MacFarlane PM. Severity of neonatal hyperoxia determines structural and functional changes in developing mouse airway. Am J Physiol Lung Cell Mol Physiol 307: L295-L301, 2014. First published June 20, 2014 doi:10.1152/ajplung.00208.2013.-Wheezing is a major long-term respiratory morbidity in preterm infants with and without bronchopulmonary dysplasia. We hypothesized that mild vs. severe hyperoxic exposure in neonatal mice differentially affects airway smooth muscle hypertrophy and resultant airway reactivity. Newborn mice were exposed to 7 days of mild (40% oxygen) or severe (70% oxygen) hyperoxia vs. room air controls. Respiratory system resistance (Rrs), compliance (Crs), and airway reactivity were measured 14 days after oxygen exposure ended under ketamine/ xylazine anesthesia. Baseline Rrs increased and Crs decreased in both treatment groups. Methacholine challenge dose dependently increased Rrs and decreased Crs in 40% oxygen-exposed mice, whereas Rrs and Crs responses were similar between 70% oxygen-exposed and normoxic controls. Airway smooth muscle thickness was increased in 40%-but not 70%-exposed mice, whereas collagen increased and both alveolar number and radial alveolar counts decreased after 40% and 70% oxygen. These data indicate that severity of hyperoxia may differentially affect structural and functional changes in the developing mouse airway that contribute to longer-term hyperreactivity. These findings may be important to our understanding of the complex role of neonatal supplemental oxygen therapy in postnatal development of airway responsiveness.
Background: Tricuspid regurgitation (TR) is common in patients receiving left ventricular assist device (LVAD) implantation. The current literature is conflicting regarding the effects of concomitant tricuspid valve repair (TVR) at LVAD implantation. We investigated the hemodynamic effects of concomitant TVR at LVAD implantation.Methods: Consecutive clinically stable LVAD outpatients who underwent hemodynamic ramp testings were enrolled in this study, and they were stratified by concomitant TVR. Results of hemodynamic ramp tests were compared between the TVR group and the non-TVR group.Results: Among 65 LVAD patients undergoing ramp tests, 34 patients had received TVR, and 31 had not. There were no significant differences in baseline characteristics between two groups except for higher degree of TR and lower pulmonary artery pulsatility index in the TVR group (P < .05 for both). Following LVAD implantation, the degree of TR improved significantly in the TVR group down to the comparable level with the non-TVR group. During ramp tests, the TVR group had steeper cardiac index slope (0.14 ± 0.12 vs 0.07 ± 0.07 L/min/m 2 /step, P = .002) and higher cardiac index at set LVAD speed (2.99 ± 0.84 vs 2.52 ± 0.42 L/min/m 2 , P = .007).
Conclusions: Concomitant TVR improves cardiac output and its response to LVAD speed change following LVAD implantation. Longitudinal clinical implications of such hemodynamic changes are unknown. K E Y W O R D S heart failure, right ventricular failure, tricuspid regurgitation
There are conflicting data regarding whether concomitant mitral valve surgery (MVS) at left ventricular assist device (LVAD) implantation is beneficial. This study aimed to assess the hemodynamic effects of concomitant MVS. Of all 73 enrolled patients, 44 patients had undergone concomitant MVS and 29 patients had not. Before LVAD implantation, MVS group had higher pulmonary capillary wedge pressure (p = 0.04). After LVAD implantation, MVS group had higher mean pulmonary artery pressure and cardiac output (CO). During the hemodynamic ramp study, MVS group had steeper CO slopes (0.18 [0.13 0.28] vs. 0.15 [0.08, 0.20] L/min/step; p = 0.04) at incremental LVAD speed and achieved a higher CO at the optimized set speed (5.5 [4.7, 6.9] vs. 4.9 [4.0, 5.7] L/min; p = 0.03). One-year freedom from death or heart failure readmission was statistically comparable between the two groups (61% vs. 80%, p = 0.20). Thus far, after LVAD implantation and concomitant MVS, patients had increased pulmonary hypertension, despite having higher CO and a better response of CO at incremental LVAD speed. The implication of hemodynamic features after concomitant MVS on clinical outcomes warrants further investigation.
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