We identified five patients with a functional disorder of the vocal cords that mimicked attacks of bronchial asthma. Paroxysms of wheezing and dyspnea were refractory to standard therapy for asthma. During episodes of wheezing, the maximal expiratory and inspiratory flow-volume relationship was consistent with a variable extrathoracic obstruction. Laryngoscopy confirmed that wheezing was due to adduction of the true and false vocal cords throughout the respiratory cycle. During asymptomatic periods the maximal flow-volume relationship and laryngoscopic examination were normal. Provocation tests for bronchial asthma were negative. A variety of personality styles and psychiatric diagnoses were represented; patients were not aware of the vocal-cord dysfunction, which uniformly and dramatically responded to speech therapy and psychotherapy. This syndrome may be a form of conversion reaction.

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Guinea pig airway smooth muscle (ASM) cells were maintained in a primary tissue culture (passages 1-3). Cells were exposed to human recombinant interleukin-1 beta (IL-1 beta; 20-100 pg/ml) or interleukin-6 (IL-6; 1-4 ng/ml) in the presence of indomethacin (1 microgram/ml) for up to 5 days. Proliferation of ASM cells was assessed with two techniques, direct counting of cells with a hemacytometer and [3H]thymidine incorporation corrected for total protein content. Hypertrophy of ASM cells was assessed by [3H]leucine incorporation (evaluation of protein synthesis), determination of total DNA content, DNA content per cell, and protein content per cell. We observed that the exposure of ASM cells to human recombinant IL-1 beta or IL-6, in all studied concentrations, significantly increased the number of cells as well as [3H]thymidine incorporation into ASM cells. We also found that exposure of ASM to these two cytokines increased [3H]leucine incorporation into the ASM cells and increased protein content and DNA content per single cell. These changes were also concentration dependent. We conclude that the two proinflammatory cytokines, IL-1 beta and IL-6, which are present in asthmatic lungs, increased the proliferation of ASM cells (hyperplasia) as well as their overall size and size of their nuclei, as measured by biochemical markers. These findings are compatible with the presence of ASM hypertrophy.

Active and passive sensitization, both in vivo and in vitro, caused significant hyperpolarization of airway smooth muscle cell preparations isolated from guinea pigs. An increase in the contribution of the electrogenic Na+ pump to the resting membrane potential was responsible for this change. Hyperpolarization, as induced by passive sensitization, was not prevented by agents that inhibit specific mediators of anaphylaxis but was abolished when serum from sensitized animals was heated. The heat-sensitive serum factor, presumably reaginic antibodies, appears to be responsible for the membrane hyperpolarization of airway smooth muscle cells after sensitization.