Does expiratory automatic endotracheal tube compensation reduce dynamic hyperinflation in a physical lung model?
In a lung model of pressure-targeted ventilation, expiratory ETT resistance caused dynamic lung hyperinflation during increases in respiratory rates, thereby reducing inspiratory tidal volume. Expiratory ATC attenuated these adverse effects.
In a mouse model of NASH, TLR9 signaling induces production of IL-1beta by Kupffer cells, leading to steatosis, inflammation, and fibrosis.