» Articles » PMID: 2536224

SR Ca Loading in Cardiac Muscle Preparations Based on Rapid-cooling Contractures

Overview
Journal Am J Physiol
Specialty Physiology
Date 1989 Jan 1
PMID 2536224
Citations 23
Authors
Affiliations
Soon will be listed here.
Abstract

The influence of rest periods on twitches and rapid-cooling contractures (RCCs) was examined in trabeculae from rabbit, rat, guinea pig, and frog ventricle and rabbit atrium. RCCs were used as a relative index of sarcoplasmic reticulum (SR) Ca content. After increasing rest duration, rabbit and guinea pig ventricles exhibit a decline of both twitch force and RCC force (rest decay). When stimulation is resumed, both twitches and RCCs recover to steady-state levels. The SR (and cells) in these tissues may lose Ca during quiescence and become reloaded with progressive stimulation. Rat ventricle and rabbit atrium exhibited an increase in both twitch and RCC tension as a function of rest duration (rest potentiation). Resumption of stimulation resulted in parallel declines of both twitch and RCC tension approaching steady state. Thus stimulation in rat ventricle and rabbit atrium may lead to a net Ca loss from the SR (and the cell) and quiescence may lead to replenishment of cellular Ca. This major difference in Ca metabolism in mammalian cardiac muscles might be due to a fundamental difference in SR properties or, alternatively, different sarcolemmal transport properties (e.g., action potential configuration, Na-pump). After long rest intervals in rabbit and guinea pig ventricle, RCCs return toward their steady-state value in considerably fewer beats than does twitch tension. This implies that something other than SR refilling is responsible for the slow phase of twitch recovery after rest. In rabbit ventricle increasing frequency or extracellular Ca concentration ([Ca]o) generally increases both twitch and RCC tension. However, decreasing [Ca]o (to 0.2 mM) does not decrease RCCs much despite a dramatic decline in twitch tension (suggesting low twitch tension despite a loaded SR). Rapid rewarming during an RCC usually results in a transient rise in tension (or rewarming "spike"), which is due to a warming-induced increase in myofilament Ca sensitivity. Differences in rewarming spikes among the tissues studied suggest differences in temperature effects on myofilament Ca sensitivity.

Citing Articles

Energy expenditure for isometric contractions of right and left ventricular trabeculae over a wide range of frequencies at body temperature.

Pham T, Zgierski-Johnston C, Tran K, Taberner A, Loiselle D, Han J Sci Rep. 2019; 9(1):8841.

PMID: 31222042 PMC: 6586799. DOI: 10.1038/s41598-019-45273-1.


Role of superoxide ion formation in hypothermia/rewarming induced contractile dysfunction in cardiomyocytes.

Schaible N, Han Y, Tveita T, Sieck G Cryobiology. 2018; 81:57-64.

PMID: 29458041 PMC: 7903890. DOI: 10.1016/j.cryobiol.2018.02.010.


The calcium-frequency response in the rat ventricular myocyte: an experimental and modelling study.

Gattoni S, Roe A, Frisk M, Louch W, Niederer S, Smith N J Physiol. 2016; 594(15):4193-224.

PMID: 26916026 PMC: 4967761. DOI: 10.1113/JP272011.


Dissociation of Calcium Transients and Force Development following a Change in Stimulation Frequency in Isolated Rabbit Myocardium.

Haizlip K, Milani-Nejad N, Brunello L, Varian K, Slabaugh J, Walton S Biomed Res Int. 2015; 2015:468548.

PMID: 25961020 PMC: 4413957. DOI: 10.1155/2015/468548.


Perturbed atrial calcium handling in an ovine model of heart failure: potential roles for reductions in the L-type calcium current.

Clarke J, Caldwell J, Horn M, Bode E, Richards M, Hall M J Mol Cell Cardiol. 2014; 79:169-79.

PMID: 25463272 PMC: 4312356. DOI: 10.1016/j.yjmcc.2014.11.017.