ABSTRACT
Investigation of the roles of prostaglandins(PGs) and leukotrienes(LTs) inthe changes of hemodynamics and hypoxic pulmonary vasoconstriction(HPV) induced bychronic cigarette smoking in Wistar rats.After exposure to either smoke or room air, rats were anesthetized, the changes ofhemodynamics and hypoxic pulmonary vasoconstriction were measured. Blood samplesdrawn through the carotid arterial cannula were analyzed with radioimmunoassay(RIA)for PGs and bioassay for LTs in plasma. The results showed that cigarette smoking for onemonth did not change the pulmonary arterial pressure nor the pulmonary vascularresistance(PVR) in rats, while the pressure response of pulmonary vessels to hypoxiawas reduced significantly, which could be abolished by indomethacin. Cigarette smokingcould increase the concentration of 6-Keto-PGF_1?but not that of TXB_2, in arterial plasma,during hypoxia and it reduced the plasma level of LTs as well. These results suggestedthat chronic cigarette smoking might have reduced HPV by two ways: i. e. increasing theptoduction of vasodilative PGs, especially PGI_2, and reducing LTs production duringhypoxia.