Benditt D G, Kriett J M, Tobler H G, Gornick C C, Detloff B L, Anderson R W
Am J Physiol. 1985 Nov;249(5 Pt 2):H1017-23. doi: 10.1152/ajpheart.1985.249.5.H1017.
This study utilized sonomicrometers transmural multipolar electrodes and cardiac electrical stimulation techniques to examine the effect on myocardial electrophysiological characteristics of altering ventricular systolic mechanical properties by transient aortic occlusion. Nine anesthetized open-chest dogs were atrially paced, and timed extrastimuli were inserted during alternate drive-train sequences at right or left ventricular (RV, LV) epicardial sites to measure ventricular effective refractory period (ERP). Sonomicrometer measurements of LV systolic mechanical parameters and both RV and LV electrophysiological findings were determined prior to and during periods of transient aortic occlusion. Aortic occlusion was applied just prior to the last beat of each eight-beat atrial drive train and released immediately following the programmed ventricular extrastimulus. Aortic occlusion increased LV systolic pressure (+42 +/- 26.6 mmHg, P less than 0.01) and diminished segmental stroke shortening (0.100 +/- 0.059 mm, P less than 0.02), shortening fraction (0.086 +/- 0.048, P less than 0.001), mean velocity of stroke shortening (0.444 +/- 0.186 mm/s, P less than 0.001), and stroke work (P less than 0.001). LV epicardial and endocardial ERP were prolonged as a result of aortic occlusion (5 +/- 7.2 and 6 +/- 6.5 ms, respectively, P less than 0.05), whereas RV ERP was unchanged. Latency of premature beats at equivalent coupling intervals was unaltered. ERP prolongation correlated most strongly with reductions of segmental stroke shortening (r = 0.928, P less than 0.001), shortening fraction (r = 0.901, P less than 0.001), and mean shortening velocity (r = 0.819, P less than 0.01). Thus transient aortic occlusion prolonged LV refractoriness, and electrophysiological changes closely paralleled the severity of systolic mechanical disturbance.
本研究利用超声微测仪、透壁多极电极和心脏电刺激技术，来检验通过短暂性主动脉阻断改变心室收缩机械特性对心肌电生理特性的影响。对9只麻醉开胸犬进行心房起搏，并在右心室或左心室（RV，LV）心外膜部位交替驱动序列期间插入定时额外刺激，以测量心室有效不应期（ERP）。在短暂性主动脉阻断之前和期间，测定LV收缩机械参数的超声微测仪测量值以及RV和LV的电生理结果。在每八次心跳的心房驱动序列的最后一次心跳之前施加主动脉阻断，并在程控心室额外刺激之后立即解除阻断。主动脉阻断使LV收缩压升高（+42±26.6 mmHg，P<0.01），节段性缩短幅度减小（0.100±0.059 mm，P<0.02），缩短分数（0.086±0.048，P<0.001），平均缩短速度（0.444±0.186 mm/s，P<0.001）和每搏功（P<0.001）。由于主动脉阻断，LV心外膜和心内膜ERP延长（分别为5±7.2和6±6.5 ms，P<0.05），而RV ERP未改变。在等效耦合间期的早搏潜伏期未改变。ERP延长与节段性缩短幅度（r = 0.928，P<0.001）、缩短分数（r = 0.901，P<0.001）和平均缩短速度（r = 0.819，P<0.01）的降低相关性最强。因此，短暂性主动脉阻断延长了LV不应期，电生理变化与收缩机械紊乱的严重程度密切平行。
