Thomas G A, Lu H, Isoda S, Hammond R L, Nakajima H, Nakajima H O, Colson M, Stephenson L W
Department of Surgery, Wayne State University, Detroit, Michigan.
Ann Thorac Surg. 1994 Oct;58(4):978-87; discussion 987-8. doi: 10.1016/0003-4975(94)90441-3.
Skeletal muscle ventricles (SMVs) were constructed from the latissimus dorsi muscle in 15 beagles. The animals were divided into two groups based on modifications in the SMV construction: group I consisted of 5 animals and group II of 10 animals. After a 3-week vascular delay and 6 to 8 weeks of 2-Hz electrical conditioning, the SMVs were connected to the thoracic aorta. In group I, counterpulsation at 33 Hz resulted in an initial 24.4% augmentation of the mean diastolic pressure, a 27.1% decrease in the presystolic pressure, and a 15.9% increase in the endocardial viability ratio. In group II, the mean diastolic pressure rose by 24.7%, the presystolic pressure decreased by 14.3%, and the endocardial viability ratio increased by 24.5%. During propranolol-induced heart failure, the percentage increase in the mean diastolic pressure was improved (12.9% before propranolol infusion versus 27.6% during propranolol infusion), as was the percentage increase in the endocardial viability ratio (11.2% versus 28.7%). Under low cardiac output conditions, SMV contraction resulted in small but statistically significant increases in the total cardiac output (4.3% at 33 Hz, 7.6% at 85 Hz). One animal in group I survived for 589 days with a functioning SMV before progressive dilation of the SMV (impending rupture) developed. Delayed rupture of the SMV sewing ring anastomosis occurred in 2 dogs. Five animals in group II are all alive, with functioning SMVs in the circulation for 377 to 464 days. No animals in group II had rupture of their SMV or showed evidence of thrombus formation.
在15只比格犬中，利用背阔肌构建骨骼肌心室（SMV）。根据SMV构建方式的不同，将动物分为两组：第一组有5只动物，第二组有10只动物。经过3周的血管延迟和6至8周的2赫兹电刺激调节后，将SMV与胸主动脉相连。在第一组中，33赫兹的反搏导致平均舒张压最初增加24.4%，收缩前期压力降低27.1%，心内膜存活比率增加15.9%。在第二组中，平均舒张压上升24.7%，收缩前期压力降低14.3%，心内膜存活比率增加24.5%。在普萘洛尔诱发心力衰竭期间，平均舒张压的增加百分比有所改善（普萘洛尔输注前为12.9%，输注期间为27.6%），心内膜存活比率的增加百分比也是如此（分别为11.2%和28.7%）。在低心输出量情况下，SMV收缩导致总心输出量有小幅度但具有统计学意义的增加（33赫兹时为4.3%，85赫兹时为7.6%）。第一组中有1只动物在SMV功能正常的情况下存活了589天，之后SMV逐渐扩张（即将破裂）。2只犬发生了SMV缝合环吻合口延迟破裂。第二组的5只动物均存活，其SMV在循环中功能正常377至464天。第二组中没有动物出现SMV破裂或血栓形成的迹象。
