Abstract
Background and aimAllow for protection of briefly ischemic tissues against the harmful effects of subsequent prolonged ischemia is a phenomennon 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.Method70 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 idenfiable 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.Results3 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 vacoular degeneration of sciatic nerves in IP group than I/R group (p < 0.05).ConclusionIP reduces the severity of I/R injury in peripheral nerve as shown by reduced tissue MDA levels at 3 th hour of reperfusion and axonal vacoulization at 7 th postischemic day.
Highlights
Background and aimAllow for protection of briefly ischemic tissues against the harmful effects of subsequent prolonged ischemia is a phenomennon called as Ischemic Preconditioning (IP)
Maximal intercellular adhesion molecule-1 (ICAM-1) expression on endoneural vessels and polymorphonuclear monocytes reaches a peak at 24 th hour and macrophages increases nearly four fold at 48–72 hour of reperfusion after a 5 h of near-complete ischemia [3]. All these cells are responsible for demyelinisation and ischemic fiber degeneration (IFD) at prolonged reperfusion after enough ischemic times in peripheral nerves [4,5]
Clinical experience related to I/R injury of peripheral nerve shows that neurologic recovery is possible, if reperfusion starts within 6 hours after ischemia [8]
Summary
Background and aimAllow for protection of briefly ischemic tissues against the harmful effects of subsequent prolonged ischemia is a phenomennon called as Ischemic Preconditioning (IP). Ischemia-reperfusion (I/R) causes oxidative injury and ischemic fiber degeneration (IFD), due to injury of the neuron and axon, after enough ischemic times, i.e.4–5 hours of peripheral nerve ischemia [1,2]. Maximal intercellular adhesion molecule-1 (ICAM-1) expression on endoneural vessels and polymorphonuclear monocytes reaches a peak at 24 th hour and macrophages increases nearly four fold at 48–72 hour of reperfusion after a 5 h of near-complete ischemia [3]. All these cells are responsible for demyelinisation and IFD at prolonged reperfusion after enough ischemic times in peripheral nerves [4,5]. Clinical experience related to I/R injury of peripheral nerve shows that neurologic recovery is possible, if reperfusion starts within 6 hours after ischemia [8]
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