Abstract
Background
Inspiratory muscle fatigue is common in severe pulmonary diseases and develops when the inspiratory effort quotient, which is the mean inspiratory pressure over maximal inspiratory pressure (PI/PIMAX), exceeds a critical value. If PIMAX is unchanged, increased PI will promote muscle fatigue. PI can be expressed as (k×VT/Cdyn)×(TI/TTOT), where k is a constant, VT is tidal volume, Cdyn is dynamic lung compliance, and TI/TTOT is inspiratory duty cycle, which is inspiratory time over the period of a respiratory cycle. The excitatory lung reflex (ELR), which can be evoked by inflammatory mediators (eg, H2O2) or hypertonic saline to cause a vagally mediated neural hyperpnea and tachypnea, may be one of the mechanisms to promote inspiratory muscle fatigue.
Methods
To investigate whether the ELR can promote inspiratory muscle fatigue I conducted experiments in anesthetized and open-chest rabbits whose lungs were made motionless. The duty cycle, amplitude of the phrenic neurogram (which is closely correlated with VT), and burst rate were examined after initiation of the ELR by injection of hypertonic saline (8.1%, 0.1 mL) into the lung parenchyma.
Results
The duty cycle, amplitude, and burst rate of the phrenic activity increased by 36±7, 15±3, and 40±8% (n=9; P<0.01), respectively. The responses were abolished by bilateral vagotomy.
Conclusions
Because Cdyn and PIMAX did not change, the ELR increased the duty cycle, phrenic amplitude, and burst rate, therefore activation of this reflex may promote inspiratory muscle fatigue and may precipitate ventilatory failure.
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