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

Patrick, Simon M.; White, Ed; Shiels, Holly A.

doi:10.1242/jeb.048546

Cited by 7 publications

(11 citation statements)

References 32 publications

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“…because it has been observed after prolonged stretch in all mammalian preparations examined to date (Alvarez et al, 1999;Calaghan and White, 1999). Our results from the axolotl are consistent with a previous study which failed to show a slow force response in the ventricle of the rainbow trout (Patrick et al, 2011) and may suggest that the slow force response evolved after amphibians diverged from the vertebrate lineage. In that paper, Patrick et al (2011) speculated that the trout heart would not benefit from the slow force response because it was already specialized for developing force at long lengths (see Farrell, 1991;Patrick et al, 2010).…”

Section: Discussionsupporting

confidence: 91%

“…The active forces and kinetic time courses produced by the muscle preparations in the current study are similar to those reported for fish (Patrick et al, 2011;Shiels et al, 2002), other amphibians (Rana temporaria) (Driedzic and Gesser, 1985) and axolotls (Meghji and Burnstock, 1983) at comparable frequencies and temperatures. However the magnitude of the Frank-Starling response (i.e.…”

Section: Discussionsupporting

confidence: 83%

“…However the magnitude of the Frank-Starling response (i.e. increase in active force when preparations were stretched from L 88% to L 98% ) was less, particularly at the colder temperature ( $ 14% increase in force), than that observed in a previous study using the same methods in trout ventricle ( $ 40% increase in force) (Patrick et al, 2011). By using a constant crosssectional area to normalize force we would have overestimated force at shorter lengths and that would reduce the amplitude of the Frank-Starling response (see Section 2) but that would not account for the difference between studies.…”

Section: Discussioncontrasting

confidence: 65%

“…Muscle preparations were stretched to quantify the FrankStarling response and the slow force response as previously described (Patrick et al, 2011). Briefly, preparations were slowly stretched from L slack to L max (the length at which maximum tension was generated) and then maintained at 98% L max (L 98% ) until the force of contraction was stable for 10 min.…”

Section: Experimental Protocolsmentioning

confidence: 99%

“…The slow force response has been observed in all mammalian ventricular preparations in which it has been investigated although it's physiological relevance is still debated. A recent study revealed that the slow force response was not observed in the ventricle of the rainbow trout (Patrick et al, 2011) calling into question the existence of the slow force response in non-mammalian vertebrate hearts. Thus, we were particularly interested to know if a slow force response was present in the amphibious axolotl heart as this could shed light on the advent of this mechanism during vertebrate evolution.…”

Section: Introductionmentioning

confidence: 99%

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Contractile properties of the axolotl ventricle at 17 and 21°C

Wignall¹,

Shiels²

2012

Journal of Thermal Biology

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 83%

Section: Discussioncontrasting

confidence: 65%

Section: Experimental Protocolsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Contractile properties of the axolotl ventricle at 17 and 21°C

Wignall¹,

Shiels²

2012

Journal of Thermal Biology

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The Zebrafish Heart as a Model of Mammalian Cardiac Function

Genge

Lin

Lee

et al. 2016

Reviews of Physiology, Biochemistry and Pharmacology

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Zebrafish (Danio rerio) are widely used as vertebrate model in developmental genetics and functional genomics as well as in cardiac structure-function studies. The zebrafish heart has been increasingly used as a model of human cardiac function, in part, due to the similarities in heart rate and action potential duration and morphology with respect to humans. The teleostian zebrafish is in many ways a compelling model of human cardiac function due to the clarity afforded by its ease of genetic manipulation, the wealth of developmental biological information, and inherent suitability to a variety of experimental techniques. However, in addition to the numerous advantages of the zebrafish system are also caveats related to gene duplication (resulting in paralogs not present in human or other mammals) and fundamental differences in how zebrafish hearts function. In this review, we discuss the use of zebrafish as a cardiac function model through the use of techniques such as echocardiography, optical mapping, electrocardiography, molecular investigations of excitation-contraction coupling, and their physiological implications relative to that of the human heart. While some of these techniques (e.g., echocardiography) are particularly challenging in the zebrafish because of diminutive size of the heart (~1.5 mm in diameter) critical information can be derived from these approaches and are discussed in detail in this article.

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The zebrafish as a novel animal model to study the molecular mechanisms of mechano-electrical feedback in the heart

Werdich

Brzezinski

Jeyaraj

et al. 2012

Progress in Biophysics and Molecular Biology

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Altered mechanical loading of the heart leads to hypertrophy, decompensated heart failure and fatal arrhythmias. However, the molecular mechanisms that link mechanical and electrical dysfunction remain poorly understood. Growing evidence suggest that ventricular electrical remodeling (VER) is a process that can be induced by altered mechanical stress, creating persistent electrophysiological changes that predispose the heart to life-threatening arrhythmias. While VER is clearly a physiological property of the human heart, as evidenced by “T wave memory”, it is also thought to occur in a variety of pathological states associated with altered ventricular activation such as bundle branch block, myocardial infarction, and cardiac pacing. Animal models that are currently being used for investigating stretch-induced VER have significant limitations. The zebrafish has recently emerged as an attractive animal model for studying cardiovascular disease and could overcome some of these limitations. Owing to its extensively sequenced genome, high conservation of gene function, and the comprehensive genetic resources that are available in this model, the zebrafish may provide new insights into the molecular mechanisms that drive detrimental electrical remodeling in response to stretch. Here, we have established a zebrafish model to study mechano-electrical feedback in the heart, which combines efficient genetic manipulation with high-precision stretch and high-resolution electrophysiology. In this model, only ninety minutes of ventricular stretch caused VER and recapitulated key features of VER found previously in the mammalian heart. Our data suggest that the zebrafish model is a powerful platform for investigating the molecular mechanisms underlying mechano-electrical feedback and VER in the heart.

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

Cited by 7 publications

References 32 publications

Contractile properties of the axolotl ventricle at 17 and 21°C

Contractile properties of the axolotl ventricle at 17 and 21°C

The Zebrafish Heart as a Model of Mammalian Cardiac Function

The zebrafish as a novel animal model to study the molecular mechanisms of mechano-electrical feedback in the heart

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