Blast overpressure has become an increasing cause of brain injuries in both military and civilian populations. Though blast's direct effects on the cochlea and vestibular organs are active areas of study, little attention has been given to the ear's contribution to the overall spectrum of blast injury. Acute autonomic responses to blast exposure, including bradycardia and hypotension, can cause hypoxia and contribute to blast-induced neurotrauma. Existing literature suggests that these autonomic responses are elicited through blast impacting the thorax and lungs. We hypothesize that the unprotected ear also provides a vulnerable locus for blast to cause autonomic responses. We designed a blast generator that delivers controlled overpressure waves into the ear canal without impacting surrounding tissues in order to study the ear's specific contribution to blast injury. Anesthetized adult rats' left ears were exposed to a single blast wave ranging from 0 to 110 PSI (0-758 kPa). Blast exposed rats exhibited decreased heart rates and blood pressures with increased blast intensity, similar to results gathered using shock tubes and whole-body exposure in the literature. While rats exposed to blasts below 50 PSI (345 kPa) exhibited increased respiratory rate with increased blast intensity, some rats exposed to blasts higher than 50 PSI (345 kPa) stopped breathing immediately and ultimately died. These autonomic responses were significantly reduced in vagally denervated rats, again similar to whole-body exposure literature. These results support the hypothesis that the unprotected ear contributes to the autonomic responses to blast.
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http://dx.doi.org/10.1016/j.joto.2018.01.001 | DOI Listing |
Sci Rep
January 2025
Department of Psychology, Division of Neuropsychology, University of Constance, Fach 905, Universitaetsstrasse 10, 78464, Constance, Germany.
Adverse early-life experiences alter the regulation of major stress systems such as the hypothalamic-pituitary-adrenal (HPA) axis. Low early-life maternal care (MC) has repeatedly been related to blunted cortisol stress responses. Likewise, an acutely increased awareness of mortality (mortality salience [MS]) also has been shown to blunt cortisol responses.
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Department of Psychiatry, The Yale Stress Center, Yale University School of Medicine, New Haven, Connecticut, USA.
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View Article and Find Full Text PDFJ Affect Disord
January 2025
Kolling Institute, Faculty of Medicine and Health, The University of Sydney, Sydney, NSW, Australia; John Walsh Centre Rehabilitation Research, Northern Sydney Local Health District, St Leonards, Sydney, NSW, Australia.
Background: Traumatic physical injuries can lead to psychological distress and increased risk of psychiatric disorders, often reflected in dysregulated autonomic responses measurable through heart rate variability (HRV). Slow-paced breathing has shown potential in enhancing HRV, but its effectiveness in injured survivors remains unexplored. This study investigates the effect of slow-paced breathing on HRV among injured survivors compared to non-injured individuals and explores the influence of psychological distress and spontaneous respiratory rate on this effect.
View Article and Find Full Text PDFJ Clin Neurol
January 2025
Department of Brain and Cognitive Engineering, Korea University, Seoul, Korea.
Background And Purpose: Obstructive sleep apnea (OSA) is associated with an increased risk of adverse outcomes, including mortality. Machine-learning algorithms have shown potential in predicting clinical outcomes in patients with OSA. This study aimed to develop and evaluate a machine-learning algorithm for predicting 10- and 15-year all-cause mortality in patients with OSA.
View Article and Find Full Text PDFEur J Haematol
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Hematology and Transplant Center, University Hospital "San Giovanni di Dio e Ruggi d'Aragona", Salerno, Italy.
Brentuximab-vedotin (BV)-induced neurotoxicity (BVIN), a frequent adverse event caused by this monoclonal antibody, is the primary reason for dose modification or drug discontinuation, and is characterized by sensory, motor, and/or autonomic peripheral nerve dysfunctions. Although reversible, BVIN can persist for months or years after treatment and negatively affect quality of life (QoL). Currently, BVIN is managed by dose adjustment or drug interruption, leading to an increased risk of disease relapse.
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