Chronic stress results in physiological and somatic changes. It has been recognized as a risk factor for several cardiovascular dysfunctions and changes in autonomic mechanisms, such as baroreflex and chemoreflex activity. However, the effects of different types of chronic stress on these mechanisms are still poorly understood. Therefore, in the present study we investigated, in adult male rats, the effect of repeated restraint stress (RRS) or chronic variable stress (CVS) on baroreflex, chemoreflex and heart rate variability in a protocol of 14 days of stress sessions. Exposure to RRS and CVS indicated no changes in basal level of neither pressure arterial nor heart rate. However, RRS and CVS were able to attenuate sympathovagal modulation and spontaneous baroreflex gain. Additionally, only RRS was able to increase the power of the low frequency band (LF) of the systolic blood pressure (SBP) spectrum, as well as the slope of linear regression of baroreflex bradycardic and tachycardic responses induced by vasoactive compounds. Additionally, our work is one of the first to show that exposure to RRS and CVS decreased the magnitude of the pressor response and potentiates respiratory responses to chemoreflex activation, which can trigger cardiovascular and respiratory pathologies. Furthermore, the basal respiratory parameters, such as minute ventilation (V_E) and tidal volume (V_T) was significantly decreased by both protocols of chronic stress. However, only CVS increased the basal respiratory frequency. In this way, the findings of the present study demonstrate the impact of chronic stress not only in depressive-like behavior, but also in alterations of the autonomic baroreflex responses and cardiocirculatory variability (systolic blood pressure and pulse interval).Our results have provided evidence that chronic stress promotes autonomic dysregulation, and impairment of baroreflex, chemoreflex and heart rate variability.

The study aimed to evaluate the antithrombotic action of Acrocomia aculeata pulp oil (AAPO) in natura, in an in vitro experimental model. AAPO was obtained by solvent extraction, and its chemical characterization was performed by gas chromatography coupled to a mass spectrometer (GC-MS). In vitro toxicity was evaluated with the Trypan Blue exclusion test and in vivo by the Galleria mellonella model. ADP/epinephrine-induced platelet aggregation after treatment with AAPO (50, 100, 200, 400, and 800 μg/mL) was evaluated by turbidimetry, and coagulation was determined by prothrombin activity time (PT) and activated partial thromboplastin time (aPTT). Platelet activation was measured by expression of P-selectin on the platelet surface by flow cytometry and intraplatelet content of reactive oxygen species (ROS) by fluorimetry. The results showed that AAPO has as major components such as oleic acid, palmitic acid, lauric acid, caprylic acid, and squalene. AAPO showed no toxicity in vitro or in vivo. Platelet aggregation decreased against agonists using treatment with different concentrations of AAPO. Oil did not interfere in PT and aPTT. Moreover, it expressively decreased ROS-induced platelet activation and P-selectin expression. Therefore, AAPO showed antiplatelet action since it decreased platelet activation verified by the decrease in P-selectin expression as well as in ROS production.

Stress may influence the autonomic regulation, pathogenesis of cardiovascular disease and play an important role in animal behavior as depression. Depression is evidenced as a significant risk factor for cardiovascular changes. This is of great importance as some studies show an association between symptoms of depression and increased risk of cardiovascular disease (CVD) morbidity. Additionality, those alterations can be alleviated by use of antidepressants such as fluoxetine, which is a selective serotonin reuptake inhibitor (SSRIs). The link between depression and cardiovascular changes is known to be mediated in part by autonomic mechanisms that contribute to the regulation of cardiovascular function. However, studies on the effects of SSRIs on cardiovascular autonomic function are inconsistent. Thus, in the present study we investigated, in adult male rats, the effect of chronic and acute treatment with fluoxetine on changes in autonomic mechanisms of baroreflex and chemoreflex induced by the repeated restraint stress (RRS) or chronic variable stress (CVS) on baroreflex and chemoreflex in a protocol of 14 days of stress sessions. The results found demonstrated that exposure to chronic stress (RRS and CVS) promove changes on cardiovascular and ventilatory responses controlled by autonomic reflexes, such as baroreflex and chemoreflex. Additionality, that chronic fluoxetine treatment for 21 days was able to prevent not only anhedonic behavior, but also of autonomic changes cardiovascular induced by chronic stress. Taken together, our results show that pharmacological treatment with fluoxetine may be also helpful to prevent cardiovascular events on account of depressive states, by correcting alterations in autonomic function.