STUDY DESIGN: The authors evaluated the vascular permeability changes of the cauda equina after lumbar laminectomy in rats. OBJECTIVES: To clarify the early vascular responses in postlaminectomy adhesive arachnoiditis. SUMMARY OF BACKGROUND DATA: Laminectomy-induced cauda equina adhesion has been visualized by postoperative serial magnetic resonance imaging in humans. In laminectomized rats, fibrinous exudation was apparent among the adhered cauda equina. To date, there has been no report of substantial changes in vascular permeability in the cauda equina after lumbar laminectomy. METHODS: Wistar rats laminectomized from L5-L6 were used for four studies; 1) Evans blue albumin tracer study; 2) horseradish peroxidase tracer study; 3) lanthanum tracer study; and 4) fluoroscein isothiocyanate-dextran (molecular weights: 20K, 70K, and 150K) tracer study. Untreated rats were used as controls. RESULTS: 1) In the laminectomized (L5-L6) area, the cauda equina tended to conglomerate from 3 hours after surgery; this was relatively resolved by 6 weeks. Extravascular leakage of Evans blue albumin in the cauda equina appeared at 3 hours after surgery and reached a plateau at 24 hours; it mostly disappeared by 6 weeks. At 24 hours after surgery, the extent of Evans blue albumin extravasation was seen in one or more levels adjacent to the laminectomized area. Evans blue albumin leakage and cauda equina adhesion started to appear in nearly a same phase after laminectomy, followed by a plateau of vascular permeability facilitating complete cauda equina adhesion by 24 hours after surgery. The restoration of Evans blue albumin leakage was noted 1 week after surgery, and tended to precede recovery of the cauda equina adhesion; 2) in the laminectomy group, Horseradish peroxidase penetrated from the lumen to the extracellular space beyond the basal laminae of the endothelial cells. Numerous horseradish peroxidase-labeled vesicles in the endothelial cells were found; 3) There was a significant increase in lanthanum distribution in the endothelial cytoplasm at the laminectomized levels. Lanthanum filled the interendothelial clefts beyond the tight junction, but did not penetrate through the perivascular basal laminae; 4) Fluoroscein isothiocyanate-dextran (20K, 70K, 150K) permeability increased in the laminectomy group, but there was no difference in extravasation of fluoroscein isothiocyanate-dextran, irrespective of the molecular weight. CONCLUSION: Laminectomy consistently induced an increase in vascular permeability in the cauda equina, an increase of vesicular transport in the endothelial cell, and opening of the tight junction early after laminectomy, suggesting breakdown of the blood nerve barrier in the cauda equina. The accelerated permeability may enhance cauda equina adhesion.
STUDY DESIGN: The authors evaluated the vascular permeability changes of the cauda equina after lumbar laminectomy in rats. OBJECTIVES: To clarify the early vascular responses in postlaminectomy adhesive arachnoiditis. SUMMARY OF BACKGROUND DATA: Laminectomy-induced cauda equina adhesion has been visualized by postoperative serial magnetic resonance imaging in humans. In laminectomized rats, fibrinous exudation was apparent among the adhered cauda equina. To date, there has been no report of substantial changes in vascular permeability in the cauda equina after lumbar laminectomy. METHODS:Wistar rats laminectomized from L5-L6 were used for four studies; 1) Evans blue albumin tracer study; 2) horseradish peroxidase tracer study; 3) lanthanum tracer study; and 4) fluoroscein isothiocyanate-dextran (molecular weights: 20K, 70K, and 150K) tracer study. Untreated rats were used as controls. RESULTS: 1) In the laminectomized (L5-L6) area, the cauda equina tended to conglomerate from 3 hours after surgery; this was relatively resolved by 6 weeks. Extravascular leakage of Evans blue albumin in the cauda equina appeared at 3 hours after surgery and reached a plateau at 24 hours; it mostly disappeared by 6 weeks. At 24 hours after surgery, the extent of Evans blue albumin extravasation was seen in one or more levels adjacent to the laminectomized area. Evans blue albumin leakage and cauda equina adhesion started to appear in nearly a same phase after laminectomy, followed by a plateau of vascular permeability facilitating complete cauda equina adhesion by 24 hours after surgery. The restoration of Evans blue albumin leakage was noted 1 week after surgery, and tended to precede recovery of the cauda equina adhesion; 2) in the laminectomy group, Horseradish peroxidase penetrated from the lumen to the extracellular space beyond the basal laminae of the endothelial cells. Numerous horseradish peroxidase-labeled vesicles in the endothelial cells were found; 3) There was a significant increase in lanthanum distribution in the endothelial cytoplasm at the laminectomized levels. Lanthanum filled the interendothelial clefts beyond the tight junction, but did not penetrate through the perivascular basal laminae; 4) Fluoroscein isothiocyanate-dextran (20K, 70K, 150K) permeability increased in the laminectomy group, but there was no difference in extravasation of fluoroscein isothiocyanate-dextran, irrespective of the molecular weight. CONCLUSION: Laminectomy consistently induced an increase in vascular permeability in the cauda equina, an increase of vesicular transport in the endothelial cell, and opening of the tight junction early after laminectomy, suggesting breakdown of the blood nerve barrier in the cauda equina. The accelerated permeability may enhance cauda equina adhesion.