Articles: pressoreceptors-physiology.
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Baroreceptors are mechanosensitive elements of the peripheral nervous system that maintain homeostasis by coordinating physiologic responses to external and internal stimuli. While it is recognized that carotid and cardiopulmonary baroreceptor reflexes modulate autonomic output to mitigate excessive fluctuations in arterial blood pressure and to maintain intravascular volume, increasing evidence suggests that baroreflex pathways also project to key regions of the central nervous system that regulate somatosensory, somatomotor, and central nervous system arousal. ⋯ The contribution of baroreceptor function to postoperative outcomes is also presented. Finally, methods that enhance baroreceptor function, which hold promise in improving postoperative and pain management outcomes, are presented.
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Reduced baroreflex sensitivity (BRS) has been reported in patients with acute cardiovascular events. We tested the hypothesis that BRS is substantially reduced in patients with spontaneous intracerebral hemorrhage (ICH) and that BRS can predict treatment outcomes. ⋯ Based on our results, BRS value at admission is a more powerful predictor of outcome than the Glasgow Coma Scale score at admission. An assay of BRS could be added as a biomarker for outcome prediction among patients with spontaneous ICH in clinical practice.
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Hypertension is the largest threat to patient health and a burden to health care systems. Despite various options, 30% of patients do not respond sufficiently to medical treatment. Mechanoreceptors in the aortic arch relay blood pressure (BP) levels through vagal nerve (VN) fibers to the brainstem and trigger the baroreflex, lowering the BP. Selective electrical stimulation of these nerve fibers reduced BP in rats. However, there is no technique described to localize and stimulate these fibers inside the VN without inadvertent stimulation of non-baroreceptive fibers causing side effects like bradycardia and bradypnea. ⋯ The presented method is robust to impedance changes, independent of the electrode's relative position, does not compromise the nerve and can run on implantable, ultra-low power signal processors.
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Anesthesia and analgesia · Mar 2012
ReviewThe Bainbridge and the "reverse" Bainbridge reflexes: history, physiology, and clinical relevance.
Francis A. Bainbridge demonstrated in 1915 that an infusion of saline or blood into the jugular vein of the anesthetized dog produced tachycardia. His findings after transection of the cardiac autonomic nerve supply and injection of the cholinergic blocking drug atropine demonstrated that the tachycardia was reflex in origin, with the vagus nerves constituting the afferent limb and a withdrawal of vagal tone the primary efferent limb. ⋯ The Bainbridge reflex is invoked throughout the anesthesia literature to describe the effect of changes in venous return on heart rate in patients in the surgical and critical care settings, but a critical analysis of the experimental and clinical evidence is lacking. Our main objectives in this review are to summarize the history of the Bainbridge reflex, to describe its anatomy and physiology, and to discuss the evidence for and against it having an influence on heart rate changes observed clinically. The interaction of the Bainbridge reflex with the arterial baroreceptor and Bezold-Jarisch reflexes is discussed.
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The nucleus tractus solitarius (NTS) is essential for orchestrating baroreflex control of blood pressure. When a change in blood pressure occurs, the information is transmitted by baroreceptor afferent fibers to the central network by glutamate binding to ionotropic glutamate receptors on second-order baroreceptor neurons. Glutamate also activates presynaptic group II and III metabotropic glutamate receptors (mGluRs), depressing both glutamate and GABA release to modulate baroreceptor signal transmission. ⋯ Group II mGluR induced-currents consisted of voltage-dependent outward and inward components, prevented by tetraethylammonium chloride and tetrodotoxin, respectively. In contrast to group II mGluR-induced hyperpolarization, there was no effect on intrinsic excitability as determined by action potential shape or firing in response to depolarizing current injections. The data suggest a novel mechanism for postsynaptic group II mGluRs to fine-tune baroreceptor signal transmission in the NTS.