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The effects of hypertonic saline on spinal cord blood flow following compression injury
P A Spera1, U S Vasthare, R F Tuma
1Department of Physiology, Temple University Hospital Philadelphia, Pennsylvania 19140, USA.
7.5% hypertonic saline was administered following spinal cord injury to test its effect on spinal cord blood flow. Four different groups of rats underwent 10 minutes of spinal cord compression (45 g) at the C3 to C5 levels. A fifth group was not injured, but received hypertonic saline (5 ml/kg) at 5, 15 and 60 minutes following injury. Somatosensory evoked potentials and spinal cord blood flow were measured prior to and for 4 hours following the injury. The administration of hypertonic saline caused a significant increase in flow when administered 5 minutes following injury. Topical nitroprusside administration did not cause any increase in spinal cord blood flow during this time period. Hypertonic saline administration at the later time periods did not increase spinal cord blood flow. The group of animals which were not injured, but received hypertonic saline also showed no significant change in flow. The somatosensory evoked response of the treated animals was maintained for 4 hours after the injury where as the untreated animals began to lose their evoked responses 3 hours after injury.
7.5% hypertonic saline was administered following spinal cord injury to test its effect on spinal cord blood flow. Four different groups of rats underwent 10 minutes of spinal cord compression (45 g) at the C3 to C5 levels. A fifth group was not injured, but received hypertonic saline (5 ml/kg) at 5, 15 and 60 minutes following injury. Somatosensory evoked potentials and spinal cord blood flow were measured prior to and for 4 hours following the injury. The administration of hypertonic saline caused a significant increase in flow when administered 5 minutes following injury. Topical nitroprusside administration did not cause any increase in spinal cord blood flow during this time period. Hypertonic saline administration at the later time periods did not increase spinal cord blood flow. The group of animals which were not injured, but received hypertonic saline also showed no significant change in flow. The somatosensory evoked response of the treated animals was maintained for 4 hours after the injury where as the untreated animals began to lose their evoked responses 3 hours after injury.