Post-Traumatic Spinal Cord Ischemia: Relationship to Injury Severity and Physiological Parameters

Alterations in lumbar spinal cord white matter blood flow (SCBF) during the initial 4 hours following contusion injury were examined in cats anesthetized with either dial-urethane or sodium pentobarbital and correlated with changes in cardiovascular parameters (MAP, HR), blood gases (pCO₂, pO₂), and pH. In the dial-urethane anesthetized cats, the effect of a severe 500 g-cm contusion on SCBF was determined at the center of the injury site vs. an adjacent site 3 mm away. At the injury site, SCBF fell progressively from a pre-injury mean of 13.9 ± 0.8 (S.E.) mg/100 g/min to a 4 hour value of 7.0 ± 1.3 (−49.6%). In contrast, SCBF in the adjacent white matter tissue was dramatically increased to 22.4 ± 1.9 ml/100 g/min (+61.2% over pre-injury; p<0.025), at 10 min post-injury falling gradually back to only slightly below the pre-injury level at 4 hours. The severe contusion resulted in prolonged hypotension and bradycardia that was significant by 10 min post-injury while arterial blood gases and pH did not change over the experimental course. A very similar post-traumatic hypoperfusion was observed at the injury site in pentobarbital anesthetized animals in regard to the time course and extent of the decline in SCBF (−55.6% at 4 hours). Although the decrease in SCBF over time was gradual, the MAP and HR were maximally depressed by 10 min post-injury. A more moderate contusion (300 g-cm) resulted in an initial hyperemia followed by a return of SCBF to the pre-injury level by 30 min with no significant change thereafter even though the MAP was depressed to nearly the same extent as in the more severely injured cats. These results demonstrate that post-traumatic spinal cord ischemia is a phenomenon localized to the spinal injury site and directly related to the injury force with moderate injury actually causing a temporary hyperemia. In addition, a significant difference in SCBF may exist between the injury site and adjacent spinal tissue only a few mm away. No correlation between the increase or decrease in SCBF and change in cardiovascular parameters or blood gases following injury is demonstrable nor does anesthetic choice seem to make a significant difference. Thus, post-traumatic changes in SCBF appear to be due to the elaboration of local mediators for the most part unrelated to concomitant alterations in spinal cord perfusion pressure.