SUMMAR Y Since previous data of our group showed increased concentrations in HPA axis hormones in sleep deprived rats, we hypothesized that this augmentation could produce effects in other hormonal systems, particularly in the sexual system. Considering that little is known about how the hormonal system changes during the recovery period after sleep deprivation (SD), our objective was to examine from what point SD alters sexual and stress-related hormones along with plasma catecholamine concentrations during 4 days. We also sought to verify the time course of their recovery after an equivalent period of recovery sleep. Rats were deprived of sleep by the platform technique for 1-4 days and were allowed to recover for the same period. Plasma catecholamines [dopamine (DA) and noradrenaline (NOR)], testosterone, estrone, progesterone, prolactin, corticosterone and adrenocorticotropic hormone (ACTH) concentrations were measured. Comparisons between groups showed that the SD procedure used in the present study produced marked alterations in almost all studied hormones from 24 h of SD, except for estrone and prolactin (which required 96 h of SD to become altered). Testosterone and estrone decreased, whereas progesterone, prolactin, corticosterone, ACTH, DA and NOR increased. During recovery period, progesterone, prolactin and corticosterone concentrations returned to control levels, whereas testosterone, estrone, NOR and DA did not. In addition, after 48 h of recovery ACTH and NOR decreased below control concentrations, remaining low until 96 h of sleep recovery. Thus, SD showed long lasting, differential effects upon these neurochemicals suggesting that each has its own pattern of responses to SD as well as variable periods of recovery.k e y w o r d s catecholamines, corticosterone, prolactin, rebound, sleep deprivation, testosterone INTRODUCTIONSleep loss is considered a health risk factor that contributes to several disease processes (Miller and Bartus, 1982), reduces longevity (Kripke, 1979) and leads to behavioral (Andersen et al., 2000(Andersen et al., , 2003Tufik et al., 1978), hormonal (Andersen et al., 2004a;Spiegel et al., 1999) and neurochemical (D'Almeida et al., 1998;Farooqui et al., 1996;Martins et al., 2004;Pedrazzoli et al., 2004) alterations.The endocrine system is responsible for physiological integration of multiple organs by different actions of the endocrine axis. However, hormonal effects are not only determined by circulating levels, but also by the time that the organ is exposed to a specific hormone. For example, an acute rise in cortisol concentration is associated with increased attention (Erickson et al., 2003) but raised concentrations, sustained chronically, reduce synaptic and neuronal populations in the hippocampus (Magarin˜os et al., 1998). Because sleep deprivation (SD) induces profound changes in the secretory patterns in distinct endocrine axes in humans, the investigation of hormone secretion could provide some insight Correspondence: Rua Napolea˜o de Barros,

IntroductionPatients and family members undergo different experiences of suffering from emotional disorders during ICU stay and after ICU discharge. The purpose of this study was to compare the incidence of anxiety, depression and post-traumatic stress disorder (PTSD) symptoms in pairs (patient and respective family member), during stay at an open visit ICU and at 30 and 90-days post-ICU discharge. We hypothesized that there was a positive correlation with the severity of symptoms among pairs and different patterns of suffering over time.MethodsA prospective study was conducted in a 22-bed adult general ICU including patients with >48 hours stay. The Hospital Anxiety and Depression Scale (HADS) was completed by the pairs (patients/respective family member). Interviews were made by phone at 30 and 90-days post-ICU discharge using the Impact of Event Scale (IES) and the HADS. Multivariate models were constructed to predict IES score at 30 days for patients and family members.ResultsFour hundred and seventy one family members and 289 patients were interviewed in the ICU forming 184 pairs for analysis. Regarding HADS score, patients presented less symptoms than family members of patients who survived and who deceased at 30 and 90-days (p<0.001). However, family members of patients who deceased scored higher anxiety and depression symptoms (p = 0.048) at 90-days when compared with family members of patients who survived. Patients and family members at 30-days had a similar IES score, but it was higher in family members at 90-days (p = 0.019). For both family members and patients, age and symptoms of anxiety and depression during ICU were the major determinants for PTSD at 30-days.ConclusionsAnxiety, depression and PTSD symptoms were higher in family members than in the patients. Furthermore, these symptoms in family members persisted at 3 months, while they decreased in patients.

