Oxidative metabolism during and following ischemia of cat spinal cord.

Spinal cord ischemia was produced by an occlusion of the thoracic descending aorta on experimental cats for the periods of 3, 5, 10, and 15 minutes. The reduction/oxidation (redox) ratio of cytochrome a,a3 was measured in vivo by reflectance spectrophotometry, simultaneously with the measurement of the following: blood pressure in the aorta distal to the occlusion; relative blood volume in the cord; oxygen tension in cord tissue; and cord potential in response to dorsal root stimulation. During aortic occlusion, the maximum increase in the redox ratio was reached somewhat more slowly than the maximum decrease in blood pressure, blood volume, and oxygen tension. Interneuron potentials began to decrease as the redox level increased, and completely disappeared soon after the redox ratio increased, and completely disappeared soon after the redox ratio increased maximally. During ischemia, therefore, oxygen consumption in the mitochondria was slightly lower than the decrease in oxygen tension; impairment of ADP phosphorylation, and accordingly that of ion pump, occurs simultaneously with the increase in the redox ratio. Recovery of the redox ratio after completion of aortic occlusion was also slightly slower than the recovery of blood pressure, blood volume, and oxygen tension. Complete recovery of interneuron potentials was much more delayed than that of the redox ratio; after 15-minute ischemia, uncoupling of ADP phosphorylation was noted. It can be concluded that the spinal cord function and metabolism are severely impaired after 15-minute occlusion.