Neuromodulation as a new avenue for resuscitation in hemorrhagic shock

Abstract

Hemorrhagic shock (HS), a major cause of early death from trauma, accounts for around 40% of mortality, with 33-56% of these deaths occurring before the patient reaches a medical facility. Intravenous fluid therapy and blood transfusions are the cornerstone of treating HS. However, these options may not be available soon after the injury, resulting in death or a poorer quality of survival. Therefore, new strategies are needed to manage HS patients before they can receive definitive care. Recently, various forms of neuromodulation have been investigated as possible supplementary treatments for HS in the prehospital phase of care. Here, we provide an overview of neuromodulation methods that show promise to treat HS, such as vagus nerve stimulation, electroacupuncture, trigeminal nerve stimulation, and phrenic nerve stimulation and outline their possible mechanisms in the treatment of HS. Although all of these approaches are only validated in the preclinical models of HS and are yet to be translated to clinical settings, they clearly represent a paradigm shift in the way that this deadly condition is managed in the future.

Non-invasive Auricular Vagus Nerve Stimulation as a Potential Treatment for Covid19-Originated Acute Respiratory Distress Syndrome

“…Furthermore, hemorrhagic shock-caused lung injury can be relieved by VNS which provokes a fall of gut permeability (Levy et al, 2012 ). VNS showed clear therapeutic effects for hemorrhagic shock mainly due to its anti-inflammatory properties while recovering lung permeability and mitigating lung injury (Powell et al, 2019 ). Thirty minutes-long VNS trains diminish TNFα and IL-6 the expression in the respiratory brainstem nuclei of developing rats, who control breathing activity of the animal (Johnson et al, 2016 ).…”

ALM Fluid Therapy Shifts Sympathetic Hyperactivity to Parasympathetic Dominance in the Rat Model of Non-Compressible Hemorrhagic Shock

“…During the early phases of hemorrhagic shock, the body compensates for blood loss by increasing heart rate (HR) and contractility, followed by baroreceptor-mediated activation of the sympathetic nervous system to increase mean arterial blood pressure (MAP) to maintain sufficient oxygen to the tissues (1,2). As ventricular filling declines and cardiac output decreases, MAP continues to fall (2). Activation of the ''fight-or-flight'' sympathetic response results in release of norepinephrine from the postganglionic nerve endings innervating the heart and other organs, and the release of norepinephrine and epinephrine from the adrenal medulla into the circulation (1,3).…”

Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress

“…The current treatments for HS include timely hemostasis, volume replacement, and whole blood or blood component therapy [ 2 – 4 ]. There have been progress in understanding hemorrhage pathophysiology and improvement in the treatment to increase survival [ 5 ]. However, the long-term consequences of HS and the development of chronic disorders, such as cardiovascular diseases including hypertension, and interventions to reduce such pathologies in survivors of HS have not been reported.…”