Search

BACKGROUND The impact of the striking perinatal circulatory changes on blood flow distribution have not to date been well examined in hypoplastic left heart syndrome (HLHS). This study aimed to document perinatal redistribution of cardiac output in HLHS compared with healthy control subjects, to further understand the impact of the perinatal transition on cerebral and systemic blood flow. METHODS Prospectively recruited HLHS case subjects (n = 31) and healthy control subjects (n = 19) underwent serial echocardiography from late fetal stages to 96 hours after birth. Combined cardiac output (CCO), systemic, pulmonary, cerebrovascular, and splanchnic flow data were compared between neonates with HLHS and control subjects, and the impact of vasoactive support and positive pressure ventilation in HLHS patients was examined. RESULTS In late gestation, CCO was similar between HLHS and control subjects, whereas middle cerebral artery (MCA) pulsatility index (PI) in HLHS was consistent with low cerebral vascular resistance. In the 96 hours after birth, CCO and pulmonary blood flow progressively increased in HLHS compared with control subjects (P < 0.001), and CCO was further increased in neonates with HLHS receiving vasoactive support (P = 0.01). Neonates with HLHS had reduced systemic and 6-24-hour superior vena cava (SVC) flow compared with control subjects (P < 0.001). Low systemic flow was further suggested by increased MCA and celiac artery PI at 6-48 hours in neonates with HLHS (P < 0.001). Systemic and SVC flow did not differ between those with and without vasoactive support. CONCLUSIONS We provide quantitative echocardiographic evidence associating impaired cerebral and systemic blood flow with perinatal hemodynamic changes in the preoperative neonate with HLHS.

The aim of this study was to evaluate left ventricular function in preterm infants from 28 days to near term using echocardiography.Thirty clinically stable preterm infants delivered at30 weeks' gestational age were prospectively enrolled. At 28 days, conventional, tissue Doppler, and speckle-tracking echocardiography evaluations of left ventricular function were performed, with comparison made to findings in 30 healthy term infants of similar postnatal age. Sixteen preterm infants underwent repeat examinations near term.Compared with controls, preterm infants at 28 days had decreased peak mitral valve (MV) E-wave velocities (P.01), E/A ratios (P.0001), annular e' velocities (P.0001), and e'/a' ratios (P.0001); increased MV E/e' ratios (P.01); and lower basal circumferential early diastolic and higher late diastolic strain rates. No significant differences were found in fractional shortening, ejection fraction, and longitudinal or circumferential strain and strain rate between preterm infants and controls. Although preterm infants at 28 days had higher heart rates compared with controls (161 ± 15 vs 142 ± 16 beats/min), no significant correlations existed between heart rate and MV E, E/A ratio, e', e'/a' ratio, and E/e' ratio. Near term, the differences in diastolic function persisted, including decreased MV e'/a' ratio (P.05), increased E/e' ratio (P.01), and increased late diastolic strain rate.Clinically stable preterm infants have normal left ventricular systolic function but altered diastolic function, with greater dependence on atrial contraction, the latter of which persists despite nearing term. These findings may be relevant to the management of preterm infants and may relate to the longer term myocardial dysfunction observed in affected adults.

In metamorphosing tadpole liver, the quantitative and qualitative changes in glycoproteins were observed by sodium dodecyl sulfate polyacrylamide gel electrophoresis and lectin-peroxidase method.

Partial hepatectomy results in an increase in the ability of the liver cells to bind 125I-labeled transferrin to surface receptors. Scatchard analysis of the binding of transferrin in regenerating rat liver indicates that this increase was due to an increase in the number of transferrin receptors on the cell surface. When we measured total cellular transferrin receptor number, we found that control and regenerating livers had identical amounts of receptor number. The increase in the surface receptor number is apparently due to the translocation of intracellular transferrin receptor to the cell surface.