Wusteman M, Boylan S, Pegg D E
Department of Biology, University of York, United Kingdom.
Cryobiology. 1996 Aug;33(4):423-9. doi: 10.1006/cryo.1996.0042.
The smooth muscle and vascular endothelium of small elastic arteries (the rabbit common carotid artery) are injured by exposure to 40% ethylene glycol (EG) at 4 degrees C, and additional damage occurs when the arteries are cooled without freezing to -20 degrees C. This paper reports attempts to reduce this injury by altering the cooling rate and temperature of exposure to the cryoprotectant. Very slow cooling (0.1 degree C/min) removed all residual smooth muscle and endothelial function when assessed in vitro after rewarming and removal of the cryoprotectant. Very rapid cooling to -20 degrees C also increased the injury, both to the endothelium and to the smooth muscle. Reducing the temperature of exposure to 40% EG from +4 degrees C to -20 degrees C had no beneficial effect on the smooth muscle but enabled the vascular endothelium to retain some functional activity. These data suggest that the mechanism responsible may be related to the physical properties of ethylene glycol rather than to a biochemical interaction with metabolic processes, and that it is a mechanism which is highly specific for the cell types involved. It also underlines the difficulties involved in the successful cryopreservation of complex tissues and organs.
小弹性动脉（兔颈总动脉）的平滑肌和血管内皮在4℃下暴露于40%乙二醇（EG）时会受到损伤，并且当动脉在未冷冻至-20℃的情况下冷却时会发生额外损伤。本文报道了通过改变冷却速率和暴露于冷冻保护剂的温度来减少这种损伤的尝试。复温并去除冷冻保护剂后在体外评估时，极慢冷却（0.1℃/分钟）会消除所有残留的平滑肌和内皮功能。极快冷却至-20℃也会增加对内皮和平滑肌的损伤。将暴露于40%EG的温度从+4℃降至-20℃对平滑肌没有有益影响，但能使血管内皮保留一些功能活性。这些数据表明，其潜在机制可能与乙二醇的物理性质有关，而非与代谢过程的生化相互作用有关，并且这是一种对所涉及的细胞类型具有高度特异性的机制。这也凸显了成功冷冻保存复杂组织和器官所面临的困难。
