At high cardiac output, diesel exhaust exposure increases pulmonary vascular resistance and decreases distensibility of pulmonary resistive vessels

Abstract

Air pollution has recently been associated with the development of acute decompensated heart failure, but the underlying biological mechanisms remain unclear. A pulmonary vasoconstrictor effect of air pollution, combined with its systemic effects, may precipitate decompensated heart failure. The aim of the present study was to investigate the effects of acute exposure to diesel exhaust (DE) on pulmonary vascular resistance (PVR) under resting and stress conditions but also to determine whether air pollution may potentiate acquired pulmonary hypertension. Eighteen healthy male volunteers were exposed to ambient air (AA) or dilute DE with a particulate matter of <2.5 μm concentration of 300 μg/m(3) for 2 h in a randomized, crossover study design. The effects of DE on PVR, on the coefficient of distensibilty of pulmonary vessels (α), and on right and left ventricular function were evaluated at rest (n = 18), during dobutamine stress echocardiography (n = 10), and during exercise stress echocardiography performed in hypoxia (n = 8). Serum endothelin-1 and fractional exhaled nitric oxide were also measured. At rest, exposure to DE did not affect PVR. During dobutamine stress, the slope of the mean pulmonary artery pressure-cardiac output relationship increased from 2.8 ± 0.5 mmHg · min · l (-1) in AA to 3.9 ± 0.5 mmHg · min · l (-1) in DE (P < 0.05) and the α coefficient decreased from 0.96 ± 0.15 to 0.64 ± 0.12%/mmHg (P < 0.01). DE did not further enhance the hypoxia-related upper shift of the mean pulmonary artery pressure-cardiac output relationship. Exposure to DE did not affect serum endothelin-1 concentration or fractional exhaled nitric oxide. In conclusion, acute exposure to DE increased pulmonary vasomotor tone by decreasing the distensibility of pulmonary resistive vessels at high cardiac output.

Exercise stress echocardiography of the pulmonary circulation and right ventricular-arterial coupling in healthy adolescents

“…Even though available validation against invasive measurements is only indirect, 3,4 exercise stress echocardiography of the pulmonary circulation to generate PAMP-flow relationships and resistive vessel distensibility calculations has been shown to be feasible and has allowed to disclose age-, sex-, environmental-related, and early stage disease alterations. The distensibility factor a has been shown to be higher in pre-menopausal women and lower in aging adults, 19 lower in young adult men of Sub-Saharan African ascendance 20 lower with chronic but not acute hypoxic exposure 2,21 or diesel exhaust exposure, 22 and lower in adolescents born by in vitro fertilization. 14 The a factor has been reported to be decreased in patients with borderline hypertension, 23 early or latent pulmonary vascular disease, 5,24 and heart failure.…”

Role of the Aryl Hydrocarbon Receptor in Sugen 5416–induced Experimental Pulmonary Hypertension

“…Importantly, the lungs are exposed to many AhR activators in airborne particulate matter. Indeed, exposure to diesel exhaust can increase pulmonary vascular tone at high cardiac output (29). Functionally, AhR has been shown to play a critical role in vascular development, angiogenesis, and cancer (30,31).…”

Cardiovascular effects of air pollution

“…When patients with stable coronary heart disease were exposed to diesel exhaust, a decrease in ischaemic threshold was observed, suggesting an adverse influence of air pollution on myocardial blood flow regulation [50]. Acute exposure to diesel exhaust is also followed by an increase in pulmonary vascular resistance and a decrease in pulmonary vessel distensibility at high cardiac output, which may participate in the influence of air pollution on an acute heart failure episode [51]. Acute arterial vasoconstriction was also observed in the systemic circulation in healthy adults exposed to diesel exhaust [52].…”