The objective of this study was to compare formula intake, the time of weaning, and growth in preterm infants (< or = 1750-g birth weight, < or = 34-wk gestation) fed a standard term or preterm infant formula after initial hospital discharge. Infants were randomized at hospital discharge to be fed a preterm infant formula from discharge to 6 mo corrected age (group A), a term formula from discharge to 6 mo (group B), or the preterm formula (discharge to term) and the term formula (term to 6 mo (group C). Infants were seen biweekly (discharge to term) and monthly (term to 6 mo), when intake was measured and anthropometry and blood sampling were performed. The results were analyzed using ANOVA. Although nutrient intake was similar, at 6 mo girls were lighter (6829 versus 7280 g) and shorter (64.4 versus 66.0 cm) than boys (p < 0.05). Patient characteristics were similar between the treatment groups. Although the volume of intake differed (B > C > A; p < 0.001), energy intake was similar in the groups. Because of differences in formula composition, protein, calcium, and phosphorus intakes differed (B < C < A; p < 0.001). Lower protein intakes were related to lower blood urea nitrogen levels (B < C < A; p < 0.001). At 6 mo, infant boys in B and C were lighter (6933, 6660 < 7949 g), shorter (65.3, 64.9 < 67.1 cm), and had a smaller head circumference (43.7, 43.7 < 44.8 cm; p < 0.05) than infants in group A. Preterm infants were found to increase their volume of intake to compensate for differences in energy density between formulas. After hospital discharge, infant boys fed a preterm formula grew faster than infant girls fed a preterm formula or infant boys fed a term formula.

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The hypothesis that endothelium-dependent components contribute to the cerebromicrovascular dilation to hypoxia in the newborn pig was addressed. Piglets anesthetized with ketamine-acepromazine and maintained on alpha-chloralose were equipped with closed cranial windows. Injury to the endothelium of pial arterioles was produced by light activation of fluorescein dye. Light/dye injury reduced the pial arteriolar dilation to hypoxia (5 min, arterial PO2 approximately 30 mmHg) from 57 +/- 9 to 19 +/- 5%. Light/dye injury abolished the pial arteriolar dilation to hypercapnia but did not affect dilation to sodium nitroprusside. The pial arteriolar dilation to hypoxia was not affected by tetrodotoxin, N(omega)-nitro-L-arginine, glibenclamide, iberiotoxin, charybdotoxin, tetraethylammonium, or 8-phenyltheophylline. Hypoxia caused increases in the cerebral cortical production of adenosine 3',5'-cyclic monophosphate and guanosine 3',5'-cyclic monophosphate. Cerebral vasodilation to hypoxia was inhibited by 5,8,11,14-eicosatetraynoic acid but was not greatly affected by cyclooxygenase or lipoxygenase inhibitors. In contrast, the cytochrome P-450 epoxygenase inhibitor miconazol decreased cerebral vasodilation to hypoxia from 45 +/- 5 to 17 +/- 4%. Therefore, the vascular endothelium appears to participate in cerebral microvascular dilation to hypoxia in newborn pigs. The mechanism may include cytochrome P-450 epoxygenase metabolites of arachidonic acid.

No abstract

Medina. Approximately forty patients a day were Received for publication January 5, 1971 examined for 3 days. At the suggestion of the epidemiologist, the patients were numbered from 150 to 272, so that the memorizing of numbers would be reduced to a minimum. The studies performed on each patient are listed below.