Effects of cigarette smoking on hemodynamics and hypoxic pulmonary vasoconstriction: role of prostaglandins and leukotrienes.
This study investigated the role of prostaglandins (PGs) and leukotrieres (LTs) in hypoxic pulmonary vasoconstriction (HPV) and in cigarette smoking-induced changes in hemodynamics and HPV in Wistar rats. Selective LTD4-LTE4 receptor antagonist LY-171883 (LY) inhibited HPV by 71.8%, while cyclooxygenase inhibitor indomethacin (IND) augmented HPV. The results indicate that LTs mediate HPV in Wistar rats. Smoking increased the level of TXB2 over control by 143.6% in plasma and 69.2% in lung tissue, concomitantly, pulmonary and systemic vascular resistance (PVR and SVR) were increased by 38.7% and 46.7%, respectively. Both LY and IND prevented the smoking-induced increase of PVR and SVR. After smoking HPV increased twofold. The increase of HPV was abolished by LY, but not by IND. Our results suggest that smoking leads to pulmonary and systemic vasoconstriction partly mediated by TXA2 and LTs; smoking also leads to an augmentation of HPV, and LTs play an important role in it.
Chen
G
G
Wang
D X
DX
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000818:Animals; D006439:Hemodynamics; D000860:Hypoxia / Q000503:physiopathology*; D015289:Leukotrienes / Q000097:blood / Q000502:physiology*; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D011651:Pulmonary Artery / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D012907:Smoking / Q000009:adverse effects*; D013929:Thromboxane B2 / Q000097:blood; D014661:Vasoconstriction
D015289:Leukotrienes; D011453:Prostaglandins; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha