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The Annals of Thoracic Surgery, Vol 37, 304-308, Copyright © 1984 by The Society of Thoracic Surgeons
NA Silverman, J Kohler, S Levitsky, DG Pavel, RB Fang and H Feinberg
Persistence of impaired ventricular function after repair of cyanotic
congenital heart defects may be due to previous exposure to chronic
hypoxemia or to perioperative ischemic injury. Clarification of this
phenomenon was sought in a canine model of cyanotic cardiovascular disease
(Group I), in which the left atrium was anastomosed proximal to the banded
pulmonary artery. Animals that had pulmonary artery banding alone (Group
II) or no prior surgical intervention (Group III) served as controls. All
Group I animals became cyanotic during the study period (arterial oxygen
tension, 38 +/- 4 mm Hg; hematocrit, 55 +/- 5%). Radionuclide-determined
ejection fractions performed three months after operation showed
significant depression of global biventricular function by 16 to 29% (p
less than 0.05) compared with groups II and III. On cardiopulmonary bypass,
all hearts were subjected to 4 degrees C potassium cardioplegic arrest and
reperfusion with serial assays for myocardial adenosine triphosphate (ATP)
and creatine phosphate (CP) levels. The ATP and CP stores in each ventricle
were similar at all sampling intervals, and preischemic levels were
comparable in cyanotic and control groups. However, ATP levels were
significantly depressed 37 to 43% from preischemic levels (p less than
0.02) after arrest and reperfusion in cyanotic dogs, but they were
preserved in Groups II and III. During ischemia, CP stores were depleted to
27% of preischemic values in Group I but only to 46 to 63% of preischemic
levels in the control groups (p less than 0.05). These data indicate that
chronic hypoxemia impairs global ventricular function and predisposes to
the accelerated depletion of high-energy phosphates during cardioplegic
arrest.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Chronic hypoxemia depresses global ventricular function and predisposes to the depletion of high-energy phosphates during cardioplegic arrest: implications for surgical repair of cyanotic congenital heart defects
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