During the past several decades, the incidence of exertional heat stroke (EHS) has increased dramatically. Despite an improved understanding of this syndrome, numerous controversies still exist within the scientific and health professions regarding diagnosis, pathophysiology, risk factors, treatment, and return to physical activity. This review examines the following eight controversies: ) reliance on core temperature for diagnosing and assessing severity of EHS; ) hypothalamic damage induces heat stroke and this mediates "thermoregulatory failure" during the immediate recovery period; ) EHS is a predictable condition primarily resulting from overwhelming heat stress; ) heat-induced endotoxemia mediates systemic inflammatory response syndrome in all EHS cases; ) nonsteroidal anti-inflammatory drugs for EHS prevention; ) EHS shares similar mechanisms with malignant hyperthermia; ) cooling to a specific body core temperature during treatment for EHS; and ) return to physical activity based on physiological responses to a single-exercise heat tolerance test. In this review, we present and discuss the origins and the evidence for each controversy and propose next steps to resolve the misconception.
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http://dx.doi.org/10.1152/japplphysiol.00452.2019 | DOI Listing |
Front Med (Lausanne)
December 2024
Department of Nursing, General Hospital of Southern Theatre Command of PLA, Guangzhou, Guangdong, China.
Introduction: Early prediction of multiple organ dysfunction syndrome (MODS) secondary to severe heat stroke (SHS) is crucial for improving patient outcomes. This study aims to develop and validate a risk prediction model for those patients based on immediate assessment indicators on ICU admission.
Methods: Two hundred eighty-four cases with SHS in our hospital between July 2009 and April 2024 were retrospectively reviewed, and categorized into non-MODS and MODS groups.
Ther Adv Hematol
January 2025
Department of Intensive Care Unit, General Hospital of Southern Theatre Command of PLA, #111 Liuhua Road, Guangzhou, 510010, Guangdong, China.
Background: Heat stroke (HS), a potentially fatal heat-related illness, is often accompanied by disseminated intravascular coagulation (DIC) early, resulting in a poorer prognosis. Unfortunately, diagnosis by current DIC scores is often too late to identify DIC. This study aims to investigate the predictors and predictive model of DIC in HS to identify DIC early.
View Article and Find Full Text PDFEnviron Res
January 2025
School of Public Health, Wuhan University of Science and Technology, Wuhan 430065, China. Electronic address:
Background: Although the association of short-term ozone and heatwave exposure with cerebrovascular disease has been well documented, it remains largely unknown whether their co-exposure could synergistically trigger ischemic stroke (IS) mortality.
Methods: We performed an individual-level, time-stratified case-crossover analysis utilizing province-wide IS deaths (n =59079) in warm seasons (May-September) during 2016-2019, across Jiangsu, eastern China. Heatwave was defined according to a combination of multiple temperature thresholds (90-97.
Mol Neurobiol
January 2025
Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi, China.
Dysregulation of long non-coding RNAs (lncRNAs) is implicated in the pathophysiology of ischemic stroke (IS). However, the molecular mechanism of the lncRNA SERPINB9P1 in IS remains unclear. Our study aimed to explore the role and molecular mechanism of the lncRNA SERPINB9P1 in IS.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 20201, USA.
Brain ischemia causes disruption in cerebral blood flow and blood-brain barrier integrity, which are normally maintained by astrocyte endfeet. Emerging evidence points to dysregulation of the astrocyte translatome during ischemia, but its effects on the endfoot translatome are unknown. In this study, we aimed to investigate the early effects of ischemia on the astrocyte endfoot translatome in a rodent cerebral ischemia and reperfusion model of stroke.
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