Assessment of spinal cord pathology following trauma using early changes in the spinal cord evoked potentials: a pharmacological and morphological study in the rat.
The possibility that spinal cord pathology following trauma can be assessed with early changes in the spinal cord evoked potentials (SCEPs) was examined in a rat model. Spinal cord injury (SCI) was produced in Equithesin-anesthetized (3 ml/kg, i.p.) rats through a longitudinal incision into the right dorsal horn at the T10-11 segments. The SCEPs were recorded with epidural electrodes placed over the T9 (rostral) segment of the cord. The SCEPs consisted of a small positive amplitude and a broad and high negative amplitude (NA). SCI resulted in an instant depression of the rostral NA that lasted for 1 h. However, the latency of NA continued to increase over time. At 5 h, spinal cord blood flow declined by 30% in the T9 segment, whereas the spinal cord water content and the permeability of the blood-spinal cord barrier (BSCB) were markedly increased. Damage to the nerve cells, glial cells, and myelin was quite common in the spinal cord, as seen by light and electron microscopy. Pretreatment with p-chlorophenylalanine, indomethacin, ibuprofen, and nimodipine attenuated the SCEP changes immediately after trauma and resulted in a marked reduction in edema formation, BSCB permeability, and blood flow changes at 5 h. However, pretreatment with cyproheptadine, dexamethasone, phentolamine, and propranolol failed to attenuate the SCEP changes after SCI and did not reduce the cord pathology. These observations suggest that early changes in SCEP reflect secondary injury-induced alterations in the cord microenvironment. Obviously, these changes are crucial in determining the ultimate magnitude and severity of cord pathology.
Laboratory of Neuroanatomy, Department of Medical Cell Biology, Box 571, Biomedical Centre, Uppsala University, SE-75123 Uppsala, Sweden. sharma@medcellbiol.uu.se
Hari Shanker
HS
Sharma
Tomas
T
Winkler
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D004396:Coloring Agents / Q000493:pharmacokinetics; D003533:Cyproheptadine / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004487:Edema / Q000473:pathology / Q000503:physiopathology; D004594:Electrophysiology; D004727:Endothelium / Q000473:pathology / Q000648:ultrastructure; D005070:Evans Blue / Q000493:pharmacokinetics; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D010134:Fenclonine / Q000494:pharmacology; D007052:Ibuprofen / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009553:Nimodipine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012702:Serotonin Antagonists / Q000494:pharmacology; D013116:Spinal Cord / Q000098:blood supply / Q000473:pathology* / Q000648:ultrastructure; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology*
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D000893:Anti-Inflammatory Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002121:Calcium Channel Blockers; D004396:Coloring Agents; D012702:Serotonin Antagonists; D003533:Cyproheptadine; D005070:Evans Blue; D009553:Nimodipine; D003907:Dexamethasone; D011433:Propranolol; D010134:Fenclonine; D007052:Ibuprofen; D007213:Indomethacin; D010646:Phentolamine