Pathophysiological Changes Occuring in Cardiovascular and Immune Systems In Response to Stress

Cardiovascular and immune system pathophysiological changes and diseases  may be attributed to stress. Sometimes stress may be beneficial when it is not 'overwhelming' as it ,may improve performance in certain cases. Modern medicine is focusing on the close relationship between stress and cardiovascular and immune system morbidity  and mortality. New therapeutic strategies have to be set in place.Brief naturalistic stressors (such as exams) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity; tended to suppress cellular immunity while preserved humoral immunity On the other hand chronic stressors were associated with suppression of both cellular and humoral immunity. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.In mammals, physiological responses such as “fight or flight.” to chronic stressors , include changes that increase the delivery of oxygen and glucose to the heart and the large skeletal muscles. The changes in Immune responses to stressful situations may be part of these adaptive responses..Pychological challenges are capable of modifying various features of the immune response

Forced Swimming-Induced Depressive-like Behavior and Anxiety Are Reduced by Chlorpheniramine via Suppression of Oxidative and Inflammatory Mediators and Activating the Nrf2-BDNF Signaling Pathway

The first-generation antihistamine chlorpheniramine (CPA) is believed to have both anxiolytic and antidepressant properties. The current study sought to assess the mechanisms behind the antidepressant and anxiolytic effects of CPA therapy concerning oxidative stress, inflammation, and nuclear factor p45 for erythroid 2-Brain-derived neurotrophic factor (Nrf2-BDNF) signaling pathway in forced swimming-induced depressive-like behavior and anxiety. Eighteen male Wistar rats (180–200 gm) rats were separated into three groups (n = 6): a stressed group (acute stress) that underwent the forced swimming test (FST) and a stressed group that received pretreatment with CPA (10 mg/kg body weight) for 3 weeks (CPA + acute stress). Animals were subsequently put through the following behavioral tests after undergoing a forced swim test (FST) for 5 min: an immobility test, open field test, and elevated plus maze test. Serum cortisol levels were measured when the rats were euthanized at the end of the experiments. Brain neurotransmitters (cortisol, serotonin, and noradrenaline), oxidative stress (SOD and MDA), inflammatory (IL-6 and IL-1) biomarkers, and the Nrf2-BDNF signaling pathway in the hippocampus and cerebral cortex tissues was determined. CPA prevented stress-induced increases in cortisol levels (p < 0.0001), decreased brain neurotransmitters, and increased oxidative stress and inflammation. CPA also upregulated the Nrf2-BDNF signaling pathway. Thus, CPA mitigates depressive-like behavior and anxiety by inhibiting oxidative stress and inflammation and upregulating the Nrf2-BDNF signaling pathway in the brain tissues