Yaku H, Slinker B K, Bell S P, LeWinter M M
Cardiology Unit, University of Vermont College of Medicine, Burlington 05405.
Am J Physiol. 1994 Mar;266(3 Pt 2):H1087-94. doi: 10.1152/ajpheart.1994.266.3.H1087.
Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)
收缩期心室直接相互作用被认为是通过室间隔以及两个心室共享的共同纤维的协调收缩而发生的。本研究的目的是评估短暂性游离壁缺血和束支传导阻滞对左向右收缩期心室相互作用的影响，这两种情况会破坏共享共同纤维的协调收缩。我们通过2分钟冠状动脉闭塞在9只原位犬心脏中产生短暂性右心室和左心室游离壁缺血，并通过心室起搏产生束支传导阻滞。为了消除串联相互作用的任何混杂效应，我们使用了突然的血流动力学扰动（主动脉缩窄），并测量收缩期相互作用增益（IG），即右心室收缩压峰值变化/左心室收缩压峰值变化（IG(peak)）以及在匹配数据采样时间的瞬时右心室压力变化/左心室压力变化（IG(inst)），同时测量主动脉缩窄前及缩窄后即刻搏动时右心室搏出量和搏功的变化。为了使室间隔压力传递对心室相互作用的贡献等效，在所有实验条件下，主动脉缩窄产生的左心室收缩压峰值变化均匹配[平均增加：64±19（标准差）mmHg]。对照IG(peak)为0.12±0.05，对照IG(inst)为0.11±0.05。无论有无完整心包，这些值在游离壁缺血或心室起搏时均未改变。在缺血或心室起搏期间，无论有无完整心包，主动脉缩窄引起的右心室搏出量和搏功变化均与零无差异。（摘要截断于250字）
