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基于快速冷却挛缩的心肌制剂中的肌浆网钙负荷

SR Ca loading in cardiac muscle preparations based on rapid-cooling contractures.

作者信息

Bers D M

机构信息

Division of Biomedical Sciences, University of California, Riverside 92521-0121.

出版信息

Am J Physiol. 1989 Jan;256(1 Pt 1):C109-20. doi: 10.1152/ajpcell.1989.256.1.C109.

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.

摘要

研究了休息期对来自兔、大鼠、豚鼠和青蛙心室以及兔心房的小梁的抽搐和快速冷却挛缩(RCC)的影响。RCC被用作肌浆网(SR)钙含量的相对指标。增加休息时间后,兔和豚鼠心室的抽搐力和RCC力均下降(休息衰减)。当恢复刺激时,抽搐和RCC均恢复到稳态水平。这些组织中的SR(以及细胞)可能在静止期失去钙,并随着逐渐刺激而重新加载钙。大鼠心室和兔心房的抽搐和RCC张力均随休息时间增加(休息增强)。恢复刺激导致抽搐和RCC张力平行下降并接近稳态。因此,大鼠心室和兔心房中的刺激可能导致SR(以及细胞)净钙流失,而静止可能导致细胞钙补充。哺乳动物心肌中钙代谢的这种主要差异可能是由于SR特性的根本差异,或者是由于不同的肌膜转运特性(例如动作电位构型、钠泵)。在兔和豚鼠心室长时间休息后,RCC在比抽搐张力少得多的搏动次数中恢复到其稳态值。这意味着除了SR再填充之外,还有其他因素导致休息后抽搐恢复的缓慢阶段。在兔心室中,增加频率或细胞外钙浓度([Ca]o)通常会增加抽搐和RCC张力。然而,将[Ca]o降低至0.2 mM(毫摩尔),尽管抽搐张力急剧下降,但RCC并没有太大降低(表明尽管SR负载,但抽搐张力较低)。在RCC期间快速复温通常会导致张力短暂升高(或复温“峰值”),这是由于复温引起的肌丝钙敏感性增加。所研究组织之间复温峰值的差异表明温度对肌丝钙敏感性的影响存在差异。

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