PULMONARY ARTERIOLES FROM RATS WITH CONGENITAL DIAPHRAGMATIC-HERNIAS ARE HYPOPLASTIC BUT NOT HYPERRESPONSIVE

Background: Infants born with congenital diaphragmatic hernias (CDH) f requently die as a result of pulmonary hypertension and persistent fet al circulation. The pulmonary vessels of infants with CDH have decreas ed total cross-sectional area, increased muscle content, and musculari zation of intraacinar arterioles that are normally not muscularized. T hese structural alterations are believed to result in exaggerated resp onses to normal vasoconstrictor stimuli. Methods: The authors used the nitrofen-induced CDH model in rats to determine whether the vasoconst rictor responses of pulmonary arterioles are exaggerated in this anima l model of CDH. The authors compared the responses of isolated third-g eneration pulmonary arterioles from normal rats and from rats with nit rofen-induced CDH to K+-induced depolarization, phenylephrine, angiote nsin II, serotonin, and the thromboxane AZ agonist, U46619. Results: I t was found that the intraluminal diameter of third-generation pulmona ry arterioles from CDH rats was significantly less than in controls (1 29 +/- 5 mu v 152 +/- 9 mu, respectively). In addition, the ratio of w all thickness to vessel internal diameter was increased in the third-g eneration pulmonary arterioles of rats with nitrofen-induced CDH (0.62 +/- 0.4 v 0.50 +/- 0.5 for controls). Responses to K+-induced depolar ization, phenylephrine, angiotensin II, serotonin, and U46619, however , were not different for pulmonary arterioles from control and CDH rat s. Conclusion: These data suggest that the structural alterations of t he pulmonary vasculature observed in infants with CDH may not cause ex aggerated vasoconstrictor responses to normal vasoconstrictor stimuli. Copyright (C) 1998 by W.B. Saunders Company.