In the range of serum vitamin concentrations found in this population, the status of vitamin A and related compounds in children appeared to have no effect on the incidence of otitis media.
Purpose of StudyRecent studies have demonstrated that in utero congenital heart disease (CHD) significantly alters the normal growth and development of the fetus. Newly published data demonstrate significant hemodynamic decreases in cardiac output, stroke volume, and ejection fraction in the fetus with CHD; however, the mechanisms by which these changes occur remain unclear. The purpose of this study was to determine the mechanisms of altered in utero hemodynamics by comparing the ventricular ejection dynamics in fetuses with CHD with normal fetuses.Methods UsedA total of 162 fetal echocardiograms were retrospectively examined. Eighty-seven were fetuses with in utero diagnosed CHD and 75 were gestational age matched normal fetuses. The gestational age range was 20 to 37 weeks. Doppler echocardiographic velocity-time plots of the aorta and pulmonary artery were digitized and coupled with 2-dimensional echocardiographic vessel diameter measurements. Measures of ejection dynamics were then derived from the time series data, including stroke volume, cardiac output, ejection time, acceleration time, mean acceleration and net developed force.Summary of ResultsCompared to gestational age matched normal fetuses, the CHD fetuses demonstrated a decrease in the net force developed (1.255 ± 0.694, p < .03), prolonged acceleration times (0.243 ± 0.075, p < .002) in the pulmonary artery (0.281 ± 0.075, p < .004) in the aorta), and normal ejection times (0.183 vs. 0.185).ConclusionsNormal ejection times suggest that afterload is not a critical determinate in the observed decreases in cardiac output, stroke volume, and ejection fraction in the fetuses with CHD. The decrease in the net developed force and prolonged acceleration times suggests decreased myocardial function as the major cause of the altered in utero hemodynamics in this population.
Cyclic stretch and oxygen are key regulators of lung development. Independently, both cyclic stretch and hyperoxia can significantly alter cell viability and proliferation. Relatively little is known however concerning the combined exposure of these factors on the distal lung epithelium. Objective: To study the effects of both cyclic stretch and hyperoxia on cell proliferation and viability using human pulmonary A549 cells. Methods: Cells were plated on collagen-coated flexible membranes and exposed to 1 Hz, 16 kPa cyclic biaxial stretch for 24, 48, and 72 hours in both normoxic (21% O2, 5% CO2) and hyperoxic (95% O2, 5% CO2) conditions. Cell proliferation was determined using manual cell counts and 3 [H] thymidine incorporation. Calcein-AM, LIVE/DEAD staining, and LDH release assays were used to assess viability. Apoptosis was measured with propidium iodide fluorescence together with annexin-V incorporation and caspase-3 activity. The reactive oxygen species, superoxide, was measured using dihydroethidium (DHE). Results: Cyclic stretch under normoxic conditions increased cell number vs. unstretched controls after 24 hours (p = .002). Cell number and 3 [H] thymidine incorporation markedly decreased following exposure to 95% O2 after 48 and 72 hours (p < .001). In contrast, both cell counts and 3 [H] thymidine incorporation following exposure to hyperoxia combined with stretch remained unchanged at 48 hours and were significantly greater vs. the unstretched hyperoxia group at 72 hours (p < .001). Calcein-AM and LIVE/DEAD analysis revealed an increase in cell death with hyperoxia after 72 hours compared to normoxia (p < .001). Cell death from hyperoxia at 72 hours was significantly attenuated when combined with stretch (p < .001). Apoptosis was not detected in any of the study groups using annexin-V and caspase-3. LDH activity was elevated after 72 hours in all the study groups vs. normoxic controls (p < .001) but did not vary between the separate study groups. Increased superoxide levels were detected in cells exposed to hyperoxia vs. normoxia using DHE fluorometric staining. Conclusion: The detrimental effects of hyperoxia on cell proliferation and nonapoptotic cell death in distal lung epithelial cells is significantly minimized when combined with cyclic stretch. The involvement of the mitogen-activated protein kinase pathways in regulating this response is currently being investigated.
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