Abstract
Objective To investigate the effect of controlled low perfusion pressure on expression of phosphor-Akt (p-Akt) and phosphor-ERK1/2 (p-ERK1/2) following spinal ischemia-reperfusion (1/R) in rabbits.Methods Thirty-six Japanese long-ear white rabbits aged 3 months weighing 2.0-2.5 kg were randomly divided into 3 groups ( n = 12 each):group sham operation (group S) ; group spinal I/R (group I/R) and group controlled low perfusion pressure (group LP).Auricular artery and femoral artery were carnulated for proximal and distal BP monitoring.A 4F catheter with a balloon at the tip was inserted into abdominal aorta.The tip was positioned 1 cm below left renal artery.Spinal ischemia was induced by inflating the balloon until the distal MAP < 20 mm Hg,and maintained for 25 min.During the first 10 min of reperfusion the distal MAP was increased to 45-55 mm Hg by partially deflating the balloon.Then the balloon was fully deflated to allow complete reperfusion.The function of lower limbs was assessed with Tarlov score (0 = no detectable movement,4 = normal function) at 1,3,7,28 d of reperfusion.Au the animals were sacrificed at 1 d of reperfusion in each group.The lumbar segment L3-5 of the spinal cord was removed for microscopic examination and determination of expression of p-Akt and p-ERK1/2 by immuno-histochemistry) and detection of neuronal apoptosis in dorsal horn (by TUNEL).Results Spinal I/R significantly decreased Tarlov scores,and increased the number of apoptotic cells and expression of p-Akt and pERK1/2 in group I/R as compared with group S.Low perfusion pressure during the 10 min at the beginning of reperfusion significantly increased Tarlov scores,decreased apoptotic index and further increased p-Akt and pERK1/2 expression in group LP compared with group I/R.The histopathological damage in the spinal cord was attenuated in group LP.Conclusion Controlled low pcrfusion pressure can reduce the spinal cord I/R injury by activating Akt and ERK1/2 and decreasing neuronal apoptosis. Key words: Hypotension,controlled; Protein-serine-threonine kinases; Mitogen-activated protein kinases; Reperfusion injury; Spinal cord
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