PDF(Pubmed)
Abstract：
In order to determine the behavior of the right ventricle, we have reviewed the existing literature in the area of cardiac remodeling, signal transduction pathways, subcellular mechanisms, β-adrenoreceptor-adenylyl cyclase system and myocardial catecholamine content during the development of left ventricular failure due to myocardial infarction. The right ventricle exhibited adaptive cardiac hypertrophy due to increases in different signal transduction pathways involving the activation of protein kinase C, phospholipase C and protein kinase A systems by elevated levels of vasoactive hormones such as catecholamines and angiotensin II in the circulation at early and moderate stages of heart failure. An increase in the sarcoplasmic reticulum Ca2+ transport without any changes in myofibrillar Ca2+-stimulated ATPase was observed in the right ventricle at early and moderate stages of heart failure. On the other hand, the right ventricle showed maladaptive cardiac hypertrophy at the severe stages of heart failure due to myocardial infarction. The upregulation and downregulation of β-adrenoreceptor-mediated signal transduction pathways were observed in the right ventricle at moderate and late stages of heart failure, respectively. The catalytic activity of adenylate cyclase, as well as the regulation of this enzyme by Gs proteins, were seen to be augmented in the hypertrophied right ventricle at early, moderate and severe stages of heart failure. Furthermore, catecholamine stores and catecholamine uptake in the right ventricle were also affected as a consequence of changes in the sympathetic nervous system at different stages of heart failure. It is suggested that the hypertrophied right ventricle may serve as a compensatory mechanism to the left ventricle during the development of early and moderate stages of heart failure.
摘要：
为了确定右心室的行为，我们回顾了心脏重塑领域的现有文献，信号转导途径，亚细胞机制，β-肾上腺素受体-腺苷酸环化酶系统和心肌儿茶酚胺含量在心肌梗塞引起的左心衰竭发展过程中。由于涉及蛋白激酶C激活的不同信号转导途径的增加，右心室表现出适应性心肌肥厚。磷脂酶C和蛋白激酶A系统通过在心力衰竭的早期和中度阶段循环中升高的血管活性激素，例如儿茶酚胺和血管紧张素II水平。在心力衰竭的早期和中度阶段，右心室观察到肌浆网Ca2转运增加，肌原纤维Ca2刺激的ATPase没有任何变化。另一方面,右心室在心肌梗死导致的严重心力衰竭阶段表现为适应性不良的心肌肥厚.在心力衰竭的中度和晚期，右心室观察到β-肾上腺素受体介导的信号转导通路的上调和下调。分别。腺苷酸环化酶的催化活性，以及Gs蛋白对这种酶的调节，早期发现肥大的右心室增强，中度和重度心力衰竭阶段。此外，在心力衰竭的不同阶段，交感神经系统的变化也影响了右心室中儿茶酚胺的储存和儿茶酚胺的摄取。建议在心力衰竭的早期和中度发展过程中，肥大的右心室可以作为左心室的代偿机制。
