Effects of hypertension and hypercarbia on spinal cord tissue oxygen in acute experimental spinal cord injury.
Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002245:Carbon Dioxide / Q000627:therapeutic use; D004285:Dogs; D005260:Female; D009638:Norepinephrine / Q000627:therapeutic use; D010100:Oxygen / Q000032:analysis*; D010102:Oxygen Inhalation Therapy; D012121:Respiration, Artificial; D013116:Spinal Cord / Q000032:analysis*; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000628:therapy
D002245:Carbon Dioxide; D010100:Oxygen; D009638:Norepinephrine