Mechanoenergetics in mechanically unloaded myocardial slices

机械卸载心肌切片中的机械能学

基本信息

批准号：
09670053
负责人：
TAKAKI Miyako
金额：
$ 1.86万
依托单位：
Nara Medical University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

项目摘要

Increasing the population of elders, increasing acute and chronic cardiovascular diseases. Thus, physiological and pathophysiological aspects of failing hearts are important issue on Scientific Research on Priority Area. However, it is little known about the energetic efficiency of Ca^<2+> handling in normal and failing hearts on the beat to beat basis. Mechanoenergetics in whole hearts revealed an 0_2 wasting effect or Ca^<2+> futile cycling during the development of failing hearts. To this end, we have recently established a new measurement system of myocardial 0_2 consumption (V0_2) per min of mechanically unloaded rat left ventricular (LV)slices. Using this system, we have revealed that an increment in V0_2(delta V0_2) by electrical stiumulation represents energy expenditure for 0a2+ handling in the excitaiton-contraction (E-C) coupling. We consider that delta V0_2 does not contain V0_2 for residual cross-bridge cycling from the results showing no effect of 2,3-butanedione monoxime (BDM) on delta V0_2. We also established a measurement system slice mechanically unloaded contraction. This contraction is expressed by the motility index. BDM largely decreased this motility index. This result also supported no V0_2 for residual crossbridge cycling was included in delta V0_2. We also revealed that V0_2 without stimulation represents basal metabolism which is much higher than in other mammalian hearts and corresponds to that in the KCI-arrested rat whole heart prepartion. We finally obtained the results showing that sarcoplasmic reticulum (SR) Ga^<2+> pump blockers, thapsigargin and cyclopiazonic acid, did not reduce basal metabolic V0_2 but both of them reduced delta V0_2by 33 and 68% and reduced the motility index by 63 and 81%. We conclude that unloaded myocardial V0_2 is composed of V0_2 for E-C coupling and basal metabolism and does not contain V0_2 for residual crossbridge cycling.

增加长老的人口，增加急性和慢性心血管疾病。因此，心脏失败的生理和病理生理方面是优先领域的科学研究的重要问题。但是，对于以正常和失败的心跳加快的心脏处理的能量效率鲜为人知。整个心脏中的机械能揭示了0_2浪费效果或Ca^<2+>在失败的心脏发展过程中徒劳的循环。为此，我们最近建立了一个新的心肌0_2消耗（V0_2）的测量系统，每分钟机械卸载的大鼠左心室（LV）切片。使用此系统，我们揭示了通过电截止图的V0_2（Delta v0_2）的增量代表了兴奋性 - 征服（E-C）耦合中0A2+处理的能量消耗。我们认为，从结果中，Delta v0_2不包含v0_2的v0_2，显示出2,3-丁烷二氧化碳（BDM）对Delta V0_2的影响。我们还建立了一个测量系统切片机械卸载的收缩。这种收缩由运动指数表示。 BDM在很大程度上降低了该运动指数。此结果还支持剩余的Crossbridge骑自行车的V0_2。我们还透露，没有刺激的V0_2代表基础代谢，这比其他哺乳动物心脏高得多，并且与KCI捕获的大鼠整个心脏育儿中相对应。我们最终获得了结果，结果表明肌质网（SR）Ga^<2+>泵盖子，thapsigargin和cyclopiazonic酸并未减少基础代谢V0_2，但它们都降低了Delta v0_2by 33和68％，并将运动指数降低了63和81％。我们得出的结论是，卸载的心肌V0_2由用于E-C耦合和基础代谢的V0_2组成，并且不包含v0_2用于残留的Crossbridge循环。