Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts
Engineered heart tissue grafts improve systolic and diastolic function in infarcted rat hearts
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DOI：
10.1038/nm1394
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发表时间：
2006-04-01
期刊：
影响因子：
82.9
通讯作者：
Eschenhagen, T
中科院分区：
文献类型：
--
作者：
Zimmermann, WH;Melnychenko, I;Eschenhagen, T
通过植入组织工程心肌来再生病变心肌的概念很耐人寻味，但缺乏令人信服的证据表明，可以产生大小和具有收缩特性的心脏组织，从而为衰竭的心脏提供相当大的支持。在这里，我们创造了大(厚度/直径，1-4 mm/15 mm)，产生力量的工程化心脏组织从新生大鼠的心脏细胞。将工程化心脏组织植入免疫抑制大鼠的心肌梗死处，可形成厚厚的心肌层。当28天后评估时，工程化心脏组织显示出与自然心肌无延迟的电耦合，没有诱发心律失常的证据。此外，与对照组(假手术和非收缩结构)相比，工程化心脏组织防止了进一步的扩张，导致梗死心肌节段的收缩期壁增厚，并改善了梗死心脏的面积缩小分数。因此，我们的研究提供了证据，证明大的收缩心肌组织移植物可以在体外构建，植入后可以存活，并可以支持梗死心脏的收缩功能。
The concept of regenerating diseased myocardium by implantation of tissue-engineered heart muscle is intriguing, but convincing evidence is lacking that heart tissues can be generated at a size and with contractile properties that would lend considerable support to failing hearts. Here we created large (thickness/ diameter, 1-4 mm/15 mm), force-generating engineered heart tissue from neonatal rat heart cells. Engineered heart tissue formed thick cardiac muscle layers when implanted on myocardial infarcts in immune-suppressed rats. When evaluated 28 d later, engineered heart tissue showed undelayed electrical coupling to the native myocardium without evidence of arrhythmia induction. Moreover, engineered heart tissue prevented further dilation, induced systolic wall thickening of infarcted myocardial segments and improved fractional area shortening of infarcted hearts compared to controls (sham operation and noncontractile constructs). Thus, our study provides evidence that large contractile cardiac tissue grafts can be constructed in vitro, can survive after implantation and can support contractile function of infarcted hearts.