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The Journal of Thoracic and Cardiovascular Surgery, Vol 100, 240-249, Copyright © 1990 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
IM Rebeyka, SA Hanan, MR Borges, KF Lee, T Yeh Jr, GE Tuchy, AS Abd-Elfattah, WG Williams and AS Wechsler
Hypothermic total circulatory arrest for repair of congenital heart lesions
in neonates requires a period of rapid core cooling on cardiopulmonary
bypass during which the myocardium is also exposed to hypothermic
perfusion. Myocardial hypothermia in the nonarrested state results in an
increase in contractility due to elevation of intracellular calcium levels.
This study was designed to test the hypothesis that rapid myocardial
cooling before cardioplegic ischemic arrest results in damage, with
impaired recovery during reperfusion. Two groups of 10 rabbit hearts were
perfused on an isolated Langendorff apparatus. Group N (normothermia) was
perfused at 37 degrees C before 2 hours of cardioplegic ischemic arrest at
10 degrees C. Group C (cooling) was perfused at 15 degrees C in the
unarrested state for 20 minutes before the same cardioplegic arrest
conditions as group N. Left ventricular isovolumic pressure measurements,
biochemical measurements from right ventricular biopsy specimens, and
ventricular necrosis as defined by tetrazolium staining were used to
compare the groups at 30 and 60 minutes of normothermic reperfusion.
Developed pressure at a constant volume was preserved in group N at 90.7
+/- 4.5 mm Hg versus 76.9 +/- 6.3 in group C after reperfusion (p less than
0.05). Diastolic compliance showed significant deterioration in group C,
with marked elevation of diastolic pressure during reperfusion (group N =
6.8 +/- 2.5 mm Hg versus group C = 38.9 +/- 6.1 after reperfusion; p less
than 0.001). Adenosine triphosphate levels were significantly higher in
group N both at end-ischemia and after reperfusion versus group C (group N
= 17.0 +/- 1.1 nmol/mg protein versus group C = 7.7 +/- 1.0 after
reperfusion; p less than 0.001). Group N had 0.4% +/- 0.4% necrosis of
ventricular mass versus 19.3% +/- 2.2% with prearrest cooling in group C (p
less than 0.0001). These results indicate that, when combined with
cardioplegic ischemic arrest, rapid myocardial cooling in the unarrested
state results in significant damage. The mechanism may be related to the
cytosolic calcium loading effect of hypothermia that is not relieved during
the subsequent period of cardioplegic arrest. Although hypothermia is an
essential component to ischemic preservation, rapid cooling contracture can
adversely influence cardioplegic myocardial protection.
ARTICLES
Rapid cooling contracture of the myocardium. The adverse effect of prearrest cardiac hypothermia
Department of Surgery, Medical College of Virginia, Richmond 23298.
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