We studied the possibility of an etiological role for endothelin-1 (ET-1) in the development of persistent pulmonary hypertension of the newborn (PPHN). Ten infants with severe PPHN requiring extracorporeal membrane oxygenation (ECMO) were studied. Pre and post pulmonary blood samples were obtained on commencing ECMO and on recovery. The samples were analyzed by radio-immunoassay. The infants with PPHN requiring ECMO had a significantly higher mean ET-1 concentration (21.1 pmol/l, S. D. 3.59) than a group of healthy controls (16.6 pmol/l, S. D. 4.44); however 8 of our 10 infants had individual ET-1 levels within our reference range for healthy newborns. Pre and post pulmonary ET-1 levels did not differ significantly and there was no evidence of a decline in ET-1 levels with resolution of PPHN. Pulmonary overproduction of ET-1 does not appear to be the cause of PPHN, although the endothelin system may still play a role in the pathophysiology of PPHN, probably mediated through changes in receptor expression.
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http://dx.doi.org/10.1515/JPM.1999.030 | DOI Listing |
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