OBJECTIVE: The mechanism underlying ischemic preconditioning (IPC) protection against spinal cord ischemia-reperfusion (I/R) injury is unclear. We investigated the role of spinal cord autoregulation in tolerance to spinal cord I/R injury induced by IPC in a rat model. METHODS: Sprague-Dawley rats were randomly assigned to four groups. IPC (P) group animals received IPC by temporary thoracic aortic occlusion (AO) with a 2F Fogarty arterial embolectomy catheter (Baxter Healthcare, Irvine, Calif) for 3 minutes. The I/R injury (I/R) group animals were treated with blood withdrawal and temporary AO for 12 minutes, and shed blood reinfusion at the end of the procedures. The P+I/R animals received IPC, followed by 5 minutes reperfusion, and then I/R procedures for 12 minutes. Sham (S) group animals received anesthesia and underwent surgical preparation, but without preconditioning or I/R injury. Neurologic function on postprocedure days 1, 3, 5, and 7 was evaluated by Tarlov scoring. Lumbar segments were harvested for histopathologic examination on day 7. To evaluate the role of autoregulation in IPC, spinal cord blood flow and tissue oxygenation were continuously monitored throughout the procedure duration. RESULTS: The Tarlov scores in the I/R group were significantly lower than those in the S, P, and P+I/R groups on days 1, 3, 5, and 7 (P < .001). No significant differences were noted between the S, P, and P+I/R groups. The numbers of surviving motor neurons in the S, P, and P+I/R groups were significantly higher than those in the I/R group (P < .001); however, the number of surviving motor neurons did not differ between the S, P, and P+I/R groups. The P group exhibited higher spinal cord blood flow (P = .001-.043) and tissue oxygenation (P = .032-.043) within the first 60 minutes after reperfusion than the S group. The P+I/R group exhibited higher spinal cord blood flow (P = .016-.045) and tissue oxygenation (P = .001-.038) within the first 60 minutes after reperfusion than the I/R group. CONCLUSIONS: IPC ameliorates spinal cord I/R injury in rats, probably mediated by triggering spinal cord autoregulation and improving local spinal cord blood flow and tissue oxygenation. This concept may be the new therapeutic targets in patients requiring aortic surgery.
OBJECTIVE: The mechanism underlying ischemic preconditioning (IPC) protection against spinal cord ischemia-reperfusion (I/R) injury is unclear. We investigated the role of spinal cord autoregulation in tolerance to spinal cord I/R injury induced by IPC in a rat model. METHODS:Sprague-Dawley rats were randomly assigned to four groups. IPC (P) group animals received IPC by temporary thoracic aortic occlusion (AO) with a 2F Fogarty arterial embolectomy catheter (Baxter Healthcare, Irvine, Calif) for 3 minutes. The I/R injury (I/R) group animals were treated with blood withdrawal and temporary AO for 12 minutes, and shed blood reinfusion at the end of the procedures. The P+I/R animals received IPC, followed by 5 minutes reperfusion, and then I/R procedures for 12 minutes. Sham (S) group animals received anesthesia and underwent surgical preparation, but without preconditioning or I/R injury. Neurologic function on postprocedure days 1, 3, 5, and 7 was evaluated by Tarlov scoring. Lumbar segments were harvested for histopathologic examination on day 7. To evaluate the role of autoregulation in IPC, spinal cord blood flow and tissue oxygenation were continuously monitored throughout the procedure duration. RESULTS: The Tarlov scores in the I/R group were significantly lower than those in the S, P, and P+I/R groups on days 1, 3, 5, and 7 (P < .001). No significant differences were noted between the S, P, and P+I/R groups. The numbers of surviving motor neurons in the S, P, and P+I/R groups were significantly higher than those in the I/R group (P < .001); however, the number of surviving motor neurons did not differ between the S, P, and P+I/R groups. The P group exhibited higher spinal cord blood flow (P = .001-.043) and tissue oxygenation (P = .032-.043) within the first 60 minutes after reperfusion than the S group. The P+I/R group exhibited higher spinal cord blood flow (P = .016-.045) and tissue oxygenation (P = .001-.038) within the first 60 minutes after reperfusion than the I/R group. CONCLUSIONS: IPC ameliorates spinal cord I/R injury in rats, probably mediated by triggering spinal cord autoregulation and improving local spinal cord blood flow and tissue oxygenation. This concept may be the new therapeutic targets in patients requiring aortic surgery.