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Cardiomechanical and biophysical effects of left ventricular assist device upon profoundly depressed heart.

左心室辅助装置对严重抑郁的心脏的心脏力学和生物物理影响。

基本信息

批准号：
16390390
负责人：
SAKAMOTO Tohru
金额：
$ 8.38万
依托单位：
Tokyo Medical and Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2004
资助国家：
日本
起止时间：
2004 至 2005
项目状态：
已结题

项目摘要

Left ventricular (IV) assist using IV drainage showed sufficient unloading effects on profoundly depressed heart, without coupled ejection to the native LV. On the volume study, end-diastolic IV volume was mildly increased and end-systolic LV volume was decreased with the increase of assisted ratio, showing the triangle loop as a whole. This volume change was large with obtaining, enough afterload reduction, and erectronmicroscopic myocardial configuration showed same results as control findings. On cell biochemical analysis in myocardium, the mRNA level in Angiotensin II type 1 receptor rose mildly, but the mRNA level in β-1 adrenergic receptor approximately showed equivalent value with "a control state". In addition, it increased to about 3 times comparing the mean value to LA drainage group, resulted in significant statistical difference between LA and IV drainage groups. Angiotensin II type 1 receptor and β-1 adrenergic receptor is the same factor as a G albuminoidal conjugation type acceptor, but this phenomenon is different from Gs, Gq in acceptor coupling factor (a transducer). It is thought that the elevation of the mRNA level of β-1 adrenergic receptor in myocardium increases during left ventricular assist is evidence indicating enough inotropic potentiality after myocardial recovery, and it is thought to be advantageous as a clinical program to achieve "Bridge to Recovery". On the other hand, IV assist with LA drainage did not showed enough afterload reduction, and resulted in persistent occurrence of intracellular edema, mitochondrial size discrepancy and myocardial disarray.In addition, the mRNA level of Angiotensin II type 1 receptor in myocardium increased, showing that afterload for left ventricle was present during IV support.

使用IV引流的左心室（IV）辅助对深度压低的心脏显示出足够的卸载作用，而没有对自体LV的耦合射血。在容量研究中，随着辅助比率的增加，舒张末期IV容量轻度增加，收缩末期LV容量减少，整体呈三角形环。这种体积变化随着获得足够的后负荷减少而变大，并且垂直电子显微镜下心肌构型显示与对照结果相同的结果。在心肌细胞生化分析中，血管紧张素Ⅱ 1型受体mRNA水平轻度升高，而β 1肾上腺素能受体mRNA水平与“对照状态”大致相当。此外，与LA引流组的平均值相比，其增加约3倍，导致LA和IV引流组之间存在显著的统计学差异。血管紧张素Ⅱ 1型受体和β 1肾上腺素能受体是一个G蛋白结合型受体，但这种现象与受体偶联因子（一种转换器）中的Gs、Gq不同。认为在左心室辅助期间心肌中β-1肾上腺素能受体mRNA水平的升高是心肌恢复后足够的变力潜力的证据，并且认为其作为实现“恢复桥”的临床方案是有利的。另一方面，IV辅助LA引流并没有表现出足够的后负荷降低，并导致细胞内水肿，线粒体大小不一致和心肌紊乱的持续发生，此外，心肌中血管紧张素II 1型受体的mRNA水平增加，表明在IV支持期间存在左心室的后负荷。