Weidemann Frank, Broscheit Jens, Eberbach Nicole, Steendijk Paul, Voelker Wolfram, Greim Clemens, Ertl Georg, Roewer Norbert, Strotmann Jörg M
Medical University Clinic, Josef-Schneider Str. 2, 97080 Würzburg, Germany.
Clin Sci (Lond). 2004 Feb;106(2):173-81. doi: 10.1042/CS20030109.
In the present study, we sought to investigate the effects of differing inotropic conditions on regional myocardial function in ischaemic segments. In an experimental pig model ( n =11), the regional deformation parameters peak systolic strain rate [SR(SYS) (peak velocity of thickening)], systolic strain [epsilon(SYS) (systolic wall thickening)] and post-systolic strain [epsilon(PST) (ongoing wall thickening after end of systole)] were measured during normal perfusion and regional ischaemia of the posterior wall. These parameters were compared with global contractility [E(ES) (end-systolic elastance)] measured by a conductance catheter. Ischaemia was induced by an active coronary hypoperfusion in the circumflex coronary artery. Measurements were done at baseline, during dobutamine and during esmolol infusion. In normal perfused hearts, SR(SYS) (4.8+/-0.2 s(-1) at baseline) increased during dobutamine infusion, decreased during esmolol infusion and correlated significantly with global E(ES). In addition, epsilon(SYS) averaged 93+/-3% at baseline and there was almost no epsilon(PST) (4+/-1%) in normal myocardium. In ischaemic myocardium, SR(SYS) and epsilon(SYS) were significantly reduced compared with normal myocardium at baseline (SR(SYS)=2.8+/-0.3 s(-1), and epsilon(SYS)=43+/-6%; P <0.001 compared with normal perfused hearts), whereas global E(ES) was unchanged. In contrast, epsilon(PST) was significantly increased in regional ischaemic segments compared with the non-ischaemic myocardium (15+/-2%; P <0.001). During the dobutamine infusion, SR(SYS) remained unchanged. In contrast, epsilon(SYS) decreased (25+/-5%; P <0.001) and epsilon(PST) increased (25+/-4%; P <0.05) significantly during dobutamine infusion in ischaemic myocardium. In ischaemic segments, an inotropic stimulation with dobutamine resulted in a shift of strain from systole (epsilon(SYS)) to post-systole (epsilon(PST)). Thus dobutamine induced ineffective myocardial work in ischaemic segments.
在本研究中，我们试图探究不同的变力状态对缺血节段局部心肌功能的影响。在一个实验猪模型（n = 11）中，在后壁正常灌注和局部缺血期间，测量局部变形参数：收缩期峰值应变率[SR(SYS)（增厚峰值速度）]、收缩期应变[ε(SYS)（收缩期壁增厚）]和收缩后期应变[ε(PST)（收缩期末期后持续的壁增厚）]。将这些参数与通过电导导管测量的整体收缩性[E(ES)（收缩末期弹性）]进行比较。通过左旋支冠状动脉主动低灌注诱导缺血。在基线、多巴酚丁胺输注期间和艾司洛尔输注期间进行测量。在正常灌注的心脏中，SR(SYS)（基线时为4.8±0.2 s⁻¹）在多巴酚丁胺输注期间增加，在艾司洛尔输注期间降低，并且与整体E(ES)显著相关。此外，ε(SYS)在基线时平均为93±3%，正常心肌中几乎没有ε(PST)（4±1%）。在缺血心肌中，与基线时的正常心肌相比，SR(SYS)和ε(SYS)显著降低（SR(SYS)=2.8±0.3 s⁻¹，ε(SYS)=43±6%；与正常灌注心脏相比，P<0.001），而整体E(ES)未改变。相反，与非缺血心肌相比，局部缺血节段中的ε(PST)显著增加（15±2%；P<0.001）。在多巴酚丁胺输注期间，SR(SYS)保持不变。相反，在缺血心肌中多巴酚丁胺输注期间，ε(SYS)显著降低（25±5%；P<0.001），ε(PST)显著增加（25±4%；P<0.05）。在缺血节段中，多巴酚丁胺的变力刺激导致应变从收缩期（ε(SYS)）转移到收缩后期（ε(PST)）。因此，多巴酚丁胺在缺血节段中诱导了无效的心肌做功。
