In situ studies of oxidative energy metabolism during transient cortical ischemia in cats

Changes in oxidative energy metabolism were monitored noninvasively during periods of transient cortical ischemia in cats by means of fluorometric observation of the redox level of intramitochondrial NADH and by dual wavelength reflectance spectrophotometry of cytochrome a. The latter technique also allowed measurements of the oxygenation state of hemoglobin and of blood volume in the optical field. We report here that incomplete ischemia is accompanied by increased levels of NADH and reduced cytochrome a, an increase in the unloading of O 2 from hemoglobin and a decrease in the blood volume, but these all turn back toward baseline with the establishment of “collateral” circulation. Complete ischemia is accompanied by sustained increased levels of reduced NAD and cytochrome a, the extent of which equaled the reduction levels produced by terminal anoxia. When short ischemic episodes were repeated, the rates of return of NAD and cytochrome a to baseline redox levels were faster after each successive ischemia, while blood volume returned at the same rate and hemoglobin saturation returned more slowly to its original state of oxygenation. We interpret that the primary lesion of short ischemic episodes is the uncoupling of oxidative phosphorylation.