Development of spinal cord ischemia after clamping of noncritical segmental arteries in the pig

Background. Blood flow to the thoracolumbar spinal cord is thought to be critically dependent on the arteria radicularis magna. We investigated whether spinal cord blood supply becomes dependent on other, noncritical, segmental arteries if spinal cord perfusion pressure (SCPP) is decreased. The SCPP is equal to the mean arterial pressure (MAP) minus the cerebrospinal fluid (CSF) pressure (SCCP = MAP - CSF). Methods. The thoracoabdominal aorta was exposed in 10 pigs. Functional integrity of spinal cord motor pathways was assessed with myogenic motor-evoked potentials after transcranial electrical stimulation (tc-MEPs). Using this technique, a group of segmental arteries not critical for spinal cord blood supply was identified. Before, during, and after clamping of the noncritical segmental arteries, spinal cord ischemia was produced by decreasing SCPP by means of increasing CSF pressure, and the SCPP threshold at which tc-MEPs showed evidence of spinal cord ischemia was determined. Ischemic SCPP thresholds, obtained during and after clamping of the noncritical segmental arteries, were compared with the ischemic threshold obtained before clamping (control value). Results. Before noncritical segmental arteries were clamped, ischemic tc-MEP changes occurred when the SCPP was below 15 ± 5 (SD) mm Hg. With a total of 9 3 (SD) segmental arteries clamped, the ischemic SCPP threshold was 48 ± 14 mm Hg (p < 0.01). After the release of all clamps, ischemia occurred at a SCPP of 15 ± 5 (SD) mm Hg. Conclusions. In this porcine experiment, clamping of originally noncritical segmental arteries significantly reduced the tolerance of the spinal cord to a decrease in SCPP.