Abstract
We examined in a rabbit model of transient spinal cord ischemia (SCI) whether isoflurane (Iso) preconditioning induces ischemic tolerance to SCI in a dose–response manner, and whether this effect is dependent on mitochondrial adenosine triphosphate-dependent potassium (K ATP) channel. Eighty-six rabbits were randomly assigned to 10 groups: Control group ( n = 8) received no pretreatment. Ischemic preconditioning (IPC) group ( n = 8) received 5 min of IPC 30 min before SCI. The Iso 1, Iso 2 and Iso 3 groups ( n = 10, 9, 8) underwent 30 min of 1.05, 2.1 and 3.15% Iso inhalation commencing 45 min before SCI. The Iso 1HD, Iso 2HD and Iso 3HD groups ( n = 9, 9, 8) each received a specific mitochondrial K ATP channel blocker, 5-hydroxydecanoic acid (5HD, 20 mg/kg), 5 min before each respective Iso inhalation. The 5HD group ( n = 8) received 5HD without Iso inhalation. The sham group ( n = 9) had no SCI. SCI was produced by infra-renal aortic occlusion via the inflated balloon of a Swan–Ganz catheter for 20 min. The Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and more viable motor nerve cells (VMNCs) in the anterior spinal cord 72 h after reperfusion than the control group ( p < 0.05). Iso 3 group showed a better neurologic outcome and more VMNCs than Iso 1 group ( p < 0.05). And, the Iso 1, Iso 2 and Iso 3 groups showed a better neurologic outcome and higher VMNC numbers than the corresponding Iso 1HD, Iso 2HD and Iso 3HD groups ( p < 0.05). This study demonstrates that Iso preconditioning protects the spinal cord against neuronal damage due to SCI in a dose–response manner via the activation of mitochondrial K ATP channels.
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