Harry S. Dweck

Parenteral nutrition in the newborn: a practical guide.

Since the first employment of total parenteral nutrition to support an infant with an anomalous gastrointestinal tract, parenteral nutrition has been resorted to regularly in treating a number of conditions encountered in pediatric practice. This article offers guidelines on the parenteral administration of nutrients, electrolytes, vitamins, and minerals to infants whose clinical conditions prevent enteral feeding. Special consideration is given to the complications of parenteral nutrition and how best to avoid or prevent them.

Variable arginine vasopressin levels in neonatal congestive heart failure

Arginine vasopressin levels in 17 neonates with cardiac disease were compared with control levels in 10 healthy newborn infants. Infants with congestive heart failure who were free of left ventricular outflow tract obstruction had a mean level of 80 +/- 18 pg/ml, which was significantly greater than the mean control level (p less than 0.001). Infants with congestive heart failure and left ventricular outflow tract obstruction had a mean vasopressin level of 3 +/- 0.7 pg/ml, which was lower than the mean control level of 6 +/- 0.7 pg/ml (p less than 0.05). The data suggest that impaired forward flow to high pressure sinoaortic and ventricular baroreceptors is necessary for vasopressin release in congestive heart failure. In left ventricular outflow tract obstruction with heart failure these receptors may be impaired or absent, leading to decreased vasopressin release. Low plasma arginine vasopressin may adversely affect circulatory homeostasis.

The nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine degrades heparan sulfate and heparin.

Nitric oxide (NO) is a powerful vascular and neural regulator. One of the breakdown products of nitric oxide is nitrite which converts to nitrous acid, a reagent routinely used for the degradation of heparin and heparan sulfate. We have recently shown that nitric oxide gas degrades heparin and heparan sulfate through a nitrous acid mechanism (Vilar et al, 1997, Biochemical Journal, 324, 473‐479). The purpose of the present study is to confirm these findings using the nitric oxide donor S‐nitroso‐N‐acetyl‐D,L‐penicillamine (SNAP) under conditions that are close to those found in vivo. The results show that 2 mM SNAP releases a steady‐state level of nitrite of over 200 μM. This level substantially degrades heparin and heparan sulfate at a pH of up to 5.0. This reaction may be important in breakdown of the glycosaminoglycan components of the extracellular matrix during normal and pathological conditions.