Coban Yusuf Kenan, Ciralik Harun, Kurutas Ergul Belge
Dept of Plastic Surgery, Sutcuimam University, School of Medicine, Kahramanmaraş, Turkey.
J Brachial Plex Peripher Nerve Inj. 2006 Sep 29;1:2. doi: 10.1186/1749-7221-1-2.
Allow for protection of briefly ischemic tissues against the harmful effects of subsequent prolonged ischemia is a phenomenon called as Ischemic Preconditioning (IP). IP has not been studied in ischemia-reperfusion (I/R) model of peripheral nerve before. We aimed to study the effects of acute IP on I/R injury of peripheral nerve in rats.
70 adult male rats were randomly divided into 5 groups in part 1 experimentation and 3 groups in part 2 experimentation. A rat model of severe nerve ischemia which was produced by tying iliac arteries and all identifiable anastomotic vessels with a silk suture (6-0) was used to study the effects of I/R and IP on nerve biochemistry. The suture technique used was a slip-knot technique for rapid release at time of reperfusion in the study. Cytoplasmic vacuolar degeneration was also histopathologically evaluated by light microscopic examination in sciatic nerves of rats at 7th day in part 2 study.
3 hours of Reperfusion resulted in an increase in nerve malondialdehyde levels when compared with ischemia and non-ischemia groups (p < 0.001 and p < 0.0001 respectively). IP had significantly lower nerve MDA levels than 3 h reperfusion group (p < 0.001). The differences between ischemic, IP and non-ischemic control groups were not significant (p > 0.05). There was also a significant decrease in vacuolar degeneration of sciatic nerves in IP group than I/R group (p < 0.05).
IP reduces the severity of I/R injury in peripheral nerve as shown by reduced tissue MDA levels at 3rd hour of reperfusion and axonal vacuolization at 7th postischemic day.
使短暂缺血组织免受随后长时间缺血的有害影响的现象称为缺血预处理(IP)。此前尚未在外周神经缺血再灌注(I/R)模型中对IP进行研究。我们旨在研究急性IP对大鼠外周神经I/R损伤的影响。
在第1部分实验中,70只成年雄性大鼠被随机分为5组,在第2部分实验中分为3组。采用丝线(6-0)结扎髂动脉和所有可识别的吻合血管建立严重神经缺血大鼠模型,以研究I/R和IP对神经生物化学的影响。在本研究中,所采用的缝合技术是一种活结技术,以便在再灌注时快速松开。在第2部分研究中,还通过光学显微镜检查对第7天大鼠坐骨神经的细胞质空泡变性进行了组织病理学评估。
与缺血组和非缺血组相比,再灌注3小时导致神经丙二醛水平升高(分别为p < 0.001和p < 0.0001)。IP组的神经丙二醛水平显著低于3小时再灌注组(p < 0.001)。缺血组、IP组和非缺血对照组之间的差异不显著(p > 0.05)。与I/R组相比,IP组坐骨神经的空泡变性也显著减少(p < 0.05)。
IP可减轻外周神经I/R损伤的严重程度,表现为再灌注第3小时组织丙二醛水平降低以及缺血后第7天轴突空泡化减少。