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钆对大鼠心脏小梁收缩力和触发的传播性收缩的影响。

Effects of gadolinium on twitch force and triggered propagated contractions in rat cardiac trabeculae.

作者信息

Zhang Y, ter Keurs H E

机构信息

Department of Medicine, Health Science Centre, University of Calgary, Alta, Canada.

出版信息

Cardiovasc Res. 1996 Jul;32(1):180-8.

PMID:8776415
Abstract

UNLABELLED

We have recently described that local contractions can be triggered by a preceding twitch in rat cardiac trabeculae in or near damaged ends of the muscle. These local contractions appeared to propagate along the trabeculae with a constant velocity; hence, they can be denoted as triggered propagated contractions (TPCs). These studies have also shown that stretch and/or subsequent shortening of the damaged ends during the twitch is necessary for the induction of TPCs.

OBJECTIVES

We tested in this study: (1) whether activation of stretch-activated channels in the damaged regions is involved in the initiation of TPCs; (2) whether activation of stretch-activated channels due to stretch of tissue adjacent to a local triggered contraction increases the velocity of propagation. As gadolinium (Gd3+) has been shown to be the most effective blocker of stretch-activated channels to date, we have studied the effects of Gd3+ on twitch force, as well as on force, triggering rate and propagation velocity of TPCs.

METHODS

TPCs were elicited by trains of 15 stimuli (2 Hz, 15-s intervals) at 20 degrees C; using HEPES solution, [Ca2+]o of 0.5 approximately 0.75 mmol/l. Laser diffraction techniques were used to measure sarcomere shortening at two sites in the trabeculae; twitch force was measured with a silicon strain gauge.

RESULTS

Gd3+ (1 to approximately 20 mumol/l) decreased both twitch force and force, triggering rate and propagation velocity of TPCs in a concentration-dependent manner. High concentrations of Gd3+ (> 20 mumol/l) almost abolished both twitch force and triggered force. The decrease of triggering rate and velocity, for the same decrease in twitch force, were not significantly larger than those by decreasing [Ca2+]o, indicating that Gd3+ did not cause an additional effect on TPCs above decreasing intracellular [Ca2+].

CONCLUSION

These observations suggest that it is not necessary to assume that Gd3+ sensitive stretch-activated channels are involved in triggering or propagation of these local contractions.

摘要

未标记

我们最近描述了在大鼠心肌小梁受损末端或其附近,局部收缩可由先前的一次抽搐引发。这些局部收缩似乎以恒定速度沿小梁传播;因此,它们可被称为触发传播性收缩(TPCs)。这些研究还表明,抽搐过程中受损末端的拉伸和/或随后的缩短对于TPCs的诱导是必要的。

目的

我们在本研究中测试了:(1)受损区域拉伸激活通道的激活是否参与TPCs的起始;(2)由于局部触发收缩附近组织的拉伸导致的拉伸激活通道的激活是否会增加传播速度。由于钆(Gd3+)已被证明是迄今为止拉伸激活通道最有效的阻滞剂,我们研究了Gd3+对抽搐力以及TPCs的力、触发率和传播速度的影响。

方法

在20℃下,用15次刺激(2Hz,间隔15秒)的序列引发TPCs;使用HEPES溶液,细胞外钙浓度([Ca2+]o)为0.5至约0.75mmol/L。采用激光衍射技术测量小梁两个部位的肌节缩短;用硅应变片测量抽搐力。

结果

Gd3+(1至约20μmol/L)以浓度依赖的方式降低了抽搐力以及TPCs的力、触发率和传播速度。高浓度的Gd3+(>20μmol/L)几乎消除了抽搐力和触发力。对于相同程度的抽搐力降低,触发率和速度的降低并不比降低细胞外钙浓度时显著更大,表明Gd3+在降低细胞内钙浓度之外,对TPCs没有额外影响。

结论

这些观察结果表明,没有必要假定Gd3+敏感的拉伸激活通道参与这些局部收缩的触发或传播。

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