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.

The role of lipoxygenase and cyclooxygenase metabolites in acute hypoxic pulmonary vasoconstriction (HPV) was studied in piglets. It has been found that acute alveolar hypoxia induced remarkable pulmonary vasoconstriction, associated with an increase in cardiac output. The hypoxic pulmonary vasoconstriction response was insignificantly attenuated after infusion of DEC. Indomethacin potentiated markedly the increase in pulmonary artery pressure and pulmonary vascular resistance and thus augmented HPV. It is inferred that hypoxic pulmonary vasoconstriction in piglet may be mediated by other important mediators in addition to leukotrienes, but modulated by prostaglandins to prevent an excessive rise in pulmonary artery pressure.

The alteration in hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking was studied in Wistar rats, piglets and in humans. The percentage change of pulmonary vascular resistance (delta PVR%) and the amplitude of the systolic wave in impedance pneumorheogram (delta H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats increased (delta PVR% from 55.0 +/- 15.6% to 102.3 +/- 12.4%), which is mainly mediated by leukotrienes (LTs); whereas HPV in piglets decreased (delta PVR% from 65.2 +/- 12.5% to 55.9 +/- 9.8%), which is mainly mediated by beta-adrenergic receptors, and HPV in humans also increased (delta H% from 20.6 +/- 2.6% to 31.1 +/- 4.1%), in which prostaglandins and leukotrienes may play the role of mediators. However, after one-month cigarette smoking, the HPV in rats fell significantly (delta PVR% 11.4 +/- 1.6%). An increase in synthesis of vasodilative prostaglandins and a decrease in leukotrienes synthesis may be the contributing factors to this alteration in HPV.

The alteration in hypoxic pulmonary vasoconstriction (HPV) induced by cigarette smoking was studied in Wistar rats, piglets and in humans. The percentage change of pulmonary vascular resistance (delta PVR%) and the amplitude of the systolic wave in impedance pneumorheogram (delta H%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats increased (delta PVR% from 55.0 +/- 15.6% to 102.3 +/- 12.4%), which is mainly mediated by leukotrienes (LTs); whereas HPV in piglets decreased (delta PVR% from 65.2 +/- 12.5% to 55.9 +/- 9.8%), which is mainly mediated by beta-adrenergic receptors, and HPV in humans also increased (delta H% from 20.6 +/- 2.6% to 31.1 +/- 4.1%), in which prostaglandins and leukotrienes may play the role of mediators. However, after one-month cigarette smoking, the HPV in rats fell significantly (delta PVR% 11.4 +/- 1.6%). An increase in synthesis of vasodilative prostaglandins and a decrease in leukotrienes synthesis may be the contributing factors to this alteration in HPV.