Cardiac atrophy in the heterotopically transplanted rat heart: in vitro protein synthesis.

Cardiac atrophy in the heterotopically transplanted rat heart: in vitro protein synthesis.
复制标题

异位移植大鼠心脏的心肌萎缩:体外蛋白质合成。

DOI:
10.1016/0022-2828(90)91481-l
复制
发表时间:
1990
影响因子:
5
通讯作者:
Schreiber,SS
Schreiber,SS
中科院分区:
医学2区
文献类型:
--
作者:
Klein,I;Hong,C;Schreiber,SS

文献摘要

被引文献

相似文献

异位心脏同种异体移植是指维持结构和功能完整的血管灌流器官。我们用这个模型研究了由心肌机械负荷引起的总心脏和左心室大小变化的时间过程。与原位(工作)心脏相比,移植后3天异位(非工作)心脏的大小缩小了19%(P<0.01)。到14天时,移植心脏的大小缩小了50%,当在4周后测量时,移植心脏的大小保持在这个萎缩的大小。在相同的血流动力学条件下,通过移植心脏和宿主心脏的同时体外灌流,测定左心室蛋白质合成。移植心脏每小时14C-赖氨酸掺入左心室总蛋白的量为21nmol,而在位心脏为50nmoL(P<0.01)。在整个研究期间,这一并入保持显著较低的水平。相反,在移植后第3天和第7天,移植左心室的蛋白质合成总量(μ摩尔赖氨酸/克蛋白氮/小时)和蛋白质合成分数都恢复到了对照组的水平。目前的研究表明,异位心脏移植导致心脏质量和总蛋白质合成迅速和可重复的下降。这些研究进一步支持了心脏做功作为调节心脏蛋白质合成的重要决定因素的作用。
Heterotopic cardiac isografts are vasculary perfused organs that maintain structural and functional integrity. We have used this model to study the time course of change in total heart and left ventricular size which results from mechanical unloading of the myocardium. When compared to thein situ(working) heart there is a 19% decrease in the size of the heterotopic (non-working) heart (P< 0.01) as early as 3 days post-transplantation. By 14 days there is 50% decrease in the size of the transplanted heart which is maintained at this atrophic size when measured after 4 weeks. Left ventricular protein synthesis was assayed by the simultaneousin vitroperfusion of the host and transplanted hearts under identical hemodynamic conditions. The hourly incorporation of14C-lysine into total left ventricular protein was 21 nmol in the transplant compared to 50 nmol in thein situheart (P< 0.01). This incorporation remained significantly lower throughout the period of study. In contrast, both the total (μmol lysine/g protein nitrogen/h) and fractional rates of protein synthesis which were lower in the transplanted left ventricle at days 3 and 7 returned to control values by day 28. The present studies demonstrate that heterotopic cardiac transplantation leads to a prompt and reproducible decline in cardiac mass and in total protein synthesis. These studies further support the role of cardiac work as an important determinant in the regulation of cardiac protein synthesis.