During hypothermic anoxic storage, low level metabolism continues and ATP levels are depleted. Soluble ATP precursors diffuse across the sarcolemma and are unavailable for high energy phosphate reformation during the reperfusion phase. The purine nucleoside adenosine serves as a nucleotide donor to replenish the adenylate charge of the myocyte during reperfusion via the purine salvage pathway. However, laboratory evidence to support this theory is lacking.43 Exogenously administered adenosine may be cleared rapidly by adenosine deaminase, converting it to inosine. Adenosine and inosine diffuse across the sarcolemma and are washed out of the interstitium upon reperfusion.
Controversy still remains regarding the optimal degree of hypothermia in terms of ischemic protection. Van Hoff and Arrhenius demonstrated that for every 10°C drop in temperature, the rate of an enzyme-catalyzed reaction was decreased from 1.5- to 4-fold.44 Therefore, cooling from 37°C to 4°C (the most commonly used practice today), decreases the metabolic rate 12- to 13-fold.45 Intracellular low molecular weight solutes depress the freezing point to -0.6°C. However, most cells do not freeze internally until less than -10°C. Rat hearts preserved in an extracellular type perfusate at 4°C had less ATP depletion, intracellular acidosis, and improved post ischemic recovery than at 15°C. Equivalent hypothermic storage in moist air versus cardioplegic solution showed no difference in functional outcomes in a rat heart transplant study47 at 10°C. Hypothermia seems to have a protective influence on the endothelium with regards to high potassium concentration mediated endothelial injury.48
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