Korpan N N
Vienna International Institute for Cryosurgery, Department of Surgery, Rudolfinerhaus, Billrothstrasse 78, A-1190 Vienna, Austria.
Technol Cancer Res Treat. 2007 Apr;6(2):59-67. doi: 10.1177/153303460700600202.
A number of theoretical and experimental studies, both in vitro and in vivo, have been performed to explain the action of low temperatures on tissue. It is now evident that the thermal parameters used in the past for freezing during cryosurgery were not precise; this may have resulted in the failure of treatment. For the first time, this report describes the early ultrastructural features of pancreatic parenchyma after low temperature exposure, i.e., cryosurgery, in vivo. We demonstrate the effect of freeze-thawing processes using temperatures of various intensities. The cryosurgical response of pancreas parenchyma, i.e., ultrastructural cellular changes in pancreas tissue, was investigated. The electronic microscopic analysis showed that, after local cryodestruction at temperatures of -80 degrees C and -180 degrees C, similar processes occurred within the pancreas tissue in the early postcryosurgical phase -- immediately and up to 24 hours after low temperature exposure on tissue. The exocrine pancreatic cells in the center of the cryozone changed upon thawing. Ultrastructural changes in the exocrine pancreatic cells, where the first signs of dystrophic processes had been noticed, were increased. These ultrastructural changes in the pancreatic cells provide a platform to better understand the mechanisms of damage and the pathogenesis of frostbite after cryosurgery. The properties of the pancreas parenchyma response after low temperature exposure provide important insights into the mechanisms of damage and the cryogenic lesion immediately after thawing in cryosurgery. Our new insights prove on the cell level that suddenly and progressively damaged pancreatic cells in the postcryosurgical zone lead to aseptic cryonecrosis and then to aseptic cryoapoptosis of vital normal tissue. The vascular capillary changes and circulatory stagnation demonstrate the anti-angiogenesis mechanism, which, together with cryoaponecrosis and cryoapoptosis, are some of the main mechanisms of biological tissue injury following the low temperature exposure.
已经进行了许多体外和体内的理论与实验研究，以解释低温对组织的作用。现在很明显，过去在冷冻手术中用于冷冻的热参数并不精确；这可能导致了治疗失败。本报告首次描述了体内低温暴露（即冷冻手术）后胰腺实质的早期超微结构特征。我们使用不同强度的温度来证明冻融过程的影响。研究了胰腺实质的冷冻手术反应，即胰腺组织中的超微结构细胞变化。电子显微镜分析表明，在-80摄氏度和-180摄氏度的局部冷冻破坏后，胰腺组织在冷冻手术后早期——在组织低温暴露后立即至24小时内——发生了类似的过程。冷冻区中心的外分泌胰腺细胞在解冻后发生了变化。外分泌胰腺细胞中最早出现营养不良过程迹象的超微结构变化增加了。胰腺细胞中的这些超微结构变化为更好地理解冷冻手术后损伤机制和冻伤的发病机制提供了一个平台。低温暴露后胰腺实质反应的特性为冷冻手术后解冻后立即出现的损伤机制和低温损伤提供了重要的见解。我们的新见解在细胞水平上证明，冷冻手术后区域中突然且逐渐受损的胰腺细胞会导致无菌性冷冻坏死，进而导致重要正常组织的无菌性冷冻凋亡。血管毛细血管变化和循环停滞表明了抗血管生成机制，该机制与冷冻凋亡和冷冻坏死一起，是低温暴露后生物组织损伤的一些主要机制。
