Abstract:BackgroundIncreased systemic cytokines and elevated brain levels of monoamines, and hydroxyl radical productions are thought to aggravate the conditions of cerebral ischemia and neuronal damage during heat stroke. Dexamethasone (DXM) is a known immunosuppressive drug used in controlling inflammation, and hydroxyethyl starch (HES) is used as a volume-expanding drug in cerebral ischemia and/or cerebral injury. Acute treatment with a combined therapeutic approach has been repeatedly advocated in cerebral ischemia… Show more
“…Animals were then returned to their cages with free access to food and water [18][19][20][21]. The following day, they were heated in a water-bath at 38°C for 5 h [22,23]. This process was repeated every 2 days.…”
Section: A Murine Model Of Cerebral Ischemiamentioning
“…Animals were then returned to their cages with free access to food and water [18][19][20][21]. The following day, they were heated in a water-bath at 38°C for 5 h [22,23]. This process was repeated every 2 days.…”
Section: A Murine Model Of Cerebral Ischemiamentioning
“…Among several mechanisms proposed to give rise to heat stroke-induced brain injury, ischemia is thought to induce restricted diffusion. Ischemia of brain tissue results from attempts of the body's autoregulatory mechanisms to divert blood flow towards periphery to dissipate excessive heat (21,22). Increased intracranial pressure secondary to venous congestion and brain edema as the result of increased permeability of blood-brain or blood-cerebrospinal fluid barrier may also…”
We report a case of heat stroke in which detection of brain injury was improved by high b-value diffusion-weighted imaging (DWI). High b-value DWI revealed moderate to marked hyperintensity at/ around bilateral dentate nuclei and part of thalami. Apparent diffusion coefficient (ADC) maps revealed ADC decrease of the dentate lesions. Routine DWI showed only mild hyperintensity of part of dentate lesions. High b-value DWI could be valuable for improved detection of heat stroke-induced brain injury.
“…In recent years, several studies have confirmed these findings in comparable rodent models of CHS (peak T core =~43.5 • C). For example, prior corticosteroid injection was shown to inhibit GI MT and improve survival [53][54][55], whereas indomethacin injection enhanced gross morphological GI hemorrhage and worsened survival [56]. Similarly, direct intravenous endotoxin injection prior to sub-lethal CHS in rodents (peak T core =~42-43 • C) unexpectedly led to fatalities in 40% of animals (versus 0% in controls; [57]), or best-case increased symptoms of multiple-organ injury [58].…”
Section: The Gi Exertional Heat Stroke Paradigmmentioning
Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.
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