Congenital diaphragmatic hernia (CDH) is associated with thoracic compression of
the lungs and heart caused by the herniated abdominal content, leading to
cardiac modifications including pressure and vascular changes. Our aim was to
investigate the experimental immunoexpression of the capillary proliferation,
activation, and density of Ki-67, VEGFR2, and lectin in the myocardium after
surgical creation of a diaphragmatic defect. Pregnant New Zealand rabbits were
operated on the 25th gestational day in order to create left-sided CDH (LCDH,
n=9), right-sided CDH (RCDH, n=9), and Control (n=9), for a total of 27 fetuses
in 19 pregnant rabbits. Five days after the procedure, animals were sacrificed,
and histology and immunohistochemistry studies of the harvested hearts were
performed. Total body weight and heart weight were not significantly different
among groups (P=0.702 and 0.165, respectively). VEGFR2 expression was increased
in both ventricles in the RCDH group (P<0.0001), and Ki-67 immunoexpression
was increased in the left ventricle in the LCDH group compared to Control and
RCDH groups (P<0.0001). In contrast, capillary density was reduced in the
left ventricle in the LCDH compared to the Control and RCDH groups (P=0.002).
Left and right ventricles responded differently to CDH in this model depending
on the laterality of the diaphragmatic defect. This surgical model of
diaphragmatic hernia was associated with different expression patterns of
capillary proliferation, activation, and density in the myocardium of the
ventricles of newborn rabbits.