Levosimendan enhances left ventricular systolic and diastolic function in conscious dogs with pacing-induced cardiomyopathy.
Levosimendan enhances left ventricular systolic and diastolic function in conscious dogs with pacing-induced cardiomyopathy.
复制标题
左西孟旦可增强患有起搏引起的心肌病的清醒犬的左心室收缩和舒张功能。
DOI：
10.1097/00005344-199705000-00001
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发表时间：
1997
影响因子：
3
通讯作者：
Warltier,DC
中科院分区：
文献类型：
--
作者：
Pagel,PS;McGough,MF;Hettrick,DA;Lowe,D;Tessmer,JP;Jamali,IN;Warltier,DC
我们研究了左西孟旦（LSM）的左心室（LV）的机械动作之前和之后的起搏诱导的心肌病在清醒的狗长期仪器测量主动脉和LV压力，+ dP/dt，内膜下段的长度，和心输出量（CO）的发展。局部前负荷可复搏功关系的斜率（Mw）用于评估心肌收缩力。用等容舒张时间常数（τ）、最大节段延长速率（dL/dt）和局部室壁僵硬度常数（KP）评价舒张功能。在不同的实验日，在开始快速心室起搏之前，将狗分配到LSM（12-或24-μg/kg负荷剂量和0.2或0.4 μg/kg/min输注）。然后以240次/min的速度对犬起搏22±2天，并在不同日期重复低剂量和高剂量LSM。LSM在开始起搏前增加了犬的M w和+ dP/dt，与心肌收缩力增强一致。LSM还改善了起搏前犬的LV舒张功能指数（τ和K p降低，dL/dt增加）。3周内快速心室起搏增加了LV舒张末期压，并产生收缩功能障碍（M w和+ dP/dt降低）和舒张功能障碍（τ和K p增加，dL/dt降低）。在左室功能障碍的情况下，LSM显著（p< 0.05）增加了Mw（54±3至98±6 mm Hg）+ dP/dt和dL/dt（57±13至72±13 mm/s），并降低了τ（66±4至52±3 ms）和Kp（1.14±0.14至0.71±0.03 mm− 1）。然而，与正常犬的研究结果相反，LSM并没有改变起搏后犬的心率和心肌耗氧量的计算指数。结果表明，LSM产生良好的改变，血流动力学和正性肌力和Lustropic效果在清醒的狗左心室功能不全。
We examined the left ventricular (LV) mechanical actions of levosimendan (LSM) before and after the development of pacing-induced cardiomyopathy in conscious dogs chronically instrumented for measurement of aortic and LV pressure,+ dP/dt, subendocardial segment length, and cardiac output (CO). The slope (M w) of the regional preload recruitable stroke work relation was used to assess myocardial contractility. Diastolic function was evaluated with a time constant of isovolumic relaxation (τ), the maximal rate of segment-lengthening velocity (dL/dt), and a regional chamberstiffness constant (K p). On different experimental days, dogs were assigned to receive LSM (12-or 24-μg/kg loading dose and 0.2 or 0.4 μg/kg/min infusion) before rapid ventricular pacing was initiated. Dogs were then paced at 240 beats/min for 22±2 days, and the low and high doses of LSM were repeated on separate days. LSM increased M w and+ dP/dt in dogs before the initiation of pacing, consistent with enhanced myocardial contractility. LSM also improved indices of LV diastolic function (decreases in τ and K p and increases in dL/dt) in dogs before pacing. Rapid ventricular pacing over a 3-week period increased LV end-diastolic pressure and produced systolic (decreases in M w and+ dP/dt) and diastolic (increases in τ and K p and decreases in dL/dt) dysfunction. LSM significantly (p< 0.05) increased M w (54±3 to 98±6 mm Hg)+ dP/dt and dL/dt (57±13 to 72±13 mm/s) and decreased τ (66±4 to 52±3 ms) and K p (1.14±0.14 to 0.71±0.03 mm− 1) in the presence of LV dysfunction. In contrast to the findings in normal dogs, however, LSM did not alter heart rate and calculated indices of myocardial oxygen consumption in dogs after pacing. The findings indicate that LSM produces favorable alterations in hemodynamics and positive inotropic and lusitropic effects in conscious dogs with left ventricular dysfunction.