The Psychophysiological Responses of the Chronic Ischemic Stroke Patients to the Acute Stress were Changed

Abstract: Mood disorder is one of the complications of stroke. The inability to cope with stress is also a prognosis of depression and anxiety. The aim of this study is to assess the response of stress system in the post stroke patients. Twelve healthy controls (HC) and twelve post-stroke patients after filling in the State-Trait Anxiety Inventory completed the Trier Social Stress Test (TSST) which induces acute stress. Salivary samples were collected to determine salivary cortisol levels and ECG record were taken in four times (before, right after stress, after two recoveries: 20 and 40 minutes after stress). ECG was also recorded during TSST and then the linear and non-linear features of Heart Rate Variability (HRV) were analyzed. The results showed that trait anxiety score and baseline salivary cortisol level were higher in post stroke than HC group (P-value <0.05). The increase of cortisol level after stress was only observed in HC that returned to baseline after the second recovery time. The stress increased the relative low frequency of HRV in both groups, however it was significantly lower in the stroke than HC group (P-value < 0.005). There was also a significant difference between alpha 1 DFA measures in stroke group and HC group (P-value <0.05). It is concluded that the impairment of the hormonal axis of stress system in the post-stroke patients that until now was not reported.

Polyhydroxylated fullerene nanoparticles attenuate brain infarction and oxidative stress in rat model of ischemic stroke.

Oxidative stress is the common underlying mechanism of damage in ischemic stroke. Therefore, we aimed to evaluate the possible protective effects of polyhydroxylated fullerene derivatives on brain infarction and oxidative/nitrosative stress in a rat model of ischemic stroke. The experiment was performed by four groups of rats (each; n=12); Sham, Control ischemia, and ischemic treatment groups (Pretreatment and Posttreatment). Brain ischemia was induced by 90 min middle cerebral artery occlusion (MCAO) followed by 24 hours reperfusion. Rats received fullerene nanoparticles at dose of 1 mg/kg 30 min before MCAO and immediately after beginning of reperfusion. Infarct volume, contents of malondialdehyde (MDA), glutathione (GSH) and nitrate as well as superoxide dismutase (SOD) activity were assessed 24 hours after termination of MCAO. Brain infarct volume was 310 ± 21 mm(3) in control group. Administration of fullerene nanoparticles before and after MCAO significantly decreased the infarct volume by 53 % (145 ± 45 mm(3)) and 81 % (59 ± 13 mm(3)), respectively. Ischemia also enhanced MDA and nitrate contents of ischemic hemispheres by 45 % and 25 % , respectively. Fullerene nanoparticles considerably reduced the MDA and nitrate contents of ischemic hemispheres before MCAO by 58 % and 17 % , respectively, and after MCAO by 38 % and 21 % , respectively. Induction of MCAO significantly decreased GSH content (19 % ) and SOD activity (52 % ) of ischemic hemispheres, whereas fullerene nanoparticles increased the GSH content and SOD activity of ischemic hemispheres by 19 % and 52 % before MCAO, respectively, and 21 % and 55 % after MCAO, respectively. Our findings indicate that fullerene nanoparticles, as a potent scavenger of free radicals, protect the brain cells against ischemia/reperfusion injury and inhibit brain oxidative/nitrosative damage.