Abstract

Thank you for the opportunity to reply to the comments and questions posed by Dr. Karamanoukian et al. 1. Persistently elevated oxygenation index, alveolar-arterial difference in partial pressure of oxygen, or both cannot explain the failure of immunoreactive endothelin-1 (irET-1) levels to decrease in infants who received extracorporeal membrane oxygenation (ECMO). These values depend on ventilator settings and the fraction of inspired oxygen concentration. Our standard of care during ECMO therapy is to use ventilation at low "rest" settings with a fraction of inspired oxygen concentration of 0.21; the calculated oxygenation index and alveolar-arterial difference in partial pressure of oxygen would necessarily be low. 2. When these data were collected, inhaled nitric oxide (NO) was not available in our nursery. We have no data correlating response to inhaled NO with levels of irET-1 but do have samples for NO- treated infants. In terms of the relation between the irET-1 level and endogenous NO production, we have no data on infants to suggest feedback modulation of the two systems. We intended to speculate that either decreased endogenous production of NO, increased production of endothelin, or both could contribute to the pulmonary vasoconstriction that characterizes persistent pulmonary hypertension. 3. Our ECMO patients received heparin; infants with persistent pulmonary hypertension who were managed conventionally received very low amounts of heparin. As stated in the discussion of our article, persistent elevation of irET-1 levels during ECMO therapy may be related to low pulmonary blood flow during bypass, resulting in either low clearance (67% of circulating endothelin-1 is cleared in the pulmonary circulation in a single pass1), or to activation of endothelin-1 production. 4. Of the eight infants with surfactant deficiency in whom the level of irET-1 was measured, only two received surfactant. Thus we cannot comment on any relation between surfactant replacement and irET-1 levels. 9/35/52855

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