Muscle Ischemia and Hypothermia

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Abstract
Following traumatic limb amputation it is common clinical practice to maintain the ischemic tissues in a hypothermic state until surgical reimplantation. Of all extremity tissues, muscle is the most sensitive to ischemia; it is therefore imperative that reperfusion be established before diffuse muscle necrosis. Although it was shown both clinically and experimentally that hypothermia prolongs the viability of ischemic skeletal muscle, the presumed mechanism by which this occurs was not confirmed at the cellular level. This study was undertaken to quantify the effect of conventional iced-saline hypothermia on anaerobic cell metabolism and high-energy phosphate depletion in traumatically devascularized muscle. 31P NMR was employed to noninvasively monitor cellular phosphocreatine (PCr), ATP and intracellular pH over time in ischemic cat hindlimb muscle under room temperature (22.degree. C) and 1.degree. C hypothermic conditions. Muscular PCr depletion was significantly retarded by tissue hypothermia but the rate of ATP depletion was not. A progressive, severe cellular acidosis was observed in the room-temperature muscle. Iced tissue cooling produced a dramatic initial rise in cell pH which significantly reduced the absolute degree of subsequent acidotic changes. These findings question the understanding of hypothermic tissue preservation, which was generally assumed to work on the basis of decreased tissue metabolism, conserving critical cellular ATP levels. The empirical benefit derived by cooling muscle in an iced medium may actually be related to the cellular alkalinization produced by tissue cooling, as this significantly mitigates the profound acidosis that would otherwise occur.