Department of Surgery, University of California Davis Medical Center, Sacramento, California 95817, USA.
Ann Thorac Surg. 2012 Oct;94(4):1241-8; discussion 1249. doi: 10.1016/j.athoracsur.2012.04.098. Epub 2012 Jul 12.
Engineered heart tissue (EHT) is being developed for clinical implantation in heart failure or congenital heart disease and therefore requires a comprehensive functional characterization and scale-up of EHT. Here we explored the effects of scale-up of self-organizing EHT and present detailed electrophysiologic and contractile functional characterization.
Fibers from EHT were generated from self-organizing neonatal rat cardiac cells (0.5×10(6) to 3×10(6)/fiber) on fibrin. We characterized contractile patterns and measured contractile function using a force transducer, and assessed force-length relationship, maximal force generation, and rate of force generation. Action potential and conduction velocity of EHT were measured with optical mapping, and transcript levels of myosin heavy chain beta were measured by reverse transcriptase-polymerase chain reaction.
Increasing the cell number per construct resulted in an increase in fiber volume. The force-length relationship was negatively impacted by increasing cell number. Maximal force generation and rate of force generation were also abrogated with increasing cell number. This decrease was not likely attributable to a selective expansion of noncontractile cells as myosin heavy chain beta levels were stable. Irregular contractile behavior was more prevalent in constructs with more cells. Engineered heart tissue (1×10(6)/construct) had an action potential duration of 140.2 milliseconds and a conduction velocity of 23.2 cm/s.
Engineered heart tissue displays physiologically relevant features shared with native myocardium. Engineered heart tissue scale-up by increasing cell number abrogates contractile function, possibly as a result of suboptimal cardiomyocyte performance in the absence of vasculature. Finally, conduction velocity approaches that of native myocardium without any electrical or mechanical conditioning, suggesting that the self-organizing method may be superior to other rigid scaffold-based EHT.
工程心脏组织 (EHT) 正在开发用于心力衰竭或先天性心脏病的临床植入,因此需要对 EHT 进行全面的功能表征和放大。在这里,我们探讨了自组织 EHT 放大的效果,并呈现了详细的电生理和收缩功能特征。
纤维从 EHT 从自组织新生大鼠心脏细胞(0.5×10(6)至 3×10(6)/纤维)在纤维蛋白上产生。我们使用力传感器来描述收缩模式和测量收缩功能,并评估力-长度关系、最大力生成和力生成速率。EHT 的动作电位和传导速度用光学映射测量,肌球蛋白重链β的转录水平用逆转录聚合酶链反应测量。
增加每个构建体的细胞数量会导致纤维体积增加。力-长度关系随着细胞数量的增加而受到负面影响。最大力生成和力生成速率也随着细胞数量的增加而被废除。这种减少不太可能归因于非收缩细胞的选择性扩张,因为肌球蛋白重链β水平保持稳定。随着细胞数量的增加,不规则的收缩行为更为普遍。工程心脏组织(1×10(6)/构建体)的动作电位持续时间为 140.2 毫秒,传导速度为 23.2 cm/s。
工程心脏组织显示出与天然心肌共享的生理相关特征。通过增加细胞数量来放大工程心脏组织会破坏收缩功能,可能是由于缺乏脉管系统导致心肌细胞性能不佳。最后,传导速度接近天然心肌,无需任何电或机械调节,表明自组织方法可能优于其他刚性支架 EHT。