Pulmonary chemoreflex

Fentanyl can evoke the pulmonary chemoreflex, as evidenced by 50% of patients in one study and 28% in another, who coughed after the administration of fentanyl through a central line (SEDA-16, 79) (8). The coughing caused by fentanyl is inhibited by terbutaline (SEDA-21, 88). 

Bombesin and gastrin-releasing peptides have been shown to sensitize C-fiber neurons to subsequent activation by capsaicin and ATP. In addition, these peptides enhance the pulmonary chemoreflex induced by C-fiber stimulants. The relevance of these observations may be heightened in small-cell lung cancers, as the cancer cells are known to secrete various peptides, including bombesin-like peptides (Gu and Lee 2005). 

Green JF, Schmidt ND, Schultz FID, Roberts AM, Coleridge HM, Coleridge JC (1984) Pulmonary C-fibers evoke both apnea and tachypnea of pulmonary chemoreflex. J Appl Physiol 57 562-567... 

The striking similarities between the cardiovascular, ventilatory, and respiratory physiological responses to inhaled irritants and allergens implies that the irritant-induced pulmonary chemoreflex comprises a subset of the more profound allergen-induced anaphylactic cardiovascular and pulmonary collapse. 

All of the foregoing cardiovascular and ventilatory and respiratoiy responses—namely, apnea followed by tachypnea, bradycardia, and increased bronchial blood flow, as well as systemic hypotension—observed in the pulmonary chemoreflex are characteristic of an anaphylactic reaction (31). An example of the cardiopulmonary responses to an inhaled allergen in a spontaneously breathing dog is shown in Figure 5. There is an increase in transpulmonary pressure indicative of an increase in airways resistance and a decrease in dynamic compliance. There is a marked apnea followed by tachypnea, a marked bradycardia and hypotension. Albeit, there may be some compensatory increase in heart rate, the induced hypotension persists. This hypotension is probably, partly, mediated by the induction of nitric oxide (NO) through the parasympathetically induced activation of nitric oxide synthase (32,33). 

There are several possible routes whereby such responses can be affected. First, there is a neural response, as evidenced by the analogous symptoms of the cardiac and pulmonary chemoreflexes. Second, mediators released from the inflammatory cells in the lungs are carried by the blood directly to the heart. Of note, C3a and C5a which are released during anaphylaxis activate cardiac, but not limg mast cells (62). Third, antigens may penetrate the airway and alveolar epithelium and enter into the vasculature and directly interact with cardiac mast cells and basophils. This latter pathway is likely important when small molecules, such as sodium diisocyanate, are inhaled, as these molecules form albumin-isocyanate conjugates that may be related to the induction of toluene diisocyanate hypersensitivity (69). 

It is notable that extremely high concentration of irritants, such as ammonia vapor, are necessary to elicit a pulmonary chemoreflex, the physiological responses... 

The pulmonary chemoreflex is activated by laryngeal sensory nerves, and... 

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