Pulmonary arterioles from rats with congenital diaphragmatic hernias are hypoplastic but not hyperresponsive.

BACKGROUND

Infants born with congenital diaphragmatic hernias (CDH) frequently die as a result of pulmonary hypertension and persistent fetal circulation. The pulmonary vessels of infants with CDH have decreased total cross-sectional area, increased muscle content, and muscularization of intra-acinar arterioles that are normally not muscularized. These structural alterations are believed to result in exaggerated responses to normal vasoconstrictor stimuli.

METHODS

The authors used the nitrofen-induced CDH model in rats to determine whether the vasoconstrictor responses of pulmonary arterioles are exaggerated in this animal model of CDH. The authors compared the responses of isolated third-generation pulmonary arterioles from normal rats and from rats with nitrofen-induced CDH to K+-induced depolarization, phenylephrine, angiotensin II, serotonin, and the thromboxane A2 agonist, U46619.

RESULTS

It was found that the intraluminal diameter of third-generation pulmonary arterioles from CDH rats was significantly less than in controls (129 +/- 5 micron v 152 +/- 9 micron, respectively). In addition, the ratio of wall thickness to vessel internal diameter was increased in the third-generation pulmonary arterioles of rats with nitrofen-induced CDH (0.62 +/- 0.4 v 0.50 +/- 0.5 for controls). Responses to K+-induced depolarization, phenylephrine, angiotensin II, serotonin, and U46619, however, were not different for pulmonary arterioles from control and CDH rats.

CONCLUSION

These data suggest that the structural alterations of the pulmonary vasculature observed in infants with CDH may not cause exaggerated vasoconstrictor responses to normal vasoconstrictor stimuli.