Bacterial recognition and induced cellular activation are fundamental for the host control of infection, yet the limit between protective and harmful response is still inexact. Forty-one patients were enrolled in this study: 14 with sepsis, 12 with severe sepsis, and 15 with septic shock. Seventeen healthy volunteers (HV) were included as control. The expression of TLR2, TLR4, CD14, CD11b, and CD11c was analyzed on monocytes surface in whole blood. sCD14 was measured in serum, and TNF-alpha, IL-6, and IL-10 cytokine levels were measured in PBMC supernatants after LPS, IL-1beta, and TNF-alpha stimuli by ELISA. An increase in sCD14 and a decreased mCD14 were found in patients as compared with HV (P < 0.001). However, no differences in the expression of TLR2, TLR4, and CD11c were found among the groups. A trend toward differential expression of CD11b was observed, with higher values found in patients with sepsis as compared with HV. A negative regulation of the inflammatory cytokine production was observed in patients with severe sepsis and shock septic in relation to sepsis and HV, regardless of the stimulus. No significant difference in IL-10 production was found among the groups. In this study, we show that the inflammatory response is associated with the continuum of clinical manifestations of sepsis, with a strong inflammatory response in the early phase (sepsis) and a refractory picture in the late phases (severe sepsis and septic shock). Correlation between cell surface receptors and cytokine production after IL-1beta and TNF-alpha stimuli and the observation of a single and same standard response with the different stimulus suggest a pattern of immunology response that is not dependent only on the expression of the evaluated receptors and that is likely to have a regulation in the intracellular signaling pathways.

Background Infection control depends on adequate microbe recognition and cell activation, yet inflammatory response may lead to organ dysfunction in sepsis. The aims of this study were to evaluate cell activation in the context of sepsis and its correlation with organ dysfunction.

There is increasing evidence to support the hypothesis that reactive oxygen species (ROS) play a role in the pathophysiology of arterial hypertension. The ROS, particularly the superoxide anions (O 2 − ), are important intracellular messengers for Angiotensin II (Ang II) action in the brain. Ang II increases the activity of NAD(P)H oxidase, the major source of O 2 − in the vasculature, and enhances O 2 − production, both systemically and in the central nervous system. 1,2,3 For instance, intracerebroventricular infusion of NAD(P)H oxidase inhibitor antagonizes the increase in renal sympathetic nerve activity (RSNA) and the pressor response induced by centrally mediated Ang II actions. 3,4 In the brain, overexpression of superoxide dismutase (SOD), the enzyme responsible for O 2 − breakdown, also abolishes the central pressor effect of the octapeptide. 5 There is evidence to suggest that the central nervous system is involved in the development and maintenance of arterial hypertension. 6 However, the precise mechanisms by which the central nervous system participates in the evolution of arterial hypertension remains unclear and depends on the specific origin and phase of the hypertensive state. It is well known that in the 2K-1C (two-kidney one-clip) Goldblatt hypertension, the rostral ventrolateral medulla (RVLM) is one of the most important regions involved in the hypertension. 7 Therefore, the first aim of the present study was to examine whether there is an increase in oxidative stress within the RVLM in 2K-1C hypertension. For this purpose, the NAD(P)H oxidase subunits (p47phox and gp91phox) and CuZnSOD mRNA expression were quantified in the RVLM of 2K-1C hypertensive rats.Tai et al. 8 found that in SHR, elevated O 2 − radical production in the RVLM was associated with increased sympathetic nervous system activity; however, this mechanism had not been tested in a renovascular hypertension model. The second aim of the present study was therefore to examine whether oxidative stress is involved in the maintenance of sympathetic vasomotor tone and hypertension in 2K-1C rats. For this purpose, we injected directly into the RVLM the antioxidant ascorbic acid (vitamin C-Vit C), that acts as a free radical Background Oxidative stress is a state in which excess reactive oxygen species (rOS) overwhelm endogenous antioxidant systems. It is known that this state has been involved in the development of hypertension. On the basis of previous data, we hypothesized that overactivity of naD(P)H oxidase-derived rOS and the lowered activity of CuZnSOD, an endogenous antioxidant within the rostral ventrolateral medulla (rVLM), could contribute to 2K-1C (two-kidney one-clip) hypertension. Moreover, to test the functional significance of whether oxidative stress was involved in the maintenance of sympathetic vasomotor tone and blood pressure in 2K-1C hypertension, we administered ascorbic acid (Vit C), an antioxidant, into the rVLM or systemically.