What We Have Done

In the last 15 years our lab has concentrated on defining the neural mechanisms of respiratory sensation and dyspnea in humans. Our major accomplishments are listed below. The Bibliography Page shows all of our relevant publications, with links to abstracts with graphics and, when available, pdf files of articles.
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   We have developed a useful laboratory model of air hunger (uncomfortable urge to breathe, starved for air, one of several sensations categorized as dyspnea). We have defined the static and dynamic stimulus-response characteristics of the air hunger response. (Banzett et al 1996, Banzett 1996)

    •     We were the first to show that air hunger is unchanged by complete paralysis of respiratory muscles, disproving the widely held view that all dyspnea arose from respiratory muscles. (Banzett et al 1989, 1990)

    •     It has been known for a century that air hunger is relieved by breathing, even when changes in blood gasses are prevented. We were the first to show this relief comes from pulmonary mechanoreceptors. (Manning et al 1992) and that this relief is the same whether the subject breathes or is mechanically ventilated. (Shea et al 1996, Bloch-Salisbury et al 1998)

    •     We were the first to show that air hunger adapts to prolonged changes in PCO2 over the course of 2-3 days. (Bloch-Salisbury et al 1996)

    •     We published the first report showing which areas of the cerebral cortex are engaged in the perception of dyspnea (air hunger). (Banzett et al 2000, Evans et al 2002)

    •     We were the first to show that pulmonary stretch receptor information lung volume is perceived, and that subjects can even detect when a single lung lobe is inflated (via bronchoscope), and can detect on which side the inflation occurs. (Banzett et al 1987, Banzett et al 1997)

    •     We have obtained the most persuasive evidence to date that the sensation of tightness in asthma arises from pulmonary receptors. (Binks et al 2001).


We are currently funded to pursue functional brain imaging of dyspnea. Having described a map of activations related to dyspnea, we can now begin to test hypotheses about the role of each of the various brain regions identified. This work is being done at the MGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging. We have also applied for funding to examine the effects of clinical brain lesions on dyspnea perception. Other projects in the near future include testing the use of aerosolized furosemide to relieve air hunger; continued studies on the afferent pathways of asthma sensation; the application of perceptual principles developed to understand pain to dyspnea.