To determine the local effects of cigarette smoke on the pulmonary vasculature, we measured pulmonary artery pressure-flow curves in isolated, blood-perfused pig lungs before and after 4 exposures to cigarette smoke. During each exposure, smoke was administered into the trachea for 3 to 4 min at a rate of 20 to 25 puffs/min and and a volume of 35 to 50 ml with a smoking machine. During hypoxia (inspired PO2 50 mmHg), when baseline vasomotor tone was high, cigarette smoke caused an acute transient vasodilation. During control (inspired PO2 200 mmHg), when baseline tone was low, no significant effect was observed. In addition to this acute effect, cigarette smoke caused a depression of the pulmonary pressor response to hypoxia, which developed gradually during the course of the experiment. Indomethacin, at perfusate concentrations of 20 and 100 μg/ml, did not significantly alter the acute vasodilating effect of smoking, suggesting that prostaglandins synthesized by cyclooxygenase were not the mediators of this response. Indomethacin did, however, prevent the gradual depression of the pulmonary vasoconstrictor response to hypoxia.
|Original language||English (US)|
|Number of pages||5|
|Journal||American Review of Respiratory Disease|
|State||Published - Dec 1 1981|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine