.
Ann Thorac Surg. 1996 Dec;62(6):1698-706; discussion 1706-7. doi: 10.1016/s0003-4975(96)00738-2.
Skeletal muscle ventricles (SMVs) are autologous pumping chambers constructed from skeletal muscle. Skeletal muscle ventricular rupture and thromboembolism have complicated chronic models of this method of skeletal muscle cardiac assist.
The SMVs were constructed from the latissimus dorsi muscle in 10 dogs. The inner surface of each SMV was lined with autologous pericardium harvested at the time of SMV construction. After a 3-week period of vascular delay and 6 weeks of electrical conditioning to convert the muscle to a fatigue-resistant state, SMVs were connected to the descending thoracic aorta and stimulated to contract during cardiac diastole.
Initial hemodynamics revealed that SMV contraction at 33 Hz increased diastolic pressure 24.7% (60.8 +/- 7.3 mm Hg versus 80.3 +/- 8.8 mm Hg). Skeletal muscle ventricle relaxation decreased presystolic pressure 14.4% (59.9 +/- 7.7 mm Hg versus 51.3 +/- 7.5 mm Hg) and decreased peak systolic pressure 4.1% (90.2 +/- 7.3 mm Hg versus 86.5 +/- 5.8 mm Hg). Hemodynamics were assessed at 1 to 2 weeks, then at 1, 2, 3, and 6 months, and at 6-month intervals thereafter. Hemodynamic performance remained stable for the duration of this study. After 2 years of pumping continuously in circulation, SMV contraction resulted in a 34.8% augmentation of diastolic pressure (63.6 +/- 6.6 mm Hg versus 85.3 +/- 6.4 mm Hg), a 17.2% decrease in presystolic pressure (54.7 +/- 3.73 mm Hg versus 45.3 +/- 4.1 mm Hg), and a 4.2% decrease in peak systolic pressure (95.3 +/- 10.4 mm Hg versus 91.3 +/- 12.3 mm Hg). Three dogs survived to 2 years with the SMVs in circulation. No animal showed evidence of thromboembolism during serial echocardiography or at autopsy and no SMVs ruptured.
These data demonstrate that SMVs can provide effective hemodynamic assist over an extended period without specific complications related to the SMVs.
骨骼肌心室（SMV）是由骨骼肌构建的自体泵腔。骨骼肌心室破裂和血栓栓塞一直是这种骨骼肌心脏辅助方法慢性模型的并发症。
在10只犬中，用背阔肌构建SMV。每个SMV的内表面衬以构建SMV时采集的自体心包。经过3周的血管延迟和6周的电调节以使肌肉转变为抗疲劳状态后，将SMV连接至胸降主动脉，并在心脏舒张期刺激其收缩。
初始血流动力学显示，33Hz的SMV收缩使舒张压升高24.7%（60.8±7.3mmHg对80.3±8.8mmHg）。骨骼肌心室舒张使收缩前期压力降低14.4%（59.9±7.7mmHg对51.3±7.5mmHg），并使收缩压峰值降低4.1%（90.2±7.3mmHg对86.5±5.8mmHg）。在1至2周时评估血流动力学，然后在1、2、3和6个月时评估，此后每隔6个月评估一次。在本研究期间，血流动力学性能保持稳定。在持续循环泵血2年后，SMV收缩使舒张压升高34.8%（63.6±6.6mmHg对85.3±6.4mmHg），收缩前期压力降低17.2%（54.7±3.73mmHg对45.3±4.1mmHg），收缩压峰值降低4.2%（95.3±10.4mmHg对91.3±12.3mmHg）。3只犬在SMV循环的情况下存活至2年。在系列超声心动图检查期间或尸检时，没有动物显示血栓栓塞的证据，也没有SMV破裂。
这些数据表明，SMV可在较长时间内提供有效的血流动力学辅助，而无与SMV相关的特定并发症。
