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Methods to improve cardiac efficiency and load matching.

提高心脏效率和负荷匹配的方法。

基本信息

批准号：
63570045
负责人：
SUGA Hiroyuki
金额：
$ 1.41万
依托单位：
National Cardiovascular Center Research Institute
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1988
资助国家：
日本
起止时间：
1988 至 1989
项目状态：
已结题

项目摘要

The heart consumes oxygen to generate free energy for the mechanical pump performance. The mechanical efficiency of the heart is 10-20% under normal loading and contractile conditions. The factors which decrease this efficiency are 1) significant level of basal metabolism, 2) oxygen wasting effect of enhanced, contractility, and 3) loss in the energy conversion from total I mechanical energy to effective mechanical work. We considered that the mechanical efficiency of the heart could be improved by 1) increasing the contractile efficiency of the heart, and 2) improving the load matching of the heart. In this project, we searched for possible methods to improve the mechanical efficiency of the heart. Through a series of appropriately designed dog heart experiments, we have found the followings: 1) Various acute positive inotropic agents increases the energy utilization for activation (membrane excitation and excitation-contraction coupling) without affecting the contractile efficiency. 2) Myocardial cooling is so far the only positive inotropic intervention which does not increase energy for activation. 3) Systolic pressure-volume area (PVA) as a measure of the total mechanical energy generated by contraction has been established as a reliable predictor of myocardial oxygen consumption (MVo_2). 4) The peak myocardial force and the time integral of force (FTI) which have been recognized to be reliable predictors of MVo_2 were shown not to be go reliable as believed. 5) Linear addition of FTI to PVA does not help improving the predictability of MVo_2.6) Epinephrine and calcium have the same oxygen cost of contractility despite their different pharmacological mechanisms of positive inotropism. These findings together impress us that it would not be easy to find methods to improve mechanical efficiency of the heart which has been usually maximized under normal loading conditions.

心脏消耗氧气来产生机械泵性能所需的自由能。在正常负荷和收缩条件下，心脏的机械效率为10-20%。降低这种效率的因素是：1）基础代谢水平显着，2）增强收缩性的耗氧效应，以及3）从总机械能到有效机械功的能量转换损失。我们认为可以通过1）提高心脏的收缩效率，2）改善心脏的负荷匹配来提高心脏的机械效率。在这个项目中，我们寻找提高心脏机械效率的可能方法。通过一系列适当设计的狗心脏实验，我们发现了以下几点：1）各种急性正性肌力药物增加了激活（膜兴奋和兴奋收缩耦合）的能量利用率，而不影响收缩效率。 2) 心肌冷却是迄今为止唯一不增加激活能量的正性肌力干预。 3) 收缩压-体积面积 (PVA) 作为收缩产生的总机械能的量度，已被确立为心肌耗氧量 (MVo_2) 的可靠预测指标。 4) 峰值心肌力和力的时间积分 (FTI) 已被认为是 MVo_2 的可靠预测因子，但事实证明并不像人们认为的那样可靠。 5) FTI线性添加到PVA无助于提高MVo_2.6)的可预测性。肾上腺素和钙尽管正性肌力作用的药理机制不同，但具有相同的收缩氧消耗。这些发现共同给我们留下了深刻的印象，找到提高心脏机械效率的方法并不容易，而心脏机械效率通常在正常负荷条件下最大化。