Agah R, Pearce J A, Welch A J, Motamedi M
Baylor College of Medicine, Houston, Texas 77030.
Lasers Surg Med. 1994;15(2):176-84. doi: 10.1002/lsm.1900150205.
A numerical model for thermal damage to human arterial tissue is presented, based on protein denaturation kinetics. The model involves determination of coefficients of rate processes A & delta E, which are tissue type-dependent (arterial tissue in this study), and definition of threshold damage. A feedback-controlled constant surface temperature device was used to induce 80 coagulative lesions of arterial human tissue ranging in temperature from 66 degrees C to 76 degrees C and in duration from 15 to 1,500 seconds. The measured coefficients were determined to be A = 5.6 x 10(63) s-1 and delta E = 430 KJ mole-1. These numerical values closely approximate the coefficients of the rate process for denaturation of collagen molecules. These and other histological observations strongly suggest collagen to be the primary coagulating component of arterial tissue at the onset of thermal coagulative damage. The ability of this model to predict onset of tissue coagulation during laser coagulation was studied using 10 postmortem human arterial samples exposed to argon laser irradiation.
基于蛋白质变性动力学，提出了一种人体动脉组织热损伤的数值模型。该模型涉及速率过程系数A和ΔE的确定，这些系数取决于组织类型（本研究中的动脉组织），并定义了损伤阈值。使用反馈控制的恒定表面温度装置，在66℃至76℃的温度范围内、15至1500秒的持续时间内，诱导了80处人体动脉组织的凝固性损伤。测得的系数确定为A = 5.6×10(63) s-1和ΔE = 430 KJ/mol。这些数值与胶原分子变性速率过程的系数非常接近。这些以及其他组织学观察强烈表明，在热凝固性损伤开始时，胶原蛋白是动脉组织的主要凝固成分。使用10个暴露于氩激光照射的死后人体动脉样本，研究了该模型预测激光凝固过程中组织凝固开始的能力。
