Chronic heart failure: a disease of the brain

摘要: The underlying mechanism for clinical and biochemical manifestations of chronic heart failure (HF) may be due in part to neurohumoral adaptations, such as activation the renin-angiotensin-aldosterone sympathetic nervous systems periphery brain. Internet search discussion with colleagues are methods this study. Since HF is associated autonomic imbalance increased nerve activity a withdrawal parasympathetic activity, it considered brain disease. This phenomenon result an systemic cerebral angiotensin II signaling because plasma humans animals HF. increase enhances through actions on both central peripheral sites during Activation different paraventricular nucleus (PVN), rostral ventrolateral medulla (RVLM), area postrema (AP) release norepinephrine, oxidative stress, inflammation leading cardiac contractility. It possible that blocking type 1 receptors decreases afferent reflex when therapy administered PVN. administration receptor blocker by injection into AP activates sympatho-inhibitory baroreflex indicating blockers act increasing activity. In HF, regions, elevates norepinephrine synthesis inhibits uptake at endings, which contribute Increased circulating enhance sympatho-excitatory chemoreflex inhibit resulting worsening can directly system via subfornical organ outflow dysfunction, failure.