Circulation, Vol 60, 158-163, Copyright © 1979 by American Heart Association
JD Sink, GL Pellom, WD Currie, WR Chitwood Jr, RC Hill and AS Wechsler
The effect of potassium cardioplegia on mitochondrial function was
evaluated in the ischemic isolated rat heart. Mitochondrial function as
well as adenosine triphosphate (ATP) levels were determined at the
initiation of ischemic contracture, at the completion of ischemic
contracture, and 20 minutes following contracture completion. Group I
received no cardioplegia prior to ischemia, while Group II received
potassium cardioplegia prior to the onset of ischemia. The respiratory
control index (RCI), which is the primary measure of the intactness of
mitochondrial function, was calculated with both a NAD (nicotinamide
adenine dinucleotide)-linked substrate and a FAD (flavin adenine
dinucleotide)-linked substrate. Potassium cardioplegia significantly
delayed ischemic contracture initiation and completion. Although the RCI
and ATP levels decreased significantly at successive levels of contracture,
there was no difference in the RCI or ATP content between Group I and Group
II at contracture initiation or completion. Unlike previous investigations
that have used a time-base to examine mitochondrial function and acute
cardiac ischemic injury, we correlated mitochondrial function with the
measurable physiologic event ischemic contracture. The data indicated that
potassium cardioplegia preserved ATP content and mitochondrial function,
and that contracture initiation and completion correlate well with specific
ATP levels and mitochondrial respiratory control. The relationship between
mitochondrial function and ATP content indicates that the beneficial effect
of potassium cardioplegia on mitochondrial function may be secondary to the
preservation of high-energy phosphate levels which provide energy for
mitochondrial maintenance.
ARTICLES
Protection of mitochondrial function during ischemia by potassium cardioplegia: correlation with ischemic contracture
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