Abstract
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 (P(pa)), 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) α-actin and double elastic laminas was assessed microscopically. CS and CH induced similar increases of P(pa) 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 α-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.
Highlights
51 guinea pigs were exposed to Cigarette smoke (CS) for 12 weeks and 32 were sham-exposed. 50% of the animals in each group were exposed to chronic hypoxia (CH) for the final 2 weeks
Animals and management 83 male Hartley guinea pigs weighing 350 g were divided into four groups: one group was exposed to CS for 12 weeks (n533); a second group was kept in a normal atmosphere for 10 weeks and subsequently exposed to an inspiratory oxygen fraction (FI,O2) of 0.12 for 2 weeks in a hypoxic chamber (CH group) (n516); a third group was exposed to CS for 12 weeks and to CH for the final 2 weeks (CSCH group) (n518); and a control group was sham-exposed to CS and kept in a normal atmosphere (n516)
Results of the present study show that both CS and CH produced a similar increase in Ppa and right ventricle (RV) hypertrophy, and that the combination of both agents had a synergistic effect on these alterations
Summary
51 guinea pigs were exposed to CS for 12 weeks and 32 were sham-exposed. 50% of the animals in each group were exposed to CH for the final 2 weeks. 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). Pulmonary hypertension is a common and serious complication of chronic obstructive pulmonary disease (COPD) It is Cigarette smoking is associated with endothelial dysfunction [3], increased expression of growth factors [4] and inflammatory cell infiltrate in considered to result from the effects of chronic pulmonary arteries [5]. These factors may induce hypoxaemia on pulmonary vessels. Structural changes in they might be related to oxidative damage [6]
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