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. 1981 Jan;193(1):99-104.
doi: 10.1097/00000658-198101000-00016.

Temporary incomplete ischemia of the legs caused by aortic clamping in man: improvement of skeletal muscle metabolism by low molecular dextran

Temporary incomplete ischemia of the legs caused by aortic clamping in man: improvement of skeletal muscle metabolism by low molecular dextran

B Eklöf et al. Ann Surg. 1981 Jan.

Abstract

Temporary infrarenal clamping of the aorta during reconstructive surgery induces incomplete ischemia of the leg muscle. After release of the clamp, severe muscle metabolic derangement with loss of high-energy phosphate compounds has been observed, indicating a dysfunction or damage of the muscle cells. In six patients operated on for occlusive aortoiliac disease, low-molecular-weight dextran (LMWD) was peroperatively administered for optimal volume loading and prevention of clotting. No heparin was used. Before, during and after the clamping period the central hemodynamics were monitored, and glycogen, glucose, lactate, pyruvate, phosphocreatine (PCr), creatine (Cr), ATP, ADP and AMP content in the thigh muscle were analyzed using enzymatic fluorometric techniques. Even though ischemia developed during the occlusion, no decline in the adenylate (ATP + ADP + AMP) or creatine (PCr + Cr) pools occurred after the clamp was released, and the energy charge of the adenine nucleotides remained unchanged. It is suggested that LMDX prevents rheologic changes impairing the microcirculation during and after the ischemic period, and thereby improves oxygenation of the muscle tissue upon reperfusion.

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