BACKGROUND
An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals.
METHODS AND RESULTS
Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44 +/- 0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59 +/- 2.2 nM (range, 0.17-8.76 nM, p less than 0.05 versus control subjects). The ouabain concentration correlated inversely with both cardiac index (r = -0.62, p less than 0.005) and mean arterial pressure (r = -0.51, p less than 0.05). However, there was no correlation between ouabain and left ventricular filling (r = 0.19, NS) or right atrial pressures (r = 0.20, NS). In 16 heart failure patients not receiving digoxin, the mean ouabain was 1.52 +/- 2.58 nM. No relation between renal function and ouabain was detected.
CONCLUSIONS
The unanticipated lack of correlation of ouabain with atrial pressures indicates that volume is not the chief determinant of ouabain concentration in patients with congestive heart failure. However, the significant relations of plasma ouabain concentration with cardiac index and mean arterial pressure imply that endogenous ouabain may be an important homeostatic factor in humans.
Objective. To determine if an early, dinically detectable patent ductus arteriosus (FDA) was associated with pulmonary hemorrhage (PH) in infants who received rescue artificial surfactant therapy.
Methods. This retrospective cohort study of 233 low birth weight infants (≤ 1700 g) who received artificial surfactant therapy for respiratory distress syndrome compared antenatal and postnatal characteristics of infants with PH and without PH. Pulmonary hemorrhage was defined by an onset of bright red blood from the endotracheal tube in quantities that resulted in increased ventilatory support and a new infiltrate on a chest radiograph.
Results. Pulmonary hemorrhage occurred in 6% (15/233) of the infants. Thirty-three percent (5/15) of the infants with PH died within 14 days of the hemorrhage. Of the 15 PH, 73% occurred within 48 hours of the first surfactant dose. Pulmonary hemorrhage was more common in male infants and infants of mothers who received antibiotic therapy during labor (P ≤ .04). Infants with PH received surfactant earlier than those without PH (P = .04). Nursery events or therapies occurring following surfactant therapy that were associated with PH included: little improvement in ventilatory efficiency index (P = .01), dopamine infusion (P = .04), and the presence of a clinically detectable PDA before, or at the time of, the PH [60% (9/15) vs 33% (71/217), P = .03]. After adjusting for severity of illness before surfactant therapy, risk of PH remained greater in infants who developed symptoms of a PDA. Dopamine support appeared to modify the association between PDA and PH.
Conclusions. In this retrospective cohort study, pulmonary hemorrhage was associated with the presence of a clinically detectable patent ductus arteriosus before, or at the time of, pulmonary hemorrhage.
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