Spinal Cord Blood Flow and Neurologic Outcome after Transient Spinal Cord Ischemia in Rabbits : Modification by Graded Hypothermia, Thiopental, and Nitric Oxide Synthase Inhibitor

脊髄虚血後の血流と神経学的予後 : 低体温,チオペンタール,一酸化窒素合成酵素阻害薬の影響

Spinal Cord Blood Flow and Neurologic Outcome after Transient Spinal Cord Ischemia in Rabbits : Modification by Graded Hypothermia, Thiopental, and Nitric Oxide Synthase Inhibitor

Creators Iida Yasuhiko

Paraplegia is the most dreaded complication after reconstruction of the thoracoabdominal aorta. For better understanding of pathophysiology of and potential protective measures against spinal cord damage following ischemia, three series of study were performed using transient lumbar spinal cord ischemia (20 min) model (aortic clamp) in New Zealand white rabbits. In the first series (n=19), spinal cord blood flow (SCBF) was measured using colored microsphere technique and a correlation between SCBF and neurologic outcome (6 h) was examined. In the second series (n=27), the effects of hypothermia (35℃, 32℃) and thiopental (a dose inducing burst and suppression in EEG) on neurologic outcome (48 h)were evaluated. In control rabbits temperature was maintained at 38℃. In the third series (n=18), the effects of nitric oxide synthase inhibitor, N^G-nitro-L-arginine-methyl-ester (L-NAME), and phenylephrine (in a dose to produce comparable elevation of systemic blood pressure) were examined. L-NAME 3mg/kg was given (over 10 min) 20 min before aortic clamp followed by an infusion (3 mg/kg/h) till the end of 6 h-reperfusion. Segmental spinal cord evoked potentials were monitored and histopathological examination was done in the second and third series. All rabbits except the thiopental group were maintained 1 % halothane before, during, and shortly after ischemia. SCBF in the lumbar region, following a marked decrease during ischemia, was significantly increased at 10 min of reperfusion and returned to preischemic level at 60 and 120 min. At 6 h, the SCBF of the paraplegic rabbits was significantly higher than preischemic value. When compared to the control group, neurologic outcome in the hypothermic groups was better, but not in the thiopental group. In L-NAME and phenylephrine groups, proximal mean blood pressure was higher by 15 mmHg and neurologic outcome was significantly better compared to the control group. Histological findings were well correlated to neurologic outcome. The results suggest that (1 ) the mechanisms other than postischemic hypoperfusion may play a role in paraplegia, (2) mild hypothermia has protective effect, while thiopental has not, and thus the protection by mild hypothermia appears to be mediated by the mechanisms other than metabolic suppression, (3) improvement of neurologic outcome with nitric oxide synthase inhibitor in this model may be attributed to the augmentation of systemic blood pressure which may possibly increase collateral blood flow to the ischemic regions.

[ISSN]0513-1731

[NCID]AN00243156