The use of computational fluid dynamics (CFD) to simulate ventilation in the major airways of the lung has been shown to demonstrate greater specificity in assessing lung function over spirometry measures and visual analysis of computed tomography (CT) images. Currently, CFD is limited to simulating ventilation in a static airway geometry derived directly from CT. It cannot be used to assess the change in ventilation as a result of acute bronchoconstriction or long term remodelling of the airway wall. We have developed a multiscale biomechanical model of bronchoconstriction in the major airways. The model integrates an active tension produced by airway smooth muscle (ASM) and the passive mechanical properties of airway walls and lung parenchyma to simulate constriction and allow assessment of changes in ventilation. Initially, a finite element model (FEM) of the mechanics of a single airway embedded in a layer of parenchyma was developed. The model was used to parameterise material laws governing the airway wall mechanics in generations 1-10 and to validate the mechanical behaviour of the model in comparison to experimental data. ASM is embedded circumferentially in the model acting at a given angle to the airway cross section. The model is used to assess the reduction in airflow in response to ASM contraction in both normal and remodelled airway wall cases and the distribution of mechanical stress in the airway wall. To extend the methodology to a patient specific setting, a CT scan of a healthy adult was segmented to obtain a surface mesh of the airway wall. A volumetric mesh encompassing the airway walls was subsequently generated for use with the FEM model. Wall thickness in the mesh is varied to represent airway wall remodelling. The single airway model was used to investigate changes in airway resistance in response to remodelling. For example, a 19.5x increase in resistance between a normal and a remodelled generation 3 airway in response to a ASM activation (15 degree fibre angle at 8 cmH2O pleural pressure) was shown. The patient specific model was used to demonstrate the change in airflow and material stress around a number of bifurcations for several prescribed ASM tensions, again demonstrating the change in flow in response to ASM constriction and airway wall thickening. We have developed a methodology for simulating bronchoconstriction on patient specific geometries. The single airway model is well validated and validation of the patient specific model against clinical data is ongoing. The method reveals the importance of the structure of airway bifurcations in governing total airflow in the major airways. The results suggest that simulating bronchoconstriction on patient specific geometries can provide insight into the reduction in ventilation due to acute ASM contraction and chronic airway wall remodelling.