Effect of Pacing‐Induced Ischemia on Left Ventricular Diastolic Pressure‐Volume Relations in Dogs with Coronary Stenoses
Effect of Pacing‐Induced Ischemia on Left Ventricular Diastolic Pressure‐Volume Relations in Dogs with Coronary Stenoses
复制标题
起搏引起的缺血对冠状动脉狭窄犬左心室舒张压-容积关系的影响
作者：
T. Serizawa;B. Carabello;W. Grossman
在10只开胸和心包开放的氯醛糖麻醉犬上，研究了心绞痛期间左室舒张特性改变的机制。为了消除反应性充血，在左前降支和回旋支冠状动脉都造成了90%的近端冠状动脉狭窄，心脏的起搏速度几乎是其静息频率的两倍(115±4到200±5次/分钟)。起搏后左室舒张末压(EDP10±2~21±2 mm Hg，P；0.001)、左室最低舒张压(5±1~13±2 mm Hg，P；0.001)、左室舒张末容量(55±3~60±2ml，P&t；0.001)、左室收缩末期容量(28±2~33±2ml，P<；0.001)、右室收缩压(RVP，27±2~32±2 mm Hg，P<；0.001)均有增加。左心室舒张期压力下降时间常数(T)(35±4~53±4毫秒，P&0.001)。LV峰值收缩压(12 1±5)mm Hg(P&t；0.001)、LV最大负dp/dt(2 30 0±15 8~1 319±15 4 mm Hg/s，P<；0.001)、LV射血分数(0.49±0.0 2~0.44±0.0 3)明显降低(P<0.0 5)，心率无明显变化。每只狗的LV舒张压-容量曲线上移；在任何舒张期容量下，压力都高于对照组。在4只犬中，突然收缩肺动脉，注入生理盐水使右室负荷急剧增加(右室压由29±1/6±1增至67±5/11±1 mm Hg，P<；0.001/P<；0.001)，并观察其对LV舒张压-容量关系的影响。与起搏诱导的缺血相比，这种关系只有很小的变化。由于在我们的缺血模型中，LV舒张压-容量曲线的上移是在没有心包的情况下发生的，并且与RVEDP的微小变化有关，因此我们得出结论，心肌舒张期特性的改变在这一现象中起着重要作用。中国保监会第46：430-439号决议，1980年
Mechanisms involved in altering left ventricular (LV) diastolic properties during angina were studied in 10 chloralose-anesthetized dogs with chest and pericardium open. Proximal coronary artery stenoses of >90% were created in both left anterior descending and circumflex coronary arteries to abolish reactive hyperemia, and the heart was paced at nearly twice its resting rate (115 ± 4 to 200 ± 5 beats/min). After pacing, increases occurred in LV end-diastolic pressure (EDP, 10 ± 2 to 21 ± 2 mm Hg, P< 0.001), LV minimum diastolic pressure (5 ± 1 to 13 ± 2 mm Hg, P< 0.001), LV end-diastolic volume (55 ± 3 to 60 ± 2 ml, P < 0.001), LV end-systolic volume (28 ± 2 to 33 ± 2 ml, P < 0.001), right ventricular (RV) systolic pressure (RVP, 27 ± 2 to 32 ± 2 mm Hg, P < 0.01), RVEDP (5 ± 1 to 6 ± 1 mm Hg, P < 0.05), and time constant (T) of LV pressure fall in diastole (35 ± 4 to 53 ±4 msec, P < 0.001). Decreases occurred in LV peak systolic pressure (121 ± 5 to 102 ± 5 mm Hg, P< 0.001), LV maximum negative dp/dt (2300 ± 158 to 1319 ± 154 mm Hg/sec, P< 0.001), and LV ejection fraction (0.49 ± 0.02 to 0.44 ± 0.03, NS), whereas heart rate was not significantly different. LV diastolic pressure-volume curves were shifted upward for each dog; at any diastolic volume, pressure was higher than control. In four dogs, the pulmonary artery was abruptly constricted, and saline was infused to produce an acute increase in RV loading (RVP, 29 ± 1/6 ± 1 to 67 ± 5/11 ± 1 mm Hg, P < 0.001/P< 0.001), and the effect on the LV diastolic pressure-volume relation was examined. Only minor changes in this relation could be detected in contrast to the changes with pacing-induced ischemia. Since the upward shift in the LV diastolic pressure-volume curve in our ischemia model occurred in the absence of the pericardium and was associated with only small changes in RVEDP, we conclude that altered myocardial diastolic properties play an important role in this phenomenon. Circ Res 46: 430-439, 1980