Mor-Avi V, Shroff S G, Robinson K A, Ng A F, Cholley B P, Marcus R H, Lang R M
Department of Medicine, University of Chicago Medical Center, Illinois 60637.
J Am Coll Cardiol. 1994 Dec;24(7):1779-85. doi: 10.1016/0735-1097(94)90187-2.
We used an isolated, crystalloid-perfused rabbit heart model to test the hypothesis that the phasic changes in left ventricular contrast are due to bubble compression and decompression during systole and diastole, respectively.
Contrast enhancement of the left ventricular cavity has been shown to decrease during ventricular systole. This phenomenon has been attributed to pressure-induced microbubble destruction. Such destruction, if confirmed, would severely confound the quantitative interpretation of contrast echocardiographic data.
A fixed volume of contrast solution (5% human albumin and Albunex, approximately 400:1 ratio) was introduced into a latex balloon placed within the left ventricular cavity of an isolated paced rabbit heart preparation (n = 12). Instantaneous left ventricular pressure was measured using a high fidelity microtip catheter and digitized on-line. The beating heart was placed in a water tank, and ultrasound images were obtained using a 7.5-MHz transducer and were recorded and digitized off-line at 12 frames/s. Simultaneously, the pacing signal was used for gated on-line acquisition of end-diastolic frames. A simple theoretic model based on surface tension physical principles was used to predict changes in bubble size and, consequently, the reflection intensity in response to the measured changes in left ventricular pressure.
We found that under peak left ventricular systolic pressures ranging from 89 to 155 mm Hg, 1) end-diastolic videointensity decreased by 8 +/- 6% (mean +/- SD) over 25 consecutive heart beats; and 2) intracyclic variations in measured videointensity were in close agreement with the theoretic calculations: 80.1 +/- 2.9% versus 80.2 +/- 4.6% of diastolic videointensity at systole.
The major cause of systolic decrease in contrast enhancement is periodic bubble compression (as opposed to bubble destruction) induced by high systolic pressures. The minor progressive decrease in end-diastolic videointensity reflects the degree of instability of Albunex microbubbles under left ventricular pressures. However, the clinical impact of these destructive effects is likely to be only minor because of the rapid transit of microbubbles through the left heart chambers and myocardial microcirculation.
我们使用离体的、晶体灌注兔心脏模型来检验以下假设，即左心室造影剂的阶段性变化分别是由于收缩期和舒张期气泡的压缩和减压所致。
已表明左心室腔的造影剂增强在心室收缩期会降低。这种现象被归因于压力诱导的微泡破坏。如果这种破坏得到证实，将严重混淆造影超声心动图数据的定量解释。
将固定体积的造影剂溶液（5%人白蛋白和Albunex，比例约为400:1）注入置于离体起搏兔心脏制剂（n = 12）左心室内的乳胶球囊中。使用高保真微尖端导管测量瞬时左心室压力并在线数字化。将跳动的心脏置于水箱中，使用7.5MHz换能器获取超声图像，并以12帧/秒的速度离线记录和数字化。同时，起搏信号用于门控在线采集舒张末期帧。基于表面张力物理原理的简单理论模型用于预测气泡大小的变化，进而预测响应于测得的左心室压力变化的反射强度。
我们发现，在左心室收缩压峰值范围为89至155 mmHg的情况下，1）在连续25次心跳过程中，舒张末期视频强度降低了8±6%（平均值±标准差）；以及2）测得的视频强度的心动周期内变化与理论计算结果密切一致：收缩期为舒张期视频强度的80.1±2.9%，而理论计算值为80.2±4.6%。
造影剂增强在收缩期降低的主要原因是高收缩压诱导的周期性气泡压缩（而非气泡破坏）。舒张末期视频强度的轻微渐进性降低反映了Albunex微泡在左心室压力下的不稳定程度。然而，由于微泡快速通过左心腔和心肌微循环，这些破坏作用的临床影响可能较小。
