Vornanen Matti
University of Eastern Finland, Department of Environmental and Biological Sciences, PO Box 111, Joensuu 80101, Finland
J Exp Biol. 2016 Jul 1;219(Pt 13):1941-52. doi: 10.1242/jeb.128439.
Environmental temperature has pervasive effects on the rate of life processes in ectothermic animals. Animal performance is affected by temperature, but there are finite thermal limits for vital body functions, including contraction of the heart. This Review discusses the electrical excitation that initiates and controls the rate and rhythm of fish cardiac contraction and is therefore a central factor in the temperature-dependent modulation of fish cardiac function. The control of cardiac electrical excitability should be sensitive enough to respond to temperature changes but simultaneously robust enough to protect against cardiac arrhythmia; therefore, the thermal resilience and plasticity of electrical excitation are physiological qualities that may affect the ability of fishes to adjust to climate change. Acute changes in temperature alter the frequency of the heartbeat and the duration of atrial and ventricular action potentials (APs). Prolonged exposure to new thermal conditions induces compensatory changes in ion channel expression and function, which usually partially alleviate the direct effects of temperature on cardiac APs and heart rate. The most heat-sensitive molecular components contributing to the electrical excitation of the fish heart seem to be Na(+) channels, which may set the upper thermal limit for the cardiac excitability by compromising the initiation of the cardiac AP at high temperatures. In cardiac and other excitable cells, the different temperature dependencies of the outward K(+) current and inward Na(+) current may compromise electrical excitability at temperature extremes, a hypothesis termed the temperature-dependent depression of electrical excitation.
环境温度对外温动物生命过程的速率具有广泛影响。动物的表现受温度影响，但包括心脏收缩在内的重要身体功能存在有限的热极限。本综述讨论了引发和控制鱼类心脏收缩速率及节律的电兴奋，因此它是鱼类心脏功能温度依赖性调节的核心因素。心脏电兴奋性的控制应足够敏感以响应温度变化，但同时又要足够稳健以防止心律失常；因此，电兴奋的热弹性和可塑性是可能影响鱼类适应气候变化能力的生理特性。温度的急性变化会改变心跳频率以及心房和心室动作电位（AP）的持续时间。长时间暴露于新的热条件会诱导离子通道表达和功能的代偿性变化，这通常会部分减轻温度对心脏AP和心率的直接影响。对鱼类心脏电兴奋最敏感的分子成分似乎是Na(+)通道，它可能通过在高温下损害心脏AP的起始来设定心脏兴奋性的热上限。在心脏和其他可兴奋细胞中，外向K(+)电流和内向Na(+)电流不同的温度依赖性可能会在极端温度下损害电兴奋性，这一假说称为电兴奋的温度依赖性抑制。
