The myocardial capillary network is altered in congenital diaphragmatic hernia in the fetal rabbit model

Abstract

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.

Unveiling fetal brain changes in congenital diaphragmatic hernia: hypoxic injury with loss of progenitor cells, neurons, and oligodendrocytes

“…Our model provides some evidence that the mechanism behind the brain changes herein reported are directly due to the mechanical compression exerted by herniated organs on the mediastinum (Figure 6). This affects not only the lungs, but also the left heart which we found to have changes suggestive of ventricular hypoplasia, as previously reported in human and experimental CDH (49, 50). We speculate that compression of the mediastinal structures results in decreased MCA flow and reduced brain perfusion, with a picture of impaired cerebral oxygenation similar to that seen in fetuses with congenital heart disease (51, 52).…”