Detwiler P W, Nicolosi A C, Weng Z C, Spotnitz H M
Department of Surgery, Columbia University College of Physicians & Surgeons, New York, NY 10032.
J Thorac Cardiovasc Surg. 1994 Sep;108(3):467-76.
The mechanism through which edema reduces left ventricular compliance has not been defined. Accordingly, diastolic properties of in situ left ventricular swine papillary muscles were studied in three groups: control (n = 6, 4 degrees to 6 degrees C), edematous (150 mOsm/L coronary perfusion, n = 6, 4 degrees to 6 degrees C), and ischemic contracture (n = 8, 28 degrees C). Lagrangian stress (sigma) and strain (epsilon) were calculated from slow stretch data and approximated by sigma = alpha(e beta epsilon-1). The natural logarithm of stress versus strain was linear over the physiologic range of 0.05 < strain < 0.40. Hypotonic perfusions (1 L x 3) progressively shifted the stress-strain relationship upward and to the left. Compared to baseline, alpha increased significantly (p < 0.05) after perfusion 3 (6.7 +/- 2.1 baseline, 12.2 +/- 6.6 perfusion 1, 12.7 +/- 3.5 perfusion 2, and 42.9 +/- 16.3 gm/cm2 perfusion 3). The constant beta did not change significantly (13.0 +/- 1.5 baseline, 13.1 +/- 1.6 perfusion 1, 13.2 +/- 1.6 perfusion 2, and 14.1 +/- 1.4 perfusion 3). Right ventricular water content increased after each perfusion (77.1% +/- 1.4% baseline, 81.6% +/- 1.3%, 84.7% +/- 1.5%, and 86.9% +/- 1.7%, p < 0.05). With ischemic contracture, alpha increased from 61.9 +/- 17.8 to 173.1 +/- 61.5 gm/cm2 (p > 0.05) and beta increased insignificantly from 6.5 +/- 0.6 to 10.6 +/- 1.8 (p = NS). In the control group all variables were unchanged after 210 minutes. We conclude that myocardial stiffness increases with myocardial edema. This may explain decreased compliance in the edematous left ventricle.
水肿降低左心室顺应性的机制尚未明确。因此,研究了三组原位猪左心室乳头肌的舒张特性:对照组(n = 6,4℃至6℃)、水肿组(150 mOsm/L冠状动脉灌注,n = 6,4℃至6℃)和缺血性挛缩组(n = 8,28℃)。根据缓慢拉伸数据计算拉格朗日应力(σ)和应变(ε),并通过σ = α(eβε - 1)进行近似。在0.05 < 应变 < 0.40的生理范围内,应力的自然对数与应变呈线性关系。低渗灌注(1L×3)使应力 - 应变关系逐渐向上和向左移动。与基线相比,灌注3次后α显著增加(p < 0.05)(基线时为6.7±2.1,灌注1次后为12.2±6.6,灌注2次后为12.7±3.5,灌注3次后为42.9±16.3 g/cm²)。常数β无显著变化(基线时为13.0±1.5,灌注1次后为13.1±1.6,灌注2次后为13.2±1.6,灌注3次后为14.1±1.4)。每次灌注后右心室含水量增加(基线时为77.1%±1.4%,分别为81.6%±1.3%、84.7%±1.5%和86.9%±1.7%,p < 0.05)。发生缺血性挛缩时,α从61.9±17.8增加至173.1±61.5 g/cm²(p > 0.05),β从6.5±0.6无显著增加至10.6±1.8(p = 无统计学意义)。在对照组中,210分钟后所有变量均无变化。我们得出结论,心肌僵硬度随心肌水肿而增加。这可能解释了水肿左心室顺应性降低的原因。