Intrauterine Growth Restriction Newborns Research Articles

Altered renal function in growth-restricted newborn piglets.

The effect of intrauterine growth restriction (IUGR) on renal hemodynamics and excretory functions was studied in 76 newborn piglets 12-27 h old. The experiments were performed on anesthetized animals divided into normal-weight piglets and IUGR piglets according to their birth weight. The "normal-weight" category included animals with a birth weight >40th percentile (piglets heavier than 1,220 g); the IUGR category included animals with a birth weight >5th and <10th percentiles (piglets with a birth weight between 733 g and 853 g). Cardiac output and renal blood flow were measured by the colored microsphere technique. Urine was collected from catheters placed in the ureters. This animal model of naturally occurring growth retardation in swine gives asymmetric growth with an increase in the mean ratio of brain weight to liver weight from 1.02 to 1.85 (P<0.01). Thus there was only a small reduction in brain weight (11%). In contrast, the reduction in the weight of liver (50%) and kidney (46%) was proportional to that in body weight (46%). Heart rate, cardiac output, arterial blood gases, and pH were similar in normal-weight and IUGR piglets, but arterial blood pressure and arterial glucose content were significantly reduced in IUGR piglets (P<0.01). Moreover, IUGR piglets had higher plasma catecholamine levels (P<0.05). Renal blood flow and renal vascular resistance were similar in the normal-weight and in the IUGR groups. However, in IUGR animals, glomerular filtration rate was significantly less than in the controls (P<0.05). Normal-weight and IUGR newborn piglets reabsorbed sodium very efficiently, the fractional sodium excretion was less than 1% in both groups. We conclude that renal blood flow is maintained in relation to kidney and body weight in IUGR newborns, but that important renal excretory functions are compromised due to IUGR.

Brain peroxidative and glutathione status after moderate hypoxia in normal weight and intra-uterine growth-restricted newborn piglets.

In order to investigate the pathogenetic factors causing the relatively frequent occurrence of brain injury in intrauterine growth-restricted newborns, lipid peroxidation products (TBAR), glutathione (GSH, GSSG) and in vitro production of reactive oxygen species (chemiluminescence, stimulated lipid peroxidation, H2O2 formation) were studied in the brain of normal weight (NW) and intra-uterine growth-restricted newborn piglets (IUGR) after 1 hour of hypoxia (FiO2 11%) and 90 min reoxygenation. Cardiocirculatory parameters and catecholamine release into the blood were also measured. In the cerebellum, higher GSH content, but also higher in vitro production of lucigenin amplified chemiluminescence were found in comparison to other brain regions, independent of growth restriction and hypoxia. Moderate hypoxia without acidosis and hypercapnia resulted in GSH depletion especially in the brain of IUGR, but no changes in GSSG concentrations were measured. Though TBAR decreased after hypoxia/reoxygenation, in some brain areas of IUGR higher TBAR values were found in comparison to NW. H2O2 formation, stimulated lipid peroxidation and lucigenin and luminol amplified chemiluminescence in the 9000 x/g supernatant of brain tissue did not reveal special response of IUGR to hypoxia/reoxygenation. Hypoxia-induced circulatory centralisation due to increased release of catecholamines into the plasma prevented oxygen deficiency also in the brain of IUGR. The role of brain monoamine metabolism in the production of reactive oxygen species, followed by greater GSH depletion and higher in vivo formation of lipid peroxides in IUGR is discussed.