McCormack P D
Aviat Space Environ Med. 1984 Jul;55(7):620-31.
Experimental results indicate that the passive mechanics (no smooth muscle action) of the larger arteries, such as the aorta and pulmonary, in humans are closely related to the elastin content at low strain and to the collagen content at high strain. In an aerial combat maneuver, the acceleration stress typically rises to a maximum, remains there for several seconds, and then falls off. The arterial wall viscoelastic property relevant here is hysteresis. The strain remaining when the stress is removed is called "permanent set." This so-called permanent set will decay away exponentially with a comparatively long time constant on the order of several hundred seconds. A first approximation to the permanent set, after a hysteresis loop has been executed, has been derived. Collagen can only stretch by 20% before failing. Choosing combat scenarios in which the maneuver is repeated at 1-min intervals so that the decay in permanent sets can be ignored, the number of maneuvers required to damage or rupture the collagen is computed for ranges of acceleration (g) values equivalent to increases in the arterial intraluminal pressures. The calculations are done for the external carotid, abdominal aorta and pulmonary arteries. For example, applying the continual recruitment of collagen fibers theory to the pulmonary artery produces the following result. The permanent set at net acceleration value of 5 g is 0.085 and the number of sequential maneuvers required to damage 2.5% of the collagen is 2.4. Based on discontinuous recruitment of 100% collagen at a strain of 1.7 in the pulmonary artery, the number of maneuvers required to rupture the collagen would be 58 at an acceleration of 5 g. At 10 g, this number falls to about 10 maneuvers. The results emphasize the importance of present protective measures, such as the use of G suits and valsalva maneuvers. But these measures can only reduce the effects predicted here, not eliminate them. The results also highlight the necessity for servo-controlled seat orientation, and for the introduction of integrating accelerometers for all aircrew to record acceleration exposure history.
实验结果表明,在人体中,诸如主动脉和肺动脉等较大动脉的被动力学特性(无平滑肌作用)在低应变时与弹性蛋白含量密切相关,在高应变时与胶原蛋白含量密切相关。在空战机动中,加速度应力通常会升至最大值,在该值保持数秒,然后下降。此处相关的动脉壁粘弹性特性是滞后现象。应力消除后剩余的应变称为“永久变形”。这种所谓的永久变形将以几百秒量级的相对较长时间常数呈指数衰减。在执行滞后回线后,已推导出永久变形的一阶近似值。胶原蛋白在断裂前只能拉伸20%。选择以1分钟间隔重复机动的战斗场景,以便可以忽略永久变形的衰减,针对与动脉腔内压力增加等效的加速度(g)值范围,计算损伤或撕裂胶原蛋白所需的机动次数。针对颈外动脉、腹主动脉和肺动脉进行了计算。例如,将胶原蛋白纤维持续募集理论应用于肺动脉会产生以下结果。净加速度值为5g时的永久变形为0.085,损伤2.5%胶原蛋白所需的连续机动次数为2.4次。基于肺动脉在应变1.7时100%胶原蛋白的不连续募集,在5g加速度下撕裂胶原蛋白所需的机动次数为58次。在10g时,该次数降至约10次。结果强调了当前保护措施的重要性,例如使用抗荷服和瓦尔萨尔瓦动作。但这些措施只能减少此处预测的影响,而不能消除它们。结果还突出了伺服控制座椅定向的必要性,以及为所有机组人员引入积分加速度计以记录加速度暴露历史的必要性。