Lai Y L, Ganesan S, Lai-Fook S J
Pharmacology and Toxicology Division, College of Pharmacy and Biomedical Engineering, Wenner-Gren Research Laboratory, University of Kentucky, Lexington 40546.
J Appl Physiol (1985). 1988 Dec;65(6):2446-52. doi: 10.1152/jappl.1988.65.6.2446.
We studied the relationship between bronchoconstriction and the degree of trapping in saline-filled lungs isolated from guinea pigs postmortem after rapid exsanguination. Airway resistance was measured in nine lungs, and in five lungs the site of airway narrowing was located radiographically. Animals were anesthetized with pentobarbital sodium, degassed by O2 absorption, then rapidly exsanguinated when O2 absorption was almost complete. Liquid trapping was assessed from the pressure-volume behaviour measured in saline-filled lungs. During a slow deflation from maximum volume, alveolar liquid pressure (Palv) was measured by the micropipette-servonulling method, airway opening pressure (Pao) by a strain gauge, and flow rate (Q) by weighing a reservoir connected to the airway. Airway resistance (Raw) was calculated at different lung volumes from the relationship: Raw = (Palv-Pao)/Q. In untreated lungs, Raw and fluid trapping were relatively high, and severe bronchoconstriction occurred at the level of the main stem and lobar bronchi. Nifedipine infusion reduced Raw 40-fold and decreased trapping. Raw was further reduced 10-fold and fluid trapping was minimal in lungs pretreated with nifedipine before exsanguination. Results suggest a close association between bronchoconstriction and fluid trapping in guinea pig lungs.
