OXYGEN DEPRIVATION AND EARLY MYOCARDIAL CONTRACTILE FAILURE - REASSESSMENT OF THE POSSIBLE ROLE OF ADENOSINE-TRIPHOSPHATE
OXYGEN DEPRIVATION AND EARLY MYOCARDIAL CONTRACTILE FAILURE - REASSESSMENT OF THE POSSIBLE ROLE OF ADENOSINE-TRIPHOSPHATE
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DOI：
10.1016/0002-9149(79)90177-2
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发表时间：
1979-01-01
影响因子：
2.8
通讯作者：
HEARSE, DJ
中科院分区：
文献类型：
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作者：
HEARSE, DJ
心肌缺氧或缺血后早期收缩衰竭的确切机制引起了人们的猜测和争议。三磷酸腺苷（ATP）缺乏是导致这种失败的简单而有吸引力的假设经常被驳回，因为当收缩活动严重减少时，细胞ATP含量只有少量减少。本文的前提是，理论上缺氧后细胞ATP含量和分布的变化可能没有得到充分考虑，以前的细胞ATP含量测量可能没有在正确的时间进行。钳夹技术可以证明心肌ATP和磷酸肌酸含量的显著降低发生在缺氧发作之后，但在收缩衰竭发作之前。因此，在缺氧的前5秒，收缩活动保持不变，而ATP减少25%，磷酸肌酸减少50%。此后，发生收缩失败，高能磷酸盐的利用率随着细胞含量处于平台或可能增加而下降。这些结果是根据早期缺氧时能量代谢的动态变化进行评估的，并表明特定细胞室中的ATP耗尽可能是早期收缩衰竭的主要触发因素。
The precise mechanism responsible for early contractile failure after the onset of myocardial anoxia or ischemia has attracted speculation and controversy. The simple and attractive hypothesis that adenosine triphosphate (ATP) deficiency is responsible for this failure has often been dismissed on the basis of claims that there is only a small reduction in cell ATP content at a time when contractile activity is severely reduced. The premise of this article is that the changes in cell ATP content and distribution that theoretically should occur after oxygen depletion may not have been adequately considered and that previous measurements of cell ATP content may not have been carried out at the correct time.Using an isolated rat heart preparation and high speed freeze-clamping techniques it has been possible to demonstrate that a substantial decrease in myocardial ATP and creatine phosphate content occurs after the onset of anoxia butbeforethe onset of contractile failure. Thus, during the first 5 seconds of anoxia contractile activity remains constant whereas ATP decreases by 25 percent and creatine phosphate by 50 percent. Thereafter, contractile failure occurs and the rate of utilization of high energy phosphates declines with the cell content at a plateau or possibly increasing. These results are assessed in the light of the dynamic changes in energy metabolism occurring in early anoxia and suggest that ATP depletion in a specific cell compartment may be the primary trigger for early contractile failure.