Temperature acclimation modifies sinoatrial pacemaker mechanism of the rainbow trout heart
Temperature acclimation modifies sinoatrial pacemaker mechanism of the rainbow trout heart
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DOI：
10.1152/ajpregu.00432.2006
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发表时间：
2007-02-01
影响因子：
2.8
通讯作者：
Vornanen, Matti
中科院分区：
文献类型：
--
作者：
Haverinen, Jaakko;Vornanen, Matti
温度驯化改变虹鳟鱼心脏窦房起搏器机制。[J] .中国生物医学工程学报，2016,32(2):559 - 563。首次出版于2006年9月28日；doi: 10.1152 / ajpregu.00432.2006。通过记录4℃（冷）和18℃（暖）环境下虹鳟鱼完整窦房组织和酶分离的起搏器细胞的动作电位（AP），验证了心率热补偿的起搏器水平起源假说。电生理记录显示，初级起搏器位于窦房瓣底部，组织学检查发现一个由肌细胞和神经细胞组成的形态学上明显的组织环。该起搏器在冷驯化条件下的内在跳动速率（46 +/- 6 APs/min）高于热驯化条件下的内在跳动速率（38 +/- 3 APs/min, P < 0.05），离体起搏器细胞的跳动速率（44 +/- 6 vs. 38 +/- 6 APs/min, P < 0.05）也存在类似差异，支持热驯化改变鱼心脏内在起搏器机制的假设。10 μ M瑞诺定和1 μ M thapsigargin抑制肌浆网（SR）在11℃时对温寒驯化的鳟鱼心率均无影响，但在18℃时使温寒驯化的鳟鱼心率从74 +/- 2降至42 +/- 6 APs/min （P < 0.05）。用0.1 μ M E-4031阻断延迟整流器K+电流（I-Kr）的半最大阻断比冷驯化鳟鱼更能降低温驯化鳟鱼的心率（从45 +/- 1到24 +/- 5 APs/min） （56 +/- 3 vs 48 +/- 2 APs/min），而冷驯化鳟鱼的IKr密度更高，AP持续时间更短（P < 0.05）。总的来说，这些研究结果表明，寒冷诱导的AP排放频率增加至少部分是由于寒冷适应的鳟鱼中IKr密度较高，而SR Ca2+释放对心率热补偿的贡献可以忽略不计。
Temperature acclimation modifies sinoatrial pacemaker mechanism of the rainbow trout heart. Am J Physiol Regul Integr Comp Physiol 292: R1023-R1032, 2007. First published September 28, 2006; doi: 10.1152/ajpregu.00432.2006. The hypothesis of pacemaker level origin of thermal compensation in heart rate was tested by recording action potentials (AP) in intact sinoatrial tissue and enzymatically isolated pacemaker cells of rainbow trout acclimated at 4 degrees C (cold) and 18 degrees C (warm). With electrophysiological recordings, the primary pacemaker was located at the base of the sinoatrial valve, where a morphologically distinct ring of tissue comprising myocytes and neural elements was found by histological examination. Intrinsic beating rate of this pacemaker was higher in cold-acclimated (46 +/- 6 APs/min) than warm-acclimated trout (38 +/- 3 APs/min; P < 0.05), and a similar difference was seen in beating rate of isolated pacemaker cells (44 +/- 6 vs. 38 +/- 6 APs/min; P < 0.05), supporting the hypothesis that thermal acclimation modifies the intrinsic pacemaker mechanism of fish heart. Inhibition of sarcoplasmic reticulum (SR) with 10 mu M ryanodine and 1 mu M thapsigargin did not affect heart rate in either warm-or cold-acclimated trout at 11 degrees C but reduced heart rate in warm-acclimated trout from 74 +/- 2 to 42 +/- 6 APs/min (P < 0.05) at 18 degrees C. At 11 degrees C, a half-maximal blockade of the delayed rectifier K+ current (I-Kr) with 0.1 mu M E-4031 reduced heart rate more in warm-acclimated (from 45 +/- 1 to 24 +/- 5 APs/min) than cold-acclimated trout (56 +/- 3 vs. 48 +/- 2 APs/min), whereas IKr density was higher and AP duration less in cold-acclimated trout (P > 0.05). Collectively, these findings suggest that a cold-induced increase in AP discharge frequency is at least partly due to higher density of the IKr in the cold-acclimated trout, whereas contribution of SR Ca2+ release to thermal compensation of heart rate is negligible.