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Prophylactic closure of the patent ductus arteriosus has been recommended as a means of decreasing the morbidity of the very low birth weight neonate. This study was undertaken in order to determine potential risk factors involved in the development of the silent ductus, its impact upon both the early cardiorespiratory symptomatology and the subsequent morbidity of the premature neonate, and finally the potential benefit to be derived from prophylactic closure in this presymptomatic stage. Infants with birth weights of 1000 g or less were studied on days 2-3 of life echocardiographically, clinically, and with determination of plasma dilator prostaglandin levels. On entry to the study, those infants with early evidence of silent left-to-right patent ductus arteriosus (PDA) shunting were randomized to receive either prophylactic indomethacin or placebo therapy. Those infants with no evidence of ductal shunting were not treated at all. Infants with silent PDAs had elevated levels of the dilator prostaglandin metabolite 6-keto PGF1 alpha on admission, although they had no echocardiographic abnormalities. No other risk factors for PDA development could be identified. Silent PDA infants had an increased incidence of subsequent symptomatic PDAs, and overall morbidity and mortality when compared with those with no evidence of PDA (silent or symptomatic). Prophylactic ductal closure decreased the incidence of subsequent PDA development, but had no effect on overall morbidity and/or mortality.

Prophylactic closure of the patent ductus arteriosus (PDA) has been recommended as a means of decreasing early respiratory distress, and thereby chronic respiratory sequelae in the very low birth weight (VLBW) neonate. This study was undertaken to evaluate some possible mechanisms for the observed failure of early indomethacin therapy to achieve such improvement. 24 VLBW infants with échocardiographie evidence of PDA were randomized to receive either indomethacin or placebo at 48 h of life; and then they were studied for clinical, metabolic and laboratory signs of ductal constriction and/or reopening. Early indomethacin conferred no improvement in respiratory sequelae. However, this was not secondary to a short-term therapeutic failure. Prophylactic indomethacin, even in the VLBW infant, was successful in decreasing dilator prostaglandin production, and probably in closing the PDA and in decreasing the number of recurrences. The implications are that even with effective ductal constriction, overall morbidity is not affected.

ABSTRACT. In a piglet model of group B fi Streptococci SVI, stroke volume index (GBS)-induced pulmonary hypertension, we have deter-CVP, central venous pressure mined hemodynamic responses to epinephrine (EPI) infusion in both the systemic and pulmonary circulations.Three groups of piglets (GBS + EPI, n = 6; GBS + ~lacebo. n = 6: ~lacebo. n = 6 ) were studied. GBS, infused intravenously -5 x l~~' o r~a n i s m s / k~/ m i n , 'reduced cardiac index and stroke volume index while elevating pulmonary artery pressure and pulmonary vascular resistance index. Systemic vascular resistance index, heart rate and aortic pressure did not change during GBS infusion. Six piglets received intravenous EPI after cardiac index had fallen by 30% during GBS infusion. At 3.5, 7.0, and 15 pg/kg/min, respectively, EPI raised aortic pressure by 18.5,31.0, and 45.0 mm Hg while EPI reduced pulmonary artery pressure by 5.2,6.3, and 8.2 mm Hg. At each dose, EPI elevated systemic vascular resistance index and lowered pulmonary vascular resistance index. At 3.5 pg/kg/ min, the elevation of aortic pressure was associated with an increase in both cardiac index and systemic vascular resistance index. At higher EPI doses, the rise in aortic pressure was accounted for entirely by an increase in systemic vascular resistance index. Systemic acid/base status and P a 0 2 did not differ among piglets who received GBS + EPI, GBS alone, or placebo. Extrapolation of these data to human infants must be approached with extreme caution. However, selective elevation of systemic blood pressure may be a feasible strategy for some infants to impede right-to-left shunting of blood often associated with sepsis-induced pulmonary hypertension. (Pediatr Res 20: 872-875,1986 The transition from in utero to ex utero existence is generally accompanied by a significant fall in PAP and PVR (1-3). Under certain circumstances, however, PAP and PVR remain elevated after birth, and persistent pulmonary hypertension may be associated with considerable derangement of cardiopulmonary dynamics in the newborn. If PAP is elevated to levels approaching AOP, blood may be shunted directly from the venous to arterial circulations, resulting in hypoxemia (1-4).Consequently, many investigators including ourselves, have attempted to identify techniques to reduce PAP and PVR selectively; that is, to effect a fall in PAP greater than a concomitant fall in AOP for any given intervention (4-7). We have developed a model of sepsis-induced pulmonary hypertension using infusion of GBS in piglets and have attempted to determine hemodynamic correlates of pathologically elevated PAP utilizing techniques not widely available clinically (7,8).In our piglet model of sepsis-induced pulmonary hypertension, we have been unable to demonstrate any agent currently approved for use in human newborns which reduces PAP and PVR to a greater extent than it lowers AOP and SVR. Others, using lambs with hypoxia-induced pulmonary hypertension, have also been unable to demonstrate such an agent (5,6,9,10). Nor, in...

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