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Indomethacin decreases cerebral and mesenteric blood flow velocities in premature infants with symptomatic patent ductus arteriosus. Low-dose indomethacin is recommended for the prevention of intraventricular hemorrhage in very low birth weight infants. The hemodynamic effects of prophylactic indomethacin have not been previously examined. We hypothesized that prophylactic indomethacin does not change cerebral and mesenteric blood flow velocities and cardiac function in very low birth weight infants. Twenty-one infants (775 to 1245 gm, 24 to 31 weeks' gestation) were studied before and after indomethacin (0.1 mg/kg) administration at 6, 30, and 54 hours of life. Mean and end-diastolic cerebral and mesenteric blood flow velocities decreased (ANOVA, p < 0.05) after prophylactic indomethacin. The 38% increase in cerebral relative vascular resistance was significantly greater than the 18% increase in mesenteric relative vascular resistance (ANOVA, p < 0.05). In five infants who were fed 1 hour after the third indomethacin dose, the postprandial mesenteric blood flow velocity was significantly greater than the mesenteric blood flow velocity before both indomethacin and feeding (ANOVA, p < 0.05). Cardiac output, stroke volume, fractional shortening, and blood pressure did not change after prophylactic indomethacin administration. We conclude that prophylactic indomethacin (1) reduces cerebral and mesenteric blood flow velocity without affecting cardiac function, (2) increases cerebral more than mesenteric relative vascular resistance, and (3) does not prevent postprandial increases in mesenteric blood flow velocity. We speculate that the increase in cerebral relative vascular resistance is a beneficial effect that contributes to protection against intraventricular hemorrhage.

A multicenter, randomized, double-blind, controlled trial compared three beractant (Survanta) administration procedures in the treatment of neonatal respiratory distress syndrome. Infants weighing > or = 600 gm with respiratory distress syndrome who required assisted ventilation were treated within 8 hours of birth with beractant administered intratracheally. Procedure A required administration in two fractional doses after removal of the infant from the ventilator. Procedure B required administration in two fractional doses through a neonatal suction valve and did not require removal of the infant from the ventilator, and procedure C required administration in four fractional doses during removal from the ventilator. Procedure C is the method used in all previous beractant studies. Of the 299 infants enrolled, 103 were randomly assigned to procedure A, 100 to procedure B, and 96 to procedure C. The results indicate no significant differences among the treatment groups in the clinical outcome measures of fractional inspired oxygen, mean airway pressure, and arterial-alveolar ratio of partial pressure of oxygen at 72 hours of life, or in the incidences of air leaks, pulmonary interstitial emphysema, or death through 72 hours of life. There were no significant differences in the lowest heart rates recorded during administration of doses, but there was less oxygen desaturation during administration of dose 1 with procedure B than with procedure A (p = 0.001), and more reflux of beractant after procedure B than after procedure C (p = 0.007). We conclude that the three procedures are equally effective and can be used to administer beractant safely and effectively. Procedure B has the advantage of allowing administration without interrupting mechanical ventilation.

Brain blood flow was determined in 21 spontaneously breathing, awake, newborn piglets during control, asphyxia, superimposed hypotension, and subsequent volume expansion (15 ml/kg of plasmanate). The piglets were divided into three groups based upon the rate of volume expansion: rapid infusion group-piglets received plasmanate in three minutes; slow infusion group-piglets received plasmanate in 30 minutes: the noninfused group-piglets did not receive plasmanate. The results showed comparable increases in brain blood flow among each group during asphyxia, and similar reduction to preasphyxia values during superimposed hypotension. Although pressure-passive changes occurred, the rate of volume expansion did not influence the magnitude of change in brain blood flow. Significantly lower arterial blood pressure and brain blood flow were observed in those piglets who did not have a plasmanate infusion. Intracranial hemorrhages were not observed at autopsy in any of the study subjects. These data indicate that rapid or slow infusion of plasmanate for volume restoration did not influence the pattern of brain blood flow and that in these relatively mature brains, intracranial bleeding was not observed. Both plasmanate infused groups had higher brain blood flows at study completion (when compared to controls), reflecting compensation for anemia to maintain adequate oxygen delivery. Furthermore, regional differences in blood flow were found during asphyxia and superimposed hypotension (brain-stem greater than cerebellum greater than cerebrum), probably reflecting compensatory protection of vital portions of the central nervous system.

Because of its effects on the cardiovascular and renin-angiotensin systems and on fluid and electrolyte homeostasis, maternal administration of ritodrine to inhibit preterm labor may cause significant alterations in renal function in the newborn infant. We determined inulin clearance, plasma renin activity, urinary arginine vasopressin excretion, and serum and urine electrolyte concentrations and osmolalities at 12 to 36 hours of life and at 6 days of life in 15 infants whose mothers had received ritodrine and in 15 infants whose mothers did not (control infants). At the time of each study, plasma ritodrine concentrations were obtained in the infants whose mothers received ritodrine. The infants whose mothers had received ritodrine had significantly lower inulin clearances and higher plasma renin activity and urinary arginine vasopressin excretion on day 1 but not on day 6. Gestational age was inversely correlated with plasma ritodrine concentration, plasma renin activity, and urinary arginine vasopressin excretion. There were no overt clinical signs of renal failure in any of the infants, and no differences in serum and urine electrolyte values, osmolality, fractional sodium excretion, or urine flow rate were observed between the groups.

We measured hematocrit, whole blood viscosity, arterial oxygen content, and cerebral blood flow in seven newborn lambs in which polycythemia and hyperviscosity were induced by partial exchange transfusion with packed red blood cells from a donor lamb. After the exchange transfusion, the hematocrit, whole blood viscosity, and arterial oxygen content were significantly elevated, whereas cerebral blood flow was reduced from baseline measurements. Sodium nitrite was then infused to reduce the arterial oxygen content to baseline values while the hematocrit and viscosity remained elevated. Under this condition, cerebral blood flow returned to baseline values. Oxygen delivery to the brain remained constant throughout the study. These results indicate that the reduction of cerebral blood flow in neonatal polycythemia and hyperviscosity is a physiologic response to increased arterial oxygen content and not a result of hyperviscosity.