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The Journal of Thoracic and Cardiovascular Surgery, Vol 81, 455-458, Copyright © 1981 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
BW Shragge, SB Digerness and EH Blackstone
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.
ARTICLES
Complete recovery of the heart following exposure to profound hypothermia
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