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induced bronchial vasoconstriction
Department of Medicine, Johns Hopkins University, Baltimore, Maryland 21224
The
pro-inflammatory characteristics of tumor necrosis factor-
(TNF-)
have been extensively characterized in in vitro systems. Furthermore,
this cytokine has been shown to play a pivotal role in airways
inflammation in asthma. Since the airway vasculature also
performs an essential function in inflammatory cell transit to the
airways, experiments were performed to determine the effects of TNF-
on bronchial vascular resistance (BVR). In anesthetized, ventilated
sheep, the bronchial artery (BA) was cannulated and perfused with
autologous blood. BVR was defined as inflow pressure/flow and averaged
6.3 ± 0.2 mmHg · ml
1 · min1 (±SE) for the 25 sheep studied. Recombinant human
TNF- (10 µg for 20 or 40 min) infused directly into the BA
resulted in a significant decrease in BVR to 87% of baseline
(P < 0.05). This vasodilation was followed by a
reversal of tone by 120 min and a sustained increase in BVR to 126% of
baseline (P < 0.05). Since others have shown TNF-
caused coronary vasoconstriction through endothelial release of
endothelin-1 (ET-1), an ET-1 antagonist was used to block bronchial
vasoconstriction. BQ-123, a selective ETA receptor antagonist, was delivered to the bronchial vasculature prior to TNF-
challenge. Attenuation of bronchial vasoconstriction was observed at
120 min (P < 0.03). Thus TNF- causes bronchial
vasoconstriction by the secondary release of ET-1. Although TNF-
exerts pro-inflammatory actions on most cells of the airways,
vasoactive properties of this cytokine likely further contribute to the
inflammatory status of the airways.
bronchial artery; tumor necrosis factor-; endothelin-1; airways
resistance; inflammation; sheep
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