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虹鳟鱼心肌对牵张没有表现出缓慢的变力性反应。

Rainbow trout myocardium does not exhibit a slow inotropic response to stretch.

机构信息

Faculty of Life Sciences, University of Manchester, 46 Grafton Street, Manchester M13 9NT, UK.

出版信息

J Exp Biol. 2011 Apr 1;214(Pt 7):1118-22. doi: 10.1242/jeb.048546.

DOI:10.1242/jeb.048546
PMID:21389196
Abstract

Mammalian myocardial studies reveal a biphasic increase in the force of contraction due to stretch. The first rapid response, known as the Frank-Starling response, occurs within one heartbeat of stretch. A second positive inotropic response occurs over the minutes following the initial stretch and is known as the slow force response (SFR). The SFR has been observed in mammalian isolated whole hearts, muscle preparations and individual myocytes. We present the first direct study into the SFR in the heart of a non-mammalian vertebrate, the rainbow trout (Oncorhynchus mykiss). We stretched ventricular trabecular muscle preparations from 88% to 98% of their optimal length and individual ventricular myocytes by 7% of their slack sarcomere length (SL). Stretch caused an immediate increase in force in both preparations, indicative of the Frank-Starling response. However, we found no significant effect of prolonged stretch on the force of contraction in either the ventricular trabecular preparations or the single myocytes. This indicates that rainbow trout ventricular myocardium does not exhibit a SFR and that, in contrast to mammals, the piscine Frank-Starling response may not be associated with the SFR. We speculate that this is due to the fish myocardium modulating cardiac output via changes in stroke volume to a larger extent than heart rate.

摘要

哺乳动物心肌研究表明,由于拉伸会导致收缩力呈双相增加。第一个快速反应,即弗兰克-斯塔林反应,在拉伸后的一个心跳内发生。第二个正性肌力反应发生在初始拉伸后的几分钟内,称为缓慢力反应(SFR)。SFR 已在哺乳动物分离的全心、肌肉制剂和单个心肌细胞中观察到。我们首次在非哺乳动物脊椎动物虹鳟鱼(Oncorhynchus mykiss)的心脏中进行了 SFR 的直接研究。我们将心室小梁肌肉制剂拉伸至其最佳长度的 88%至 98%,并将单个心室心肌细胞拉伸至其松弛肌节长度(SL)的 7%。拉伸导致两种制剂的力立即增加,表明存在弗兰克-斯塔林反应。然而,我们发现延长拉伸对心室小梁制剂或单个心肌细胞的收缩力没有显著影响。这表明虹鳟鱼心室心肌不表现出 SFR,并且与哺乳动物不同,鱼类的弗兰克-斯塔林反应可能与 SFR 无关。我们推测这是由于鱼类心肌通过改变每搏量而不是心率来更大程度地调节心输出量。

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