Chronic obstructive pulmonary disease (COPD) is characterised by a poorly reversible airflow limitation. It is a complex disease associated with both pulmonary and systemic vascular inflammation, linked to subsequent development of cardiovascular complications including pulmonary hypertension. Inflammatory mediators and hypoxia promote endothelial damage causing an imbalance between vasodilator and vasoconstrictor intermediaries, thus altering vascular tone. These lead to increased smooth muscle cell proliferation and vasoconstriction as well as vascular remodelling and subsequently resulting in an increased pulmonary arterial pressure.1,2 The pathogenesis of systemic effects of COPD has not yet been fully elucidated. Pulmonary artery (PA) was dissected from normoxic control (C) and chronically hypoxic (CH – 10% O2; 1 week) Wistar rats and 2 mm segments of the vessels were mounted on a wire myograph in physiological saline (95% O2, 5% CO2, 37oC). U46691 was used to generate a pre-tone and a cumulative dose-response curve for a vasodilator (carbachol -CC or sodium nitroprusside -SNP) was constructed. A pro-inflammatory cytokine (TNF-α, IL-8 or IL-β) was then added for 1 hour before vasodilator responses were re-assessed. Right ventricular (RV) to left ventricular and septum (LV+S) ratio was used to assess RV hypertrophy in control and chronic hypoxic rats. All procedures were in accordance with current UK legislation. Significance was taken as P<0.05. One week hypoxia induced a significant increase in RV hypertrophy in rats (C= 0.27±0.026, CH= 0.40±0.028 n=3 t-test). Our preliminary data on control and CH rats did not show any significant difference in the maximum percentage of the endothelial dependent vasodilation by CC (C= 62±8.1% n=8, control+IL-8= 57±6.5% n=8, CH= 83±16.1% n=3 CH+IL-8= 68±7.6% n=3 ANOVA). CH increased the maximum vasodilatation by endothelial independent vasodilator, SNP by ~25% when compared to the control (CH=36±3.9% n=3, C=45±6.3% n=4) and the addition of IL-8 augmented SNP induced vasodilation in both groups (control+IL-8= 41±5.7% n=6, CH+IL-8= 30±3.1% n=3). However, these differences did not reach significance in both groups. Our findings suggest that (1) acute cytokine exposure has little effect on vasoreactivity; (2) one-week CH can cause structural changes in RV, even though a functional difference was not observed in PA vasodilatation in the same time. This might represent a difference in the time course for structural changes to be observed in the cardiovascular and pulmonary systems consequent to CH, or that hypoxia and pro-inflammatory cytokine effects are synergistic, and future longitudinal studies are planned.