Effects of different ventilation strategies on lung injury in newborn rabbits

Abstract

Our data demonstrate that different ventilation regimes can induce lung injury and that the interaction effects of the FiO(2), the PIP and the RT may play crucial roles in the pathogenesis of lung injury.

Animal models of bronchopulmonary dysplasia. The preterm and term rabbit models

“…Both term and preterm rabbits (delivered between 27 and 29 days of gestation) have been used in short-term (Յ16 h) experiments involving mechanical ventilation. These models have tested the effects of the administration of surfactant (24,30,64,86), of varying conventional mechanical ventilation and oxygen strategies (52), and of conventional vs. high-frequency oscillatory ventilation (88), as well as the effects of conventional ventilation on SP-A and KGF (36). With animal weights ranging from ϳ25 to 35 g at 27 days gestation, the preterm model allowed ventilation via an 18-gauge catheter inserted into the trachea (30,88).…”

“…RABBIT MODELS OF BPD reach adolescence by the close of exposure at 5-6 wk (although, unlike the human, their alveoli are still developing rapidly at that stage), allowing early evaluation of near-adult animals following a neonatal perturbation (67). Rabbit models are also cost effective compared with larger animal models, but large enough to permit perturbations, including nebulized treatments, mechanical ventilation and pulmonary function testing, and easy isolation of individual cells, even among newborn or premature animals (1,30,36,52,64,86,88,95). Neonatal rabbits weigh ϳ50 g, slightly above the size of an adult mouse, and even premature (27-29 days) rabbits have weights in the range of a mouse's 30 g. The once-daily feeding behavior of term rabbits allows mothers to be placed in the exposure chamber for brief periods once daily, avoiding the need for gavage feeding or cross-fostering and rotating mothers to prevent oxygen toxicity to the mothers.…”

“…Hyperoxia is the most common reported exposure, but investigators have used FI O 2 ranging from 0.55 to 1.0 for the acute injury portion of their models (37,75,122). Acute hyperoxia exposures have varied in length from short-term models under 24 h to up to 11 days of exposure, with exposures from 7 to 11 days producing similar results (26,52,54,77,104,112). Bacterial exposure and malnutrition as models have been explored infrequently, although the findings from those experiments suggest that investigators should be sensitive to the effects of nutrition and infection on their models and that these factors may be important in the human newborn (45,78).…”

“…Furthermore, the term newborn recovery model has not been critically evaluated for morphometric similarities to or differences from the human infant recovering from BPD. Premature rabbit kits have been maintained briefly on mechanical ventilation, showing evidence that it is possible to manipulate the model in this manner (30,36,52,64,86,88). However, there are no published longer-term exposures to both hyperoxia and mechanical ventilation that would mimic more fully the exposures faced by the human premature infant.…”

Brain caspase-3 and intestinal FABP responses in preterm and term rats submitted to birth asphyxia

“…However, the indiscriminate use of this intervention may be potentially toxic to various organs of the NB, resulting in serious diseases and intensifying the development of injuries ( 18 ). After asphyxia, during the reperfusion period, molecular oxygen in the tissue reacts with hypoxanthine and triggers production of free radical species causing tissue damage ( 19 - 21 ).…”