Airway sensors play an important role in control of breathing. Recently, it was found that pulmonary slowly adapting stretch receptors (SARs) cease after a brief excitation following sodium pump blockade by ouabain. This deactivation can be explained by overexcitation. If this is true, mechanical stimulation of the SARs should also lead to a deactivation. In this study, we recorded unit activity of the SARs in anesthetized, open-chest, and mechanically ventilated rabbits and examined their responses to lung inflation at different constant pressures. Forty-seven of 137 units had a clear deactivation during the lung inflation. The deactivation threshold varied from unit to unit. For a given unit, the higher the inflation pressure, the sooner the deactivation occurs. For example, the SARs deactivated at 3.0 +/- 0.3 and 4.8 +/- 0.4 s when the lungs were inflated to constant pressures of 30 and 20 cmH(2)O, respectively (n = 25, P < 0.0001). The units usually ceased after a brief intense discharge. In some units, their activity shifted to a lower level, indicating a pacemaker switching. Our results support the notion that SARs deactivate due to overexcitation.

Background: Positive end-expiratory pressure (PEEP) is commonly used in clinical settings. It is expected to affect the input from slowly adapting pulmonary stretch receptors (SARs), leading to altered cardiopulmonary functions. However, we know little about how SARs behave during PEEP application. Objectives: Our study aimed to characterize the behavior of SARs during PEEP application. Methods: We recorded single-unit activities from 18 SARs in the cervical vagus nerve and examined their response to an increase of PEEP from 3 to 10 cm H₂O for 20 min in anesthetized, open-chest and mechanically ventilated rabbits. Results: The mean activity of the units increased immediately from 35.7 to 80.5 impulses per second at the fifth breath after increasing PEEP (n = 14, p < 0.001) and then gradually returned to 56.5 impulses per second at the end of 20 min of PEEP application (p < 0.001). In the meantime, peak airway pressure increased from 9.3 to 32.7 cm H₂O, and then gradually returned to 29.4 cm H₂O (n = 18; p < 0.05) after 20 min. The remaining four units ceased firing at 34.7 s (range 10-56 s) after their initial increased activity upon 10 cm H₂O PEEP application. The unit activity resumed as the PEEP was returned to 3 cm H₂O. Conclusions: High PEEP stimulates SARs and SAR activity gradually returns towards the baseline via multiple mechanisms including receptor deactivation, neural habituation and mechanical adaptation. Understanding of the sensory inputs during PEEP application will assist in developing better strategies of mechanical ventilation.

No abstract