Cigarette smoke (CS) and chronic hypoxia (CH) can produce pulmonary
hypertension. Similarities and differences between both exposures and their interaction have
not been explored. The aim of the present study was to investigate the effects of CS and CH, as
single factors or in combination, on the pulmonary circulation in the guinea pig.
51 guinea pigs were exposed to CS for 12 weeks and 32 were sham-exposed. 50% of the animals
in each group were additionally exposed to CH for the final 2 weeks.We measured pulmonary artery
pressure (Ppa), and the weight ratio between the right ventricle (RV) and left ventricle plus the
septum. Pulmonary artery contractility in response to noradrenaline (NA), endothelium-dependent
vasodilatation and distensibility were evaluated in organ bath chambers. The number of small
intrapulmonary vessels showing immunoreactivity to smooth muscle (SM) a-actin and double
elastic laminas was assessed microscopically.
CS and CH induced similar increases of Ppa and RV hypertrophy (p,0.05 for both), effects that
were further enhanced when both factors were combined. CH increased the contractility to NA
(p,0.01) and reduced the distensibility (p,0.05) of pulmonary arteries. Animals exposed to CS
showed an increased number of small vessels with positive immunoreactivity to SM a-actin
(p,0.01) and those exposed to CH a greater proportion of vessels with double elastic laminas
(p,0.05).
We conclude that CH amplifies the detrimental effects of CS on the pulmonary circulation by
altering the mechanical properties of pulmonary arteries and enhancing the remodelling of
pulmonary arterioles.
