Systemic production of prostacyclin and thromboxane A2 does not correlate with patency of the ductus arteriosus in very low birth weight infants.
Urinary excretion of prostacyclin and thromboxane metabolites (2,3-dinor-6-ketoprostaglandin F1 alpha, thromboxane B2, and 2,3-dinor-thromboxane B2) as indices of systemic biosynthesis was prospectively determined in nine premature infants during the first 10 days of life, by gas chromatography-mass spectrometry. The patients ranged in gestational age from 27 to 29 weeks and in birth weight from 720 to 980 gm. Four infants developed symptomatic patent ductus arteriosus (PDA). Excretion of all metabolites exceeded adult values on the basis of body surface area at birth, reached a maximum on the fourth day of life, was related to urine output, and did not distinguish patients with and without symptomatic PDA. We conclude that neither circulating prostacyclin nor thromboxane A2 contribute significantly to the pathophysiology of symptomatic PDA in very low birth weight infants.
D015121:6-Ketoprostaglandin F1 alpha / Q000031:analogs & derivatives / Q000652:urine; D004374:Ductus Arteriosus, Patent / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D008401:Gas Chromatography-Mass Spectrometry; D005865:Gestational Age; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007235:Infant, Premature, Diseases / Q000378:metabolism*; D011446:Prospective Studies; D013929:Thromboxane B2 / Q000031:analogs & derivatives / Q000652:urine
D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C028965:2,3-dinor-thromboxane B2; C028290:2,3-dinor-6-ketoprostaglandin F1alpha; D011464:Epoprostenol