Complete recovery of the heart following exposure to profound hypothermia.
Cold injury has been suggested as a potential limitation to the use of temperatures below 10 degrees to 15 degrees C in clinical myocardial preservation. The isolated effects of profound hypothermia on myocardial function and energy metabolism were studied in the working rat heart preparation. Each heart was isolated and stabilized; then initial aortic flow, coronary flow, and heart rate were measured. The heart then was perfused in the Langendorf mode with oxygenated Krebs-Henseleit buffer for 20 minutes at 0.5 degree, 4 degrees, 10 degrees, 15 degrees, or 20 degrees C. After being rewarmed to 37 degrees C, the heart was returned to the working mode for final functional measurements. In a control group, the perfusion was kept at 37 degrees C. Recovery of function in hearts exposed to hypothermic perfusion was not significantly different from that observed in the hearts kept at 37 degrees C. When cold exposure time to 0.5 degree C perfusion was extended to 2 hours, heart function still returned to the same level as that of control hearts maintained at 37 degrees C, and adenosine triphosphate (ATP) and glycogen levels were higher than those in the control group. Thus, under these conditions, cold exposure per se, even for 2 hours at temperatures near 0 degree C, has no deleterious effect upon myocardial function and energy metabolism.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003080:Cold Temperature / Q000009:adverse effects*; D003326:Coronary Circulation; D004734:Energy Metabolism; D006003:Glycogen / Q000378:metabolism; D006321:Heart / Q000502:physiology*; D006339:Heart Rate; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009926:Organ Preservation; D051381:Rats; D013997:Time Factors
D000255:Adenosine Triphosphate; D006003:Glycogen; D007770:L-Lactate Dehydrogenase