The cough reflex (CR) and the expiration reflex (ER) are two defensive reflexes from the respiratory tract, the latter mainly from the larynx. Both are elicited by mechanical and chemical irritation of the airway mucosa, and are a characteristic of airway diseases, but they have different functions. The CR first draws air into the lungs, to accentuate the subsequent expulsive phase; the ER consists of a strong expiration, to prevent aspiration of material into the lungs. They have different sensory pathways, central nervous circuits, and physiological and pharmacological modulations. In practice, coughing often consists of a combination of the two reflexes, a cough bout, epoch or attack. Articles on cough usually do not distinguish between the two reflexes, or whether the coughs are single events or epochs; they usually only measure frequency of expiratory efforts, and neglect other aspects. Current methods for measuring and assessing cough are described, with indications of when the use of these methods may be important. (+info)
Raising end-expiratory volume relieves air hunger in mechanically ventilated healthy adults.
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Air hunger is an unpleasant urge to breathe and a distressing respiratory symptom of cardiopulmonary patients. An increase in tidal volume relieves air hunger, possibly by increasing pulmonary stretch receptor cycle amplitude. The purpose of this study was to determine whether increasing end-expiratory volume (EEV) also relieves air hunger. Six healthy volunteers (3 women, 31 +/- 4 yr old) were mechanically ventilated via a mouthpiece (12 breaths/min, constant end-tidal Pco(2)) at high minute ventilation (Ve; 12 +/- 2 l/min, control) and low Ve (6 +/- 1 l/min, air hunger). EEV was raised to approximately 150, 400, 725, and 1,000 ml by increasing positive end-expiratory pressure (PEEP) to 2, 4, 6, and 8 cmH(2)O, respectively, for 1 min during high and low Ve. The protocol was repeated with the subjects in the seated and supine positions to test for the effect of shifting baseline EEV. Air hunger intensity was rated at the end of each breath on a visual analog scale. The increase in EEV was the same in the seated and supine positions; however, air hunger was reduced to a greater extent in the seated position (13, 30, 31, and 44% seated vs. 3, 9, 23, and 27% supine at 2, 4, 6, and 8 cmH(2)O PEEP, respectively, P < 0.05). Removing PEEP produced a slight increase in air hunger that was greater than pre-PEEP levels (P < 0.05). Air hunger is relieved by increases in EEV and tidal volume (presumably via an increase in mean pulmonary stretch receptor activity and cycle amplitude, respectively). (+info)
Airway mechanoreceptor deactivation.
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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. (+info)
The effect of increased background resistance on the resistive load threshold for eliciting the respiratory-related evoked potential.
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The detection threshold (DeltaR(50)) of resistive (R) loads is a function of the total background resistance (R(0)). Increased R(0) increases the DeltaR(50), but the ratio DeltaR(50)/R(0) remains constant. The respiratory-related evoked potential (RREP) is elicited only by R loads greater than the cognitive detection threshold, DeltaR(50). We hypothesized that the RREP Nf, P1, and N1 peaks will be elicited only when the added load DeltaR/R(0) is greater than the normal detection threshold, DeltaR(50)/R(0) = 0.30. We also hypothesized that when the R(0) is increased by adding extrinsic R, the RREP will not be elicited if the DeltaR/R(0) is less than the 0.30 ratio. RREPs were recorded with healthy volunteers (n = 20) respiring through a non-rebreathing valve. Three inspiratory R loads that spanned the DeltaR(50)/R(0) = 0.30 detection threshold were presented in two conditions: 1) no added R(0) (R1 < 0.30, R2 > 0.30, R3 > 0.30); and 2) increased R(0) = 13.3 cmH(2)O.l(-1).s (R1 < 0.30, R2 < 0.30, R3 > 0.30). For the control R(0), P1, Nf, and N1 peaks of the RREP were elicited by both R2 and R3, and not present with R1. The increased R(0) decreased R2/R(0) > 1.5 to R2/R(0) < 0.15. With increased R(0), the R1 and R2 loads did not elicit the RREP, but the Nf, P1, and N1 peaks were present for R3. These results demonstrate that the RREP is present if the DeltaR is above the cognitive detection threshold, and the RREP is absent if the load is below the detection threshold. When the R(0) is increased to make the DeltaR/R(0) less than the detection threshold, the DeltaR no longer elicits the RREP. (+info)
The expiration reflex from the trachea and bronchi.
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The expiration reflex (ER) is a forced expiratory effort against a closed glottis that subsequently opens to eject laryngeal debris and prevent aspiration of material. It is distinct from the cough reflex. Its source is usually assumed to be restricted to the larynx and vocal folds, and its possible origin from the tracheobronchial (TB) tree has been suggested but never studied. The current authors re-analysed previous records with mechanical or chemical stimulation of the TB tree to see if an ER can consistently be elicited, and to see whether it has properties similar to that from the larynx and vocal folds. A random review was made of some of the extensive literature on TB "cough" to see if it confirmed the authors' conclusions. The TBER was consistently seen in cats and rabbits, either alone or followed by cough. These results are consistent with many studies in other species, including humans. It was enhanced, relative to cough, by inflation of the lungs and by general anaesthesia. Tracheobronchial expiration reflex occurs frequently with mechanical stimulation of the tracheobronchial tree. It differs fundamentally from many of the properties of "true" cough. Its features similar to the laryngeal expiration reflex suggest that both should be labelled "expiration reflexes" and not cough. Its existence should be taken into account in experimental, and possibly clinical, studies on tracheobronchial cough. (+info)
Voltage-gated sodium channels in nociceptive versus non-nociceptive nodose vagal sensory neurons innervating guinea pig lungs.
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Responses of slowly and rapidly adapting receptors in the airways of rabbits to changes in the Starling forces.
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1. The responses of the rapidly adapting receptors (RARs) and the slowly adapting receptors (SARs) of the airways to changes in the Starling forces regulating fluid exchange in the pulmonary extravascular space were investigated in anaesthetized rabbits. The hydrostatic pressure in the pulmonary microvasculature was raised by partial obstruction of the mitral valve (mean left atrial pressure increased by approximately 5 and 10 mmHg above the control values) and the concentration of plasma proteins was reduced by plasmapheresis (the total plasma protein concentration reduced by 18%). 2. There was a significant correlation between the action potentials generated by RARs and mean left atrial pressure (n = 12). A similar response was not observed in SARs (n = 12). 3. After plasmapheresis, there was an increase in the resting activity of the RARs (n = 5). In addition, the stimulus-response curve relating mean left atrial pressure and RAR activity was significantly shifted to the left compared to the one elicited before plasmapheresis. Plasmapheresis failed to influence the activity of SARs (n = 5). 4. Obstruction of the pulmonary lymph flow by raising the afterload in the right external jugular vein caused a significant increase in the activity of RARs (n = 6). This response was also maintained during the entire period of lymphatic obstruction. 5. The results show that manipulation of the Starling forces within the lung influences the RAR activity profoundly. It is suggested that the stimulus for the RARs may be a function of the fluid fluxes in the pulmonary extravascular space. (+info)