ObjectiveIncreased glucose 6-phosphate dehydrogenase activity has been demonstrated in
heart failure. This study sought to assess myocardial glucose 6-phosphate
dehydrogenase activity in retraining of the subpulmonary ventricle of adult goats.
MethodsEighteen adult goats were divided into three groups: traditional (fixed banding),
sham, and intermittent (adjustable banding, daily 12-hour systolic overload).
Systolic overload (70% of systemic pressure) was maintained during a 4-week
period. Right ventricle, pulmonary artery and aortic pressures were measured
throughout the study. All animals were submitted to echocardiographic and
hemodynamic evaluations throughout the protocol. After the study period, the
animals were killed for morphological and glucose 6-phosphate dehydrogenase
activity assessment.ResultsA 55.7% and 36.7% increase occurred in the intermittent and traditional right
ventricle masses, respectively, when compared with the sham group
(P<0.05), despite less exposure of intermittent group to
systolic overload. No significant changes were observed in myocardial water
content in the 3 groups (P=0.27). A 37.2% increase was found in
right ventricle wall thickness of intermittent group, compared to sham and
traditional groups (P<0.05). Right ventricle glucose
6-phosphate dehydrogenase activity was elevated in the traditional group, when
compared to sham and intermittent groups (P=0.05).ConclusionBoth study groups have developed similar right ventricle hypertrophy, regardless
less systolic overload exposure of intermittent group. Traditional systolic
overload for adult subpulmonary ventricle retraining causes upregulation of
myocardial glucose 6-phosphate dehydrogenase activity. It may suggest that the
undesirable "pathologic systolic overload" is influenced by activation of penthose
pathway and cytosolic Nicotinamide adenine dinucleotide phosphate availability.
This altered energy substrate metabolism can elevate levels of free radicals by
Nicotinamide adenine dinucleotide phosphate oxidase, an important mechanism in the
pathophysiology of heart failure.