Zarem H A, Hayden B, Soderberg R, Ringham J M, Gabriel K
Department of Surgery, UCLA School of Medicine.
Plast Reconstr Surg. 1988 Nov;82(5):865-71. doi: 10.1097/00006534-198811000-00022.
In order to study the preservation of ischemic tissue, an in vivo end-artery model was designed using the rabbit ear. Ear surface-area necrosis and ear edema were quantitatively evaluated for 14 postoperative days in a total of 107 rabbits. The LD50 of ischemic injury was determined by effecting 8, 10, and 12 hours of circulatory arrest. Using a 12-hour ischemic interval in this model, methylprednisolone decreased edema formation (p less than 0.01) and dramatically halted the progression of ischemic injury to necrosis (p less than 0.05) when administered within 5 hours after the onset of ischemia and continued for 3 postoperative days. A single perioperative dose of methylprednisolone was ineffective in decreasing edema formation and preserving tissue. Administration of steroids greater than 5 hours after the onset of ischemia was similarly ineffective even when administered for 3 postoperative days.
为了研究缺血组织的保存，使用兔耳设计了一种体内终末动脉模型。对总共107只兔子术后14天的耳表面积坏死和耳水肿进行了定量评估。通过造成8、10和12小时的循环停止来确定缺血性损伤的半数致死剂量（LD50）。在该模型中使用12小时的缺血间隔，当在缺血开始后5小时内给予甲基强的松龙并持续3个术后日时，其可减少水肿形成（p<0.01）并显著阻止缺血性损伤向坏死的进展（p<0.05）。围手术期单次给予甲基强的松龙在减少水肿形成和保存组织方面无效。即使在术后3天给予，在缺血开始后5小时以上给予类固醇同样无效。
