Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease
Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. The current paradigm in the pathophysiology and prevention of H...
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| Format: | Journal Article |
| Language: | English |
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2018
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| Online Access: | https://hdl.handle.net/10356/89249 http://hdl.handle.net/10220/47061 |
| _version_ | 1811693370639122432 |
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| author | Lim, Chin Leong |
| author2 | Lee Kong Chian School of Medicine (LKCMedicine) |
| author_facet | Lee Kong Chian School of Medicine (LKCMedicine) Lim, Chin Leong |
| author_sort | Lim, Chin Leong |
| collection | NTU |
| description | Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. The current paradigm in the pathophysiology and prevention of HS focuses predominantly on heat as the primary trigger and driver of HS, which has not changed significantly for centuries. However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. Exposure to heat and exercise stresses independently promote the translocation of lipopolysaccharides (LPS) from gram-negative bacteria in the gut to blood in the circulatory system. Blood concentration of LPS can increase to a threshold that triggers the systemic inflammatory response, leading to the downstream ramifications of cellular and organ damage with sepsis as the end point i.e., heat sepsis. The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS. |
| first_indexed | 2024-10-01T06:50:36Z |
| format | Journal Article |
| id | ntu-10356/89249 |
| institution | Nanyang Technological University |
| language | English |
| last_indexed | 2024-10-01T06:50:36Z |
| publishDate | 2018 |
| record_format | dspace |
| spelling | ntu-10356/892492020-11-01T05:25:48Z Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease Lim, Chin Leong Lee Kong Chian School of Medicine (LKCMedicine) Heat Stroke Endotoxemia Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. The current paradigm in the pathophysiology and prevention of HS focuses predominantly on heat as the primary trigger and driver of HS, which has not changed significantly for centuries. However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. Exposure to heat and exercise stresses independently promote the translocation of lipopolysaccharides (LPS) from gram-negative bacteria in the gut to blood in the circulatory system. Blood concentration of LPS can increase to a threshold that triggers the systemic inflammatory response, leading to the downstream ramifications of cellular and organ damage with sepsis as the end point i.e., heat sepsis. The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS. Published version 2018-12-18T07:23:01Z 2019-12-06T17:21:09Z 2018-12-18T07:23:01Z 2019-12-06T17:21:09Z 2018 Journal Article Lim, C. L. (2018). Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease. Antioxidants, 7(11), 149-. doi: 10.3390/antiox7110149 https://hdl.handle.net/10356/89249 http://hdl.handle.net/10220/47061 10.3390/antiox7110149 en Antioxidants © 2018 The Author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). 18 p. application/pdf |
| spellingShingle | Heat Stroke Endotoxemia Lim, Chin Leong Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease |
| title | Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease |
| title_full | Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease |
| title_fullStr | Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease |
| title_full_unstemmed | Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease |
| title_short | Heat sepsis precedes heat toxicity in the pathophysiology of heat stroke—a new paradigm on an ancient disease |
| title_sort | heat sepsis precedes heat toxicity in the pathophysiology of heat stroke a new paradigm on an ancient disease |
| topic | Heat Stroke Endotoxemia |
| url | https://hdl.handle.net/10356/89249 http://hdl.handle.net/10220/47061 |
| work_keys_str_mv | AT limchinleong heatsepsisprecedesheattoxicityinthepathophysiologyofheatstrokeanewparadigmonanancientdisease |