Department of Biomedical Engineering, School of Electrical and Computer Engineering, and Center for Biomedical Engineering, University of Campinas (UNICAMP), R. Alexander Fleming, 163, Cidade Universitária Zeferino Vaz, Campinas, SP, 13083-881, Brazil.
J Comp Physiol B. 2018 Nov;188(6):929-937. doi: 10.1007/s00360-018-1183-0. Epub 2018 Sep 14.
Insect and vertebrate hearts share the ability to generate spontaneously their rhythmic electrical activity, which triggers the fluid-propelling mechanical activity. Although insects have been used as models in studies on the impact of genetic alterations on cardiac function, there is surprisingly little information on the generation of the inotropic activity in their hearts. The main goal of this study was to investigate the sources of Ca for contraction in Tenebrio molitor hearts perfused in situ, in which inotropic activity was assessed by the systolic variation of the cardiac luminal diameter. Increasing the pacing rate from 1.0 to 2.5 Hz depressed contraction amplitude and accelerated relaxation. To avoid inotropic interference of variations in spontaneous rate, which have been shown to occur in insect heart during maneuvers that affect Ca cycling, experiments were performed under electrical pacing at near-physiological rates. Raising the extracellular Ca concentration from 0.5 to 8 mM increased contraction amplitude in a manner sensitive to L-type Ca channel blockade by D600. Inotropic depression was observed after treatment with caffeine or thapsigargin, which impair Ca accumulation by the sarcoplasmic reticulum (SR). D600, but not inhibition of the sarcolemmal Na/Ca exchanger by KB-R7943, further depressed inotropic activity in thapsigargin-treated hearts. From these results, it is possible to conclude that in T. molitor heart, as in vertebrates: (a) inotropic and lusitropic activities are modulated by the heart rate; and (b) Ca availability for contraction depends on both Ca influx via L-type channels and Ca release from the SR.
昆虫和脊椎动物的心脏都具有自发产生有节奏的电活动的能力,这种电活动触发了流体推动的机械活动。尽管昆虫已被用于研究遗传改变对心脏功能的影响的模型,但关于它们心脏的变力活性的产生,信息却惊人地很少。本研究的主要目的是研究在原位灌流的 T. molitor 心脏中收缩的 Ca 来源,其中通过心脏内腔直径的收缩期变化来评估变力活性。将起搏率从 1.0 增加到 2.5 Hz 会降低收缩幅度并加速松弛。为了避免变力活性的变化引起的变力干扰,这种变化已被证明在影响 Ca 循环的操作期间在昆虫心脏中发生,因此在接近生理速率的电起搏下进行实验。将细胞外 Ca 浓度从 0.5 增加到 8 mM 以对 D600 阻断 L 型 Ca 通道敏感的方式增加了收缩幅度。在用咖啡因或 thapsigargin 处理后观察到变力抑制,这会损害肌浆网 (SR) 对 Ca 的积累。D600,但不是 KB-R7943 抑制肌膜 Na/Ca 交换器,进一步抑制了 thapsigargin 处理的心脏的变力活性。从这些结果可以得出结论,在 T. molitor 心脏中,与脊椎动物一样:(a)变力和顺应性活性受心率调节;和 (b)收缩的 Ca 可用性取决于通过 L 型通道的 Ca 内流和从 SR 释放的 Ca。