Vascular reactivity
To assess the effect of both CS-exposure and ebselen treatment on vessel function, thoracic aorta was excised from the mice and all perivascular fat removed. Vessels were placed into carbogen-bubbled (95% O2, 5% CO2) cold Krebs buffer (composition in mmol/L: NaCl 119, KCl 4.7, MgSO4 1.17, NaHCO3 25, KH2PO4 1.18, CaCl2 2.5, glucose 5.5). The aortae were cut into four 2 mm rings and mounted onto the pins of the myograph system (Danish Myo Technology A/S, Model 610M) with the resting tension increased to 5mN which was determined to give an effective arterial wall pressure of ~100mmHg (13.3kPa) thus mimicking in vivoconditions. Following a 30-minute equilibration, aortic rings were exposed to 0.5 x 10-3M of the thromboxane A2 agonist U46619 (Cayman Chemical, USA) to induce the maximal vascular contraction, defined as 100%. In each ring, both endothelial integrity and smooth muscle function were assessed using cumulative doses of acetylcholine (ACh, 1x10-8M to 1x10-5M) (Thermo Fisher Scientific, USA) and sodium nitroprusside (SNP, 1x10-8M to 1x10-5M) (Thermo Fisher Scientific, USA) respectively in sub-maximally contracted aorta (50-60% of maximal U46619 contraction) with all experiments ran in duplicate and compared to sham or sham + vehicle treated mice.