Faculty Bibliography

In the present study, we examined the effects of various levels of oxygen tension on spinal cord blood flow while using somatosensory evoked potentials to monitor spinal cord sensory function during hypoxia. In this experiment, six adult, mongrel dogs were heparinized and placed on right atrial-femoral artery bypass with an oxygenator in the bypass circuit. The aorta was cross-clamped proximal to the left subclavian artery, and bypass flow and fluid balance were adjusted so as to maintain a distal aortic perfusion pressure of greater than 80 mm Hg. Oxygen flow to the oxygenator was lowered by graded decrements to provide decreasing levels of oxygen tension, which ultimately approached pure venoarterial bypass. Each successive oxygen level was maintained for 30 minutes. Spinal cord blood flow was measured with radioactive microspheres, and latency and amplitude of somatosomatic evolved potentials were continuously monitored. The somatosensory evolved potential signal was invariably present as long as the distal aortic pressure was greater than 80 mm Hg; there were several transient hypotensive episodes (less than 5 minutes), which were accompanied by reversible loss of somatosensory evolved potentials. The spinal cord blood flow increased from 13.6 to 119.7 ml/100 gm/min as the distal oxygen tension fell to a mean value of 30 mm Hg, while latency of somatosensory evolved potentials increased 19.3% and amplitude decreased 43.3%. These results suggest the following conclusions: (1) In response to hypoxia, spinal cord blood flow dramatically increases and somatosensory evolved potentials deteriorate (increase in latency and decrease in amplitude). (2) However, during prolonged hypoxia, spinal cord sensory function can be maintained by sufficiently high flow rates and perfusion pressures. (3) Somatosensory evolved potentials can be used to monitor continuously spinal cord sensory function under these conditions