Effect of cigarette smoking on hypoxic pulmonary vasoconstriction and its relation to animal species and period of smoking

Summary

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 (δPVR%) and the amplitude of the systolic wave in impedance pneumorheogram (δH%) were used to estimate the strength of HPV. It was observed that immediately after acute cigarette smoking, HPV in rats increased (δPVR% from 55,0 ±15.6% to 102.3 ±12.4%), which is mainly mediated by leukotrienes (LTs); whereas HPV in piglets decreased (δPVR% from 65.2 + 12.5% to 55.9 ±9.8%), which is mainly mediated by β-adrenergic receptors, and HPV in humans also increased (δH% 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 (δPVR% 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.