AJP - Heart and Circulatory Physiology, Vol 252, Issue 1 89-H99, Copyright © 1987 by American Physiological Society
Pulmonary edema in dogs fails to cause reflex responses
W. B. Wead, S. S. Cassidy and R. C. Reynolds
Pulmonary edema has been proposed as a stimulus for pulmonary C-fibers.
Stimulation of pulmonary C-fibers causes depression of cardiovascular
function and either tachypnea or apnea. Our objective was to determine
whether pulmonary edema, induced by either increasing pulmonary vascular
permeability with alloxan or hydrostatic challenges, would elicit
depression of cardiovascular function or changes in frequency of
inspiratory activity. Utilizing a preparation in which the left pulmonary
vessels and left airway were isolated, we monitored systemic blood pressure
(BP), heart rate (HR), and diaphragm contractions (DC) in 13 anesthetized
dogs. Injection of alloxan into the left pulmonary artery (LPA) produced
transient decreases in HR, BP, and frequency of DC within 20 s of injection
with no subsequent cardiorespiratory changes up to 5 min. These alloxan
injections also caused coagulation necrosis. Generation of hydrostatic
pulmonary edema in the left lung caused no changes in HR, BP, or in the
frequency and amplitude of DC. We conclude that alloxan does stimulate
reflex cardiorespiratory depression consistent with C-fiber stimulation,
but these reflex responses are probably caused by alloxan's caustic effect
and not by the resultant edema. We also conclude that pulmonary edema
induced by increased hydrostatic pressure does not evoke any reflex
cardiovascular responses or changes in frequency of inspiratory activity.
