Does [ Propofol depress the activity of hypoglossal nerve more than that of phrenic nerve in rabbits ]?
During the sedation with low dose of propofol, we need to pay attention to potential upper airway obstruction. In addition to the above, high doses of propofol could reduce spontaneous inspiratory drive, and we need to keep both upper airway patency and sufficient ventilation.
Based on these findings, we postulate a new mechanism of cardiac toxicity based on the PTM-driven accumulation of desmin amyloid-like oligomers. Phosphorylation and cleavage as well as oligomers formation are reduced by treatment (CRT) indicating a relationship between the three. Finally, the decrease of desmin amyloid-like oligomers with CRT or small molecules points both to a general mechanism of HF based on desmin toxicity that is independent of protein mutations and to novel potential therapies.