ENERGY COSTS vary with an organ's functional needs. The same relationship applies within different regions of the same organ. In vivo regional differences in O t consumption are known within some organs, e.g., white and gray matter of the cerebral cortex, subepicardium, and subendocardium of the left ventricle, and cortex and medulla of the kidney. "3 Only qualitative evidence for these differences exist. We have developed a technique that can quantitatively measure these differences in regional O 2 consumption under different functional conditions. Regional Oj extraction is measured, using our recently developed microspectrophotometric technique, 4 -B and regional blood flow is determined with radioactive microspheres. Regional O 2 consumption is calculated from these data by the Fick principle.This method of determination of regional O, consumption has been applied to the heart where there are clear differences in cardiac work between the right, left, and septal ventricular walls. Until now, there has been no way to quantitate this difference in terms of O 2 consumption. Differences in blood flow have been reported between the ventricular walls, 6 ' 7 but no disparity has been found between the average arteriovenous O t difference of the right, septal, and left ventricular walls, although within the left ventricular wall some regional arteriovenous O s saturation differences exist. 8 We have studied O t extraction and flow in the same dog and determined differences in O t consumption between the ventricular walls.In the left ventricular free wall, there has been some qualitative evidence for regional differences in O 2 consumption as a function of depth within the wall. The

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1. Ischaemia of a portion of the myocardium in the dog heart was produced by tying off a small branch of a coronary artery: flow in the occluded region was reduced from 5 to 82% of the initial value. 2. The effect of inhalation of 5% CO2 in air on relative tissue PO2 and perfusion in normal and partially ischaemic myocardium was determined. 3. After 10 min inhalation of 5% CO2, there was an increase in tissue perfusion as measured by hydrogen desaturation; the increase was inversely proportional to the degree of flow reduction. 4. Relative intramyocardial PO2 measured polarographically, decreased with occlusion and increased after CO2 inhalation; the changes were inversely proportional to the degree of reduction in PO2. 5. The increase in flow after CO2 inhalation suggests that partially ischaemic myocardial tissue is capable of further vasodilation.

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