Right ventricular contractile protein function in rats with left ventricular myocardial infarction
Right ventricular contractile protein function in rats with left ventricular myocardial infarction
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DOI：
10.1152/ajpheart.1996.271.1.h73
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发表时间：
1996-07-01
影响因子：
4.8
通讯作者：
Little, WC
中科院分区：
文献类型：
--
作者：
deTombe, PP;Wannenburg, T;Little, WC
我们研究了左心室（LV）心肌梗死（MI后24周; n = 6）和假手术大鼠（n = 7）诱导的实验性心力衰竭（HF）大鼠右心室（RV）分离的心脏小梁的收缩功能。肌节长度（SL）采用激光衍射技术测量，力（F）采用硅应变片测量。通过计算机反馈控制，SL始终保持恒定。HF与显著的LV扩张和肺充血相关。在完整的RV抽搐小梁中，HF与细胞外Ca 2+浓度（[Ca 2 +]（o））= 1.5 mM时F-SL关系的抑制和SL = 2.0 μ m时F-[Ca 2 +]（o）关系的抑制有关。HF还与SL = 2.0 pm时这些RV小梁（皮肤纤维）化学透化后测量的F-细胞内[Ca 2 +]关系的显著抑制相关。我们的研究结果表明，减少力的发展，在这个模型的HF是由于，在一定程度上，抑制功能的收缩丝。
We studied contractile function in cardiac trabeculae isolated from the right ventricles (RV) of rats with experimental heart failure (HF) induced by left ventricular (LV) myocardial infarction (24 wk post-MI; n = 6) and from sham-operated rats (n = 7). Sarcomere length (SL) was measured by laser diffraction techniques, and force (F) was measured by silicon strain gauge. SL was kept constant at all times by computer feedback control. HF was associated with marked LV dilation and pulmonary congestion. In intact, RV twitching trabeculae, HF was associated with a depression of the F-SL relation at extracellular Ca2+ concentration ([Ca2+](o)) = 1.5 mM and a depression of the F-[Ca2+](o) relation at SL = 2.0 mu m. HF was also associated with a significant depression of the F-intracellular [Ca2+] relation at SL = 2.0 pm measured after chemical permeabilization of these RV trabeculae (skinned fibers). Our results suggest that reduced force development in this model of HF is due, in part, to depressed function of the contractile filaments.