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老年心肌收缩持续时间延长。

Prolonged contraction duration in aged myocardium.

作者信息

Lakatta E G, Gerstenblith G, Angell C S, Shock N W, Weisfeldt M L

出版信息

J Clin Invest. 1975 Jan;55(1):61-8. doi: 10.1172/JCI107918.

DOI:10.1172/JCI107918
PMID:1109181
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC301717/
Abstract

Isometric performance at 29degreesC was measured in left ventricular trabeculae carneae from young adult (6-mo) and aged (25-mo) rats (n equals 18 in each group). Active tension and maximal rate of tension development did not differ with age, but contraction duration was 255plus or minus6 ms in the young adult and 283plus or minus6 ms in the aged group (P less than0.001). Although catecholamine content per gram heart weight was less in the aged myocardium, additional experiments showed that neither 1 times 10-6 M propranolol nor pretreatment with 6-hydroxydopamine eliminated the age difference in contraction duration. To determine if this age difference resulted from a prolonged active state, electromechanical dissociation and the overshoot of contraction duration during recovery from hypoxia were measured. During paired stimulation greater mechanical refractoriness was found in aged muscles (P less than0.01), but intracellular action potential recordings showed no age difference in the electrical refractory period. On recovery from hypoxia, contraction duration overshoot was 117plus or minus 4percent of control in the young and 138plus or minus 4percent of control in the aged muscles (P less than0.01). The greater electromechanical dissociation and greater overshoot in contraction duration following hypoxia in aged myocardium suggests that prolonged contraction duration in aged myocardium results from a prolonged active state rather than changes in passive properties or myocardial catecholamine content.

摘要

在29摄氏度下,对年轻成年(6个月)和老年(25个月)大鼠的左心室肉柱进行等长性能测量(每组n = 18)。主动张力和张力发展的最大速率在年龄上没有差异,但年轻成年组的收缩持续时间为255±6毫秒,老年组为283±6毫秒(P<0.001)。尽管老年心肌每克心脏重量中的儿茶酚胺含量较低,但进一步的实验表明,1×10-6M普萘洛尔或用6-羟基多巴胺预处理均不能消除收缩持续时间的年龄差异。为了确定这种年龄差异是否由延长的活动状态引起,测量了电机械分离和缺氧恢复过程中收缩持续时间的超调。在成对刺激期间,老年肌肉中发现更大的机械不应期(P<0.01),但细胞内动作电位记录显示电不应期没有年龄差异。从缺氧恢复时,年轻肌肉收缩持续时间超调为对照的117±4%,老年肌肉为对照的138±4%(P<0.01)。老年心肌中更大的电机械分离和缺氧后收缩持续时间更大的超调表明,老年心肌收缩持续时间延长是由延长的活动状态引起的,而不是被动特性或心肌儿茶酚胺含量的变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/301717/a1dd89dfe771/jcinvest00165-0072-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/301717/e8ccb6360700/jcinvest00165-0072-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/301717/a1dd89dfe771/jcinvest00165-0072-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/301717/e8ccb6360700/jcinvest00165-0072-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/301717/a1dd89dfe771/jcinvest00165-0072-b.jpg

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