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Journal of Applied Physiology, Vol 69, Issue 6 1953-1960, Copyright © 1990 by American Physiological Society
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C. R. Killingsworth, N. E. Robinson, T. Adams, R. K. Maes, C. Berney and E. Rozanski
Department of Physiology, Michigan State University, East Lansing 48824-1314.
Airway responsiveness was studied in cats 3 or 6 days after exposure to feline herpesvirus I. Control cats were sham inoculated with tissue culture media. Intrathoracic airway caliber was evaluated by pulmonary resistance (RL) and dynamic compliance (Cdyn). Trachealis shortening was quantitated with microfoil strain gauges, which measured the external diameter of tracheal ring 4. Airway smooth muscle contraction was produced using vagal stimulation and local infusion of acetylcholine. The diameter of tracheal ring 4 decreased with increasing frequency of vagal stimulation, and there was more constriction at 3 (PID3) than at 6 days postinfection (PID6) or in control cats. RL increased and Cdyn tended to decrease with increasing frequency of stimulation, but there was no difference between control and infected cats. Infected and control cats did not differ in their response to locally infused acetylcholine. Virus was consistently cultured from conjunctival, nasal, and oral mucous membranes, trachea, and main stem bronchi at PID3 but not from the trachea and main stem bronchi at PID6. Virus was never isolated distal to the main stem bronchi. Tracheal hyperresponsiveness to vagal stimulation correlates with the presence of virus at PID3 and is apparently presynaptic in origin.
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