TY - JOUR
T1 - Vascular effects of cigarette smoke in isolated pig lungs
AU - Gilman, M. J.
AU - Sylvester, J. T.
AU - Kennedy, T. P.
AU - Menkes, H. A.
AU - Traystman, R. J.
PY - 1981/12/1
Y1 - 1981/12/1
N2 - 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.
AB - 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.
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M3 - Article
C2 - 7305109
AN - SCOPUS:0019787453
SN - 0003-0805
VL - 124
SP - 549
EP - 553
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 5
ER -