This study aimed to determine whether low dietary Se content affects the function and mechanisms mediating the vascular relaxation of rat aortas, and to test the role of oxidative stress in observed differences. Male Sprague Dawley (SD) rats were maintained for 10 weeks on low Se (low-Se group; N = 20) or normal Se content (norm-Se group; N = 20) rat chow. Dose responses to acetylcholine (ACh; 10⁻⁹–10⁻⁵M) and the response to reduced pO₂ were tested in noradrenaline-precontracted aortic rings in the absence/presence of the nitric oxide synthase (NOS) inhibitor nitro-l-arginine methyl ester (l-NAME), the cyclooxygenase 1 and 2 (COX-1, 2) inhibitor Indomethacin, and the antioxidative agent Tempol in tissue bath. mRNA expression of glutathione peroxidase 1 (GPx1), catalase (CAT), and Cu/Zn superoxide dismutase (SOD) was measured in rat aortas. Oxidative stress (Thiobarbituric Acid Reactive Substances; TBARS), antioxidative plasma capacity (ferric reducing ability of plasma assay; FRAP), and protein levels of GPx1 were measured in plasma and serum samples, respectively. Reduced ACh-induced relaxation (AChIR) (dominantly mediated by NO) in the low-Se group compared to the norm-Se group was restored by Tempol administration. Hypoxia-induced relaxation (HIR) (dominantly mediated by COX-1, 2), TBARS, and FRAP as well as GPx1 serum concentrations were similar between the groups. mRNA GPx1 expression in rat aortas was significantly decreased in the low-Se compared to the norm-Se group. These data suggest that low dietary Se content increases the local oxidative stress level, which subsequently affects the NO-mediated vascular response.

Aim: To determine optimal duration of transient middle cerebral artery occlusion (t-MCAO) for a stroke model in female diabetic Sprague-Dawley (SD) rats. Methods: Streptozotocin-induced type-1 diabetic SD female rats (n = 25, 12 weeks old, five groups; n = 5 per group) were subjected to different duration of t-MCAO (20, 30, 45, 60 and 90 minutes) followed by reperfusion. A control group of rats without diabetes (n = 5) was subjected to 30 minutes of t-MCAO followed by reperfusion. Twenty-four hours after reperfusion, infarct volumes were evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Results: Intra-ischaemic reductions of regional cerebral blood flow (rCBF) were similar in all groups (68–75% of baseline values). Reperfusion was significantly impaired in the 90-minute ischaemia group (56–62% vs 80–125% in other groups). Twenty minutes of t-MCAO induced a small infarct (3 ± 5% of ischaemic hemisphere). Thirty minutes of ischaemia produced a significantly larger infarct (46 ± 6%). In the 45 and 60 minute groups, ischaemia infarct was 52 ± 5% and 59 ± 3% of the ischaemic hemisphere, respectively. Ischaemia of 90’ led to a massive stroke (89 ± 6% of ischaemic hemisphere encompassing the whole striatum (22 ± 3%) and almost the whole MCA irrigated cortex area (67 ± 6%)). Thirty minutes of t-MCAO did not produce stroke in the control group. Conclusion: The diabetic rat stroke model should be different from the non-diabetic, because female type-1 diabetic SD rats are highly sensitive to brain ischaemia and it is necessary to significantly shorten the duration of t-MCAO, optimally to 30 minutes.