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J Appl Physiol (May 24, 2007). doi:10.1152/japplphysiol.01286.2006
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Submitted on November 14, 2006
Accepted on April 28, 2007

AIRWAY MECHANORECEPTOR DEACTIVATION

Juan Guardiola1, Mary Proctor1, Hua Feng Li1, Rajeesh Punnakkattu1, Shuxin Lin2, and Jerry Yu1*

1 Medicine, University of Louisville, United States
2 Medicine, University of Louisville, Louisville, Kentucky, United States

* To whom correspondence should be addressed. E-mail: j0yu0001{at}louisville.edu.

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 over-excitation. 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. 47 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 sec when the lungs were inflated to constant pressures of 30 and 20 cm H2O, 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 over-excitation.







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