Functional assessment of hyperoxia-induced lung injury after preterm birth in the rabbit

Abstract

Verbeken E, Deprest J. Functional assessment of hyperoxia-induced lung injury after preterm birth in the rabbit.

Transplacental Administration of Rosiglitazone Attenuates Hyperoxic Lung Injury in a Preterm Rabbit Model

“…The pups were allowed spontaneous and regular breathing and were thereafter assigned to one of the three different groups. They were kept for 24 h or 7 days at 32°C, with twice daily feeding and antibiotic administration as previously described [11]. …”

“…The rabbit is considered as a large animal, and as alveolization already starts prior to birth, lung development in rabbits is more closely related to that in humans than rodents. Furthermore, it is possible to test lung function, as we and others earlier described [11]. …”

338: Proton-pump inhibitor omeprazole attenuates hyperoxia induced lung injury

“…To deliver the pups, a cesarean section was performed at day 28 of gestation (term = 31 days) as previously described [26]. The pups used for the dose finding study at time point 0 were immediately euthanized with an intraperitoneal injection of T61…”

“…Pups were anesthetized with ketamine (35 mg/kg) and xylazin (6 mg/kg) as previously described [26]. A FlexiVent analysis [28], an invasive measurement which is the gold standard for lung function testing in vivo, was performed on anesthetized pups and the following parameters were assessed: airway resistance (Rn), tissue damping (resistance, G) and tissue elasticity (H) using Primewave-8 forced oscillation and the total lung capacity (A), static compliance (Cst) and static elastance (Est) using the pressure-volume perturbation.…”

Divergent fibroblast growth factor signaling pathways in lung fibroblast subsets: where do we go from here?

“…Along these lines, the conditional, inducible deletion FGF ligands in mesenchymal cells would permit validation of the autocrine loop idea for the ligand/receptor pairs in vivo. Given the apparent importance of divergent FGF signaling pathways to alveologenesis, addressing these ideas in a pathological context is very important: in particular, to extend these studies to explore roles for the proposed Fgf18/Fgfr3 and Fgf10/Fgfr1 signaling pathways in arrested alveolarization, for example the blunted secondary septation seen in rodent (5,34) or other animal models (12,41,50) of BPD, where mesenchymal cell dynamics are altered (49).…”