Goldstein J A, Tweddell J S, Barzilai B, Yagi Y, Jaffe A S, Cox J L
Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri 63110.
J Am Coll Cardiol. 1992 Mar 1;19(3):704-11. doi: 10.1016/s0735-1097(10)80296-7.
To determine whether modulation of systolic ventricular interaction influences right ventricular performance during right heart ischemia, the effects of septal ischemia and inotropic stimulation were studied in 15 dogs in an open chest preparation. Right coronary branch occlusions led to right ventricular dilation and free wall dyskinesia, reversed septal curvature and reduced left ventricular diastolic volume. In systole, the septum thickened but bulged paradoxically into the right ventricle generating an active but depressed right ventricular systolic pressure (28.9 +/- 5.5 to 22.1 +/- 4.5 mm Hg), with associated decreases in right ventricular stroke work (5.66 +/- 0.94 to 1.92 +/- 0.53 g.m/m2) and left ventricular systolic pressure (123 +/- 11 to 80 +/- 10 mm Hg). Septal ischemia induced systolic septal thinning, left ventricular dilation and decreased left ventricular systolic pressure (80 +/- 10 to 55 +/- 10 mm Hg) and stroke work. Although the extent of paradoxic septal displacement increased, there were further decrements in right ventricular systolic pressure (22.1 +/- 4.5 to 18.7 +/- 4.3 mm Hg) and stroke work (1.92 +/- 0.53 to 0.7 +/- 0.2 g.m/m2). Dopamine infusion augmented left ventricular free wall contraction and increased left ventricular systolic pressure (55 +/- 10 to 172 +/- 17 mm Hg) and stroke work. Although systolic septal thinning persisted, the extent of paradoxic septal displacement increased strikingly and, despite continued right ventricular free wall dyskinesia, right ventricular systolic pressure increased (18.7 +/- 4.3 to 39.6 +/- 6.2 mm Hg) as did right ventricular stroke work (0.7 +/- 0.2 to 7 +/- 1.6 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)
为了确定收缩期心室相互作用的调节是否会影响右心缺血期间的右心室功能，在15只开胸制备的犬中研究了室间隔缺血和变力刺激的影响。右冠状动脉分支闭塞导致右心室扩张和游离壁运动障碍，室间隔弯曲逆转，左心室舒张末期容积减小。在收缩期，室间隔增厚，但反常地凸入右心室，产生一个活跃但降低的右心室收缩压（从28.9±5.5降至22.1±4.5 mmHg），同时右心室搏功（从5.66±0.94降至1.92±0.53 g.m/m2）和左心室收缩压（从123±11降至80±10 mmHg）也相应降低。室间隔缺血导致收缩期室间隔变薄、左心室扩张以及左心室收缩压（从80±10降至55±10 mmHg）和搏功降低。尽管反常的室间隔移位程度增加，但右心室收缩压（从22.1±4.5降至18.7±4.3 mmHg）和搏功（从1.92±0.53降至0.7±0.2 g.m/m2）进一步降低。多巴胺输注增强了左心室游离壁收缩，增加了左心室收缩压（从55±10升至172±17 mmHg）和搏功。尽管收缩期室间隔变薄持续存在，但反常的室间隔移位程度显著增加，并且尽管右心室游离壁运动障碍持续存在，但右心室收缩压（从18.7±4.3升至39.6±6.2 mmHg）和右心室搏功（从0.7±0.2升至7±1.6 g.m/m2）均增加。（摘要截短于250字）
