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大鼠心肌中的后收缩和兴奋-收缩偶联。

Aftercontractions and excitation-contraction coupling in rat cardiac muscle.

作者信息

ter Keurs H E, Backx P H, de Tombe P P, Mulder B J

机构信息

Department of Medicine, Faculty of Medicine, University of Calgary, Alta, Canada.

出版信息

Can J Physiol Pharmacol. 1988 Sep;66(9):1239-45. doi: 10.1139/y88-204.

Abstract

Calcium loading in cardiac muscle may cause spontaneous contractions (SC). We observed that SC move at a constant rate (Vsc) through isolated rat myocytes and trabeculae. Factors that influence the properties of SC were studied with Nomarsky microscopy and laser diffraction techniques. Myocytes and trabeculae were superfused with Krebs-Henseleit solution (21 degrees C, pH 7.35; Ca2+, 0.5-7 mM). Vsc in myocytes and within cells of trabeculae ranged between 50 and 150 micron/s. After a train of 3-25 stimuli at 2 Hz, SC in trabeculae started at a site of damage in a region 250 micron in length throughout the muscle. This regional contraction then moved at a constant rate (Vsc) along the length of the muscle. Vsc increased from 0.1 to 15 mm/s with stimulation and Ca2+. Under conditions of calcium loading, spontaneous twitches also occurred throughout the trabeculae, often as triggered arrhythmias. These twitches were always preceded by SC. The range of observed Vsc could be predicted by the Ca2+-induced Ca2+ release hypothesis. We postulated that the contraction by virtue of focal calcium release from the sarcoplasmic reticulum (SR) and was stimulated this process together with the processes of diffusion into the cytosol, binding to calmodulin and troponin, sequestration by the SR, and subsequent induction of Ca2+ release from the adjacent SR. The parameters used for the kinetics of binding, release, and sequestration were obtained from those reported in the literature. The minimal and maximal velocities derived from the simulation were 0.09 and 25 mm/s, respectively. The method of solution involved writing the diffusion equation as a difference equation in the spatial coordinates. Thus, bounded, coupled, and ordinary differential equations in time were generated. The coupled equations were solved by using Gear's sixth order predictor--corrector algorithm for stiff equations along with reflective boundaries. These calculations were performed on the Cyber 205 at the University of Calgary.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

心肌中的钙负荷可能会引发自发收缩(SC)。我们观察到SC以恒定速率(Vsc)穿过分离的大鼠心肌细胞和小梁。利用诺马斯基显微镜和激光衍射技术研究了影响SC特性的因素。心肌细胞和小梁用克雷布斯 - 亨泽莱特溶液(21℃,pH 7.35;Ca2 +,0.5 - 7 mM)进行灌流。心肌细胞和小梁细胞内的Vsc范围在50至150微米/秒之间。在2赫兹频率下施加3 - 25次刺激的序列后,小梁中的SC在整个肌肉中长度为250微米的损伤部位开始。这种局部收缩然后以恒定速率(Vsc)沿着肌肉长度移动。随着刺激和Ca2 +的增加,Vsc从0.1增加到15毫米/秒。在钙负荷条件下,小梁中也会出现自发抽搐,通常表现为触发的心律失常。这些抽搐总是先于SC出现。观察到的Vsc范围可以通过钙诱导钙释放假说来预测。我们推测这种收缩是由于肌浆网(SR)的局灶性钙释放引起的,并且扩散到细胞质、与钙调蛋白和肌钙蛋白结合、被SR隔离以及随后诱导相邻SR释放Ca2 +的过程共同刺激了这一过程。用于结合、释放和隔离动力学的参数取自文献报道。模拟得出的最小和最大速度分别为0.09和25毫米/秒。求解方法包括将扩散方程写成空间坐标中的差分方程。因此,生成了有界、耦合的时间常微分方程。通过使用Gear的用于刚性方程的六阶预测 - 校正算法以及反射边界来求解耦合方程。这些计算是在卡尔加里大学的Cyber 205计算机上进行的。(摘要截断于250字)

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