Key result
A simple model increasing activation rate 1.6-fold reproduced experimental results showing that allergen sensitization increases early shortening velocity without increasing force in airway smooth muscle.
Sensitized animals serve as a model for reactive airway disease, where increased activation rate explains rapid early shortening without increased force.
No immediate clinical implications for asthma; extends validation of activation rate models in animal airway smooth muscle.
It has been reported that sensitization of animals to allergens increases both early shortening velocity and myosin light-chain kinase of their airway smooth muscle without increasing force generated by these muscles. Since early shortening sets muscle length for the duration of a contraction, these responses might be expected to produce greater airway obstruction. Here, it is explained how the more rapid early shortening without increased force production is predicted by the 2-stage process of activation followed by contraction posited by the crossbridge theory of contraction when the rate, but not the extent, of activation is increased. The experimental results are reproduced by a simple model in which activation rate is increased 1.6-fold without any other changes in contractile parameters. These results reinforce suggestions that sensitized animals are a model for reactive airway disease.
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Ford et al. (2007) studied Reactive airway disease / Asthma. Sensitization to allergens (increased activation rate) vs. Unsensitized state was evaluated on Early shortening velocity and force production. A simple model increasing activation rate 1.6-fold reproduced experimental results showing that allergen sensitization increases early shortening velocity without increasing force in airway smooth muscle.
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