1994 Fiscal Year Final Research Report Summary
Experimental studies of pathophysiology and treatment of spinal cord ischemia
| Project/Area Number |
05454423
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Yamaguchi University |
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Principal Investigator |
SAKABE Takefumi Yamaguchi University, School of Medicine Professor, 医学部, 教授 (40035225)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUMOTO Mishiya Yamaguchi University, Hospital Research Associate, 医学部・附属病院, 助手 (60243664)
NAKAKIMURA Kazuhiko Yamaguchi University, Hospital Assistant Professor, 医学部・附属病院, 講師 (50180261)
ISHIKAWA Toshizoh Yamaguchi University, School of Medicine Research Associate, 医学部, 助手 (90034991)
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| Project Period (FY) |
1993 – 1994
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| Keywords | spinal cord ischemia / spinal cord blood flow / paraplegia / nitric oxide / excitatory amino acid / hypothermia |
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| Research Abstract |
Background and Purpose : Paraplegia is a serious complication after surgery of thoracic aortic aneurysm. Basic studies concerning pathophysiology of and protection against ischemic damage of the spinal cord are of great importance. Using a rabbit or rat model of spinal cord ischemia, we investigated the pathophysiology of the spinal cord ischemia and evaluated the potential protective measures against the neurologic damage.
Methods : Spinal cord ischemia was produced by occluding infrarenal aorta in rabbits or by occluding thoracic aorta in rats for 20 minutes. Spinal cord blood flow in rabbits was measured by colored microsphere method in a peri-ischemic period. Segmental spinal cord evoked potential (SSCEP) was monitored. Excitatory amino acids in CSF of the rat were measured using an intrathecal microdialysis probe. In the outcome study, rabbits were subjected to either normothermic ischemia under halothane or thiopental (burst-suppression on EEG) anesthesia, or hypothermic (35ﾟC or
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32ﾟC) ischemia under halothane anesthesia. In another series, rabbits were subjected to normothermic ischemia after pretreatment with L-NAME,phenylephrine, or vehicle. Phenylephrine was administered to increase mean arterial blood pressure to the same level as the L-NAME group. Rabbits were allowed to recover and were graded neurologically at 48 hours after ischemia.
Results : After induction of ischemia, SSCEP disappeared within 20 minutes and returned back to preischemic pattern in 20-30 minutes. At 10 minutes after recirculation, moderate hyperemia was observed in L4-L7 spinal cord. No hypoperfusion was detected after 60 and 120 minutes of recirculation. Spinal cord blood flow increased after 6 hours of recirculation in paraplegic animals. The glutamate concentration in the CSF increased 2.5 fold during ischemia and returned to the preischemic level after 1 hour recirculation. In the outcome studies, the hypothermia groups (both 35ﾟC and 32ﾟC) exhibited no neurologic deficit while the thiopental group exhibited neurologic deficit similar to that of the control group. Rabbits pretereated with L-NAME showed significantly better neurologic outcome compared with vehicle controls. Rabbits pretreated with phenylephrine exhibited no neurologic deficit.
Conclusions : These results show that deterioration of motor function after spinal cord ischemia is neither due to delayd hypoperfusion nor nitric oxide toxicity and that glutamate may play a role in the ischemic injury. A slight decrease in body temperature in the peri-ischemic period provides significant protection, while thiopental, in a dose to produce maximal metabolic depression, does not protect the spinal cord. Less
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