P2872
J Appl Physiol 1993 May;74(5):2380-6
Respiratory and cardiovascular effects of inhaled and intravenous
bradykinin, PGE2, and PGF2 alpha in dogs.
Karlsson JA, Sant'Ambrogio FB, Forsberg K, Palecek F, Mathew OP,
Sant'Ambrogio G.
AB Draco, Pharmacology 1, Lund, Sweden.
Prostaglandins (PGs) and bradykinin act as potent respiratory irritants
in both normal and asthmatic subjects, but their sites of action are
unknown. We compared the cardiorespiratory effects of bradykinin, PGE2,
and PGF2 alpha nebulized into the isolated "in situ" larynx, inhaled
into the tracheobronchial tree, and injected intravenously in
anesthetized spontaneously breathing dogs. Laryngeal administration only
resulted in a brief burst of rapid shallow breaths produced by
bradykinin (1,000 micrograms/ml) in one of five dogs. Tracheobronchial
administration of bradykinin (1,000 micrograms/ml) increased breathing
rate and tidal volume (VT) in four of seven dogs without changing
cardiovascular parameters, whereas PGE2 (500 micrograms/ml) caused
similar effects in two of six dogs. Lower concentrations of both agents
were essentially without effect. PGF2 alpha (50-500 micrograms/ml)
inhaled into the lower airway increased breathing rate, reduced VT, and
caused a concentration-dependent bronchoconstriction that was
significantly reduced by atropine. Inhaled PGF2 alpha only slightly
increased arterial blood pressure (5.8 2.8%) and heart rate (12.0
6.4%). Intravenous PGF2 alpha (5 micrograms/kg) increased upper and
lower airway resistances, which were accompanied by a decrease in
breathing rate and VT, hypertension, and bradycardia. Bradykinin (1
micrograms/kg) and PGE2 (1 and 3 micrograms/kg) produced apnea followed
by rapid shallow breathing, bradycardia, and hypotension. These results
indicate that the tracheobronchial tree is considerably more responsive
to aerosolized bradykinin, PGE2, and PGF2 alpha than the laryngeal
region. Moreover, the stronger effects produced by intravascular
administration suggest a greater accessibility of rapidly adapting
stretch receptors and C-fiber endings from the vascular bed than from
the airway lumen.