Romero P V, Rodriguez B, Lopez-Aguilar J, Manresa F
Servei de Pneumologia i Unitat de Recerca Experimental, Ciutat Sanitaria i Universitaria de Bellvitge, 08907 L'Hospitalet de Llobregat, Barcelona, Spain.
J Appl Physiol (1985). 1998 Mar;84(3):1040-7. doi: 10.1152/jappl.1998.84.3.1040.
To investigate whether changes of tissue resistance (Rti) during methacholine (MCh)-induced constriction correspond to an intrinsic mechanism or are an artifact of increased airways inhomogeneity, rabbits were studied after exposure to air (n = 7) or 1.5 parts/million O3 (n = 6). Animals were anesthetized and mechanically ventilated. Tracheal flow and pressure (Ptr) and four alveolar capsule pressures (Pcap) were measured during 3 min after administration of an intrajugular bolus of 0.8 mg/ml MCh. By adjustment of the equation of motion [P(t) = E . V(t) + R . dV(t)/dt + P0] [where P(t), V(t), and dV(t)/dt are pressure, volume, and flow as a function of time, respectively, E is elastance, R is resistance, and P0 is end-expiratory pressure] to Ptr, lung resistance (RL) and dynamic elastance (EL) were determined breath by breath. Rti and airways resistance (Raw) were determined from Pcap in phase with rate of change of pulmonary expansion. Hysteresivity (eta) was calculated. Parallel inhomogeneity was estimated from the coefficients of variation (CV) of every Pcap at end inspiration and end expiration. Increase in CV significantly lagged Rti, RL, and eta. A linear relationship between EL and Raw was observed. Our results suggest that changes in tissue mechanics during the transition to the constricted state are not artifactual.
