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 Pageshows all of our relevant publications, with links to abstracts with graphics and, when available, pdf files of articles.
• 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 have shown this laboratory model to be useful in understanding clinical treatments. (Banzett et al 2011)
• 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, Banzett et al 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 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 test the use of aerosolized furosemide to relieve air hunger — NIH R01 NR12009