Anesthetic Preconditioning with Sevoflurane Does Not Protect the Spinal Cord After an Ischemic-Reperfusion Injury in the Rat
David A. Zvara, Andrew J. Bryant, Dwight D. Deal, Mario P. DeMarco, Kevin M. Campos, C.M. Mansfield, Michael Tytell
Abstract
David A. Zvara, Andrew J. Bryant, Dwight D. Deal, Mario P. DeMarco, Kevin M. Campos, C.M. Mansfield, Michael Tytell
Abstract
In Brief Anesthetic preconditioning (APC) is a protective mechanism, whereby exposure to a volatile anesthetic renders a tissue resistant to a subsequent ischemic insult. We hypothesized that APC of the rat spinal cord with sevoflurane would reduce neurologic deficit after an ischemic-reperfusion injury. Rats were randomly assigned to 1 of 5 groups. The ischemic preconditioning (IPC) group (n = 14) had 3 min of IPC, 30 min of reperfusion, and 12 min of ischemia. The chronic APC (cSEVO) group (n = 14) had 1 h of APC with 3.5% sevoflurane on each of 2 days before ischemia. The acute APC (aSEVO) group (n = 14) had 1 h of APC with 3.5% sevoflurane followed by a 1-h washout period before the induction of ischemia. The controls (n = 14) underwent no preconditioning before ischemia. IPC attenuated the ischemia-reperfusion injury, whereas aSEVO and cSEVO groups were no better than control animals. Histologic evaluation of the spinal cord showed severe neurologic damage in all groups except for the IPC group and sham-operated rats. APC with sevoflurane did not reduce neurologic injury in a rat model of spinal cord ischemia. Traditional ischemic preconditioning had a strong protective benefit on neurologic outcome. IMPLICATIONS: Paraplegia remains a devastating consequence of descending and thoracoabdominal aortic operations that have a period of obligate spinal cord ischemia. This research demonstrated no benefit of anesthetic preconditioning in attenuating this type of injury.
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In Brief Anesthetic preconditioning (APC) is a protective mechanism, whereby exposure to a volatile anesthetic renders a tissue resistant to a subsequent ischemic insult. We hypothesized that APC of the rat spinal cord with sevoflurane would reduce neurologic deficit after an ischemic-reperfusion injury. Rats were randomly assigned to 1 of 5 groups. The ischemic preconditioning (IPC) group (n = 14) had 3 min of IPC, 30 min of reperfusion, and 12 min of ischemia. The chronic APC (cSEVO) group (n = 14) had 1 h of APC with 3.5% sevoflurane on each of 2 days before ischemia. The acute APC (aSEVO) group (n = 14) had 1 h of APC with 3.5% sevoflurane followed by a 1-h washout period before the induction of ischemia. The controls (n = 14) underwent no preconditioning before ischemia. IPC attenuated the ischemia-reperfusion injury, whereas aSEVO and cSEVO groups were no better than control animals. Histologic evaluation of the spinal cord showed severe neurologic damage in all groups except for the IPC group and sham-operated rats. APC with sevoflurane did not reduce neurologic injury in a rat model of spinal cord ischemia. Traditional ischemic preconditioning had a strong protective benefit on neurologic outcome. IMPLICATIONS: Paraplegia remains a devastating consequence of descending and thoracoabdominal aortic operations that have a period of obligate spinal cord ischemia. This research demonstrated no benefit of anesthetic preconditioning in attenuating this type of injury.
Key concepts: Medicine, Sevoflurane, Anesthesia, Anesthetic, Ischemic preconditioning, Reperfusion injury, Ischemic reperfusion injury, Myocardial Reperfusion Injury