The declamping shock has been attributed to reactive hyper-emia with pooling of blood in the legs, metabolic acidosis following Inctate aceumulation in the ischemic leg muscles and hyperkalemia. We have studied eight patients undergoing arterial reconstruction with temporary aortic occlusion, in six cases because of obstructive arterioselerotic disease and in two cases for aortic aneurysm. Muscle biopsies from the lateral vastus muscle as well as blood samples from the iliac vein, the superior caval vein and the radial artery were taken before clamping of the aorta.,just before declamping, and 20 minutes after restitution of leg blood flow. ATP, ADP, AMP, phospho-creatine (PCr), creatine (Cr), glycogen, glucose, lactate, pyru-vate and NH4 + from the immediately frozen muscle biopsies as well as lactate and pyruvate in the iliac vein and central venous blood were determined with an enzymatic, fluorometric technique. Only one patient reacted with a temporary hypotension at declamping. Arterial pH was unaffected during the operation, and no hyperkalemia was noted. During clamping of the aorta an increased lactate/pyruvate ratio in muscle indicated tissue hypoxia. Energy charge (EC) was, however, unchanged and the adenylate pool was maintained possibly due to a decrease in PCr. In spite of the restitution of blood flow after declamping of the aorta, no normalization of the metabolic state was seen, not even 20 minutes after the release of the clamp. EC was still unchanged but a significant decrease of both the adenylate and creatine pools was seen. These findings might indicate a damage of the mitochondria and the cellular membranes in skeletal muscle after temporary arterial occlusion.