Human skeletal Muscle Energy Metabolism During and after Complete Tourniquet Ischemia

Abstract

The extent of cellular metabolic deterioration and its reversibility was studied on human skeletal muscle needle biopsies during operations in bloodless field. The tissue levels of high energy phosphates and glycolytic metabolites were analyzed after various times of tourniquet ischemia and compared to contralateral control extremity levels. In the ischemic extremity the phosphocreatine (CrP) levels decreased by 40% within 30-60 min and after 60-90 min a 60% reduction was found. No significant ATP changes occurred. Lactate levels increased by 225% after 30-60 min and by 300% after 60-90 min. The glucose and G-6-P levels increased slightly and indicated glycogenolysis. The rate of the metabolic changes decreased with ischemia time. In the control leg no significant metabolic changes could be seen. After the release of the tourniquet there was a rapid restoration of the phosphagen content and clearance of lactate in the ischemic leg. Near control levels of these substances were seen already after 5 min. The present results show that clinical tourniquet ischemia of up to 90 min duration produces less pronounced metabolic alterations than those seen in working muscle.

Quantifying delays in the recognition and management of acute compartment syndrome

“…[22][23][24][25] We suspect, in addition, that physicians have been falsely reassured by tourniquet studies, which have suggested that muscle can tolerate up to 3 hours of ischemia. [15][16][17][18] However, tourniquet-induced ischemia may be less damaging than ACS-induced ischemia. In the only study to address this possibility, Heppenstal and associates 16 found that pH and phosphocreatine recovered rapidly and fully in dogs subjected to tourniquet-ischemia, but only slowly and partially in ACS-induced ischemia.…”

“…11,14 Current knowledge of muscle ischemia tolerance is derived from tourniquet-induced ischemia models, which suggest that muscle can tolerate up to 3 hours of ischemia before necrosis ensues. [15][16][17][18] However, a recent McGill University study of 76 patients who underwent fasciotomy 19 estimated that 35% of all ACS patients and 72% of those who developed necrosis did so within 2 hours of injury -earlier than the 3-hour safe period suggested by ischemia models.…”

Chronology of mitochondrial and cellular events during skeletal muscle ischemia-reperfusion

“…This energy is provided by ATP molecules, for which storage is limited (ϳ35-55 mol/mg protein) (2,64,66).…”

“…Skeletal muscle can increase its ATP turnover, allowing it to transition from rest to exercise/ contractile activity, where different energy-producing substrates (high-energy phosphate compounds, glucose, glycogen, and lipids) can be oxidized (49,66,84,135). The most concentrated substrates in skeletal muscle are glycogen and phosphocreatine (PCr) (192), with higher PCr levels in glycolytic muscles (26).…”

The Effect of Pneumatic Tourniquets on Skeletal Muscle Physiology

“…The venous blood supply from ischaemic limbs in man shows a significant fall in Po, and pH after 30 minutes whilst the Pco, is raised (Wilgis 1971). Other studies in man have demonstrated a reduction of muscle phosphocreatine and a rise in lactate levels after 30 minutes; however, the amount of ATP shows no marked change after 90 minutes (Haljamae & Enger 1975). Paul (1961) found a block in neuromuscular transmission after 13 minutes in a rat muscle nerve preparation subject to anoxia, whilst the muscle fibres of the preparation remained sensitive to direct electrical stimulation for 40 minutes.…”