Heat stroke (HS) is a fatal disease caused by thermal damage in the body, and it has a very high mortality rate. In 2015, the People’s Liberation Army Professional Committee of Critical Care Medicine published the first expert consensus on HS in China, Expert consensus on standardized diagnosis and treatment for heat stroke . With an increased understanding of HS and new issues that emerged during the HS treatment in China in recent years, the 2015 consensus no longer meet the requirements for HS prevention and treatment. It is necessary to update the consensus to include the latest research evidence and establish a new consensus that has broader coverage, is more practical and is more in line with China’s national conditions. This new expert consensus includes new concept of HS, recommendations for laboratory tests and auxiliary examinations, new understanding of diagnosis and differential diagnosis, On-site emergency treatment and In-hospital treatment, translocation of HS patients and prevention of HS.

Heat stroke is the most severe type of heat illness, it is often accompanied by severe multiorgan damage and has a high fatality rate. In January 2020, based on new research evidence and the experiences of Chinese experts in heat stroke, the Expert Group of Heat Stroke Prevention and Treatment of the Chinese People’s Liberation Army (PLA) and the Professional Committee of Critical Care Medicine of the Chinese PLA jointly issued a new Expert Consensus on the Diagnosis and Treatment of Heat Stroke in China . This article aims to interpret and supplement the major updates to the new consensus.

Heat stroke (HS) is a critical condition with extremely high mortality. Heat acclimation (HA) is widely recognized as the best measure to prevent and protect against HS. Preventive administration of oral rehydration salts III (ORSIII) and probiotics have been reported to sustain intestinal function in cases of HS. This study established a rat model of HA that was treated with probiotics-based ORS (ORSP) during consecutive 21-day HA training. The results showed that HA with ORSP could attenuate HS-induced hyperthermia by regulating thermoregulatory response. We also found that HA with ORSP could significantly alleviate HS-induced multiple organ injuries. The expression levels of a series of heat-shock proteins (HSPs), including HSP90, HSP70, HSP60, and HSP40, were significantly up-regulated from the HA training. The increases in intestinal fatty acid binding protein (I-FABP) and D-Lactate typically seen during HS were decreased through HA. The representative TJ proteins including ZO-1, E-cadherin, and JAM-1 were found to be significantly down-regulated by HS, but sustained following HA. The ultrastructure of TJ was examined by TEM, which confirmed its protective effect on the intestinal barrier protection following HA. We also demonstrated that HA raised the intestinal levels of beneficial bacteria Lactobacillus and lowered those of the harmful bacteria Streptococcus through 16S rRNA gene sequencing. These findings suggest that HA with ORSP was proven to improve intestinal thermotolerance and the levels of protective gut microbiota against HS.

Heat stroke (HS) is a severe condition associated with prolonged exposure to high temperatures, leading to systemic inflammation and multi-organ damage. Disruption of the intestinal barrier plays a crucial role in HS progression by allowing endotoxins to enter circulation and trigger widespread inflammation. Lactoferrin (LF), known for its immune-modulating and barrier-protective properties, shows promise in mitigating HS-related damage. This study investigated the protective effects of LF on the intestinal barrier under HS conditions using in vitro and in vivo models. In Caco-2 cell monolayers exposed to heat stress, LF improved barrier integrity by increasing transepithelial electrical resistance (TEER) and maintaining tight junctions. In mice, LF supplementation enhanced heat tolerance, delayed HS onset, and reduced multi-organ damage, whereas LF knockout (KO) mice exhibited exacerbated damage. Further analysis revealed that heat stress induced ferroptosis by suppressing GPX4 and SLC7A11, contributing to intestinal injury. LF alleviated ferroptosis by upregulating these proteins and reducing Fe²⁺ accumulation, reactive oxygen species (ROS) generation, and lipid peroxidation. Additionally, LF inhibited heat stress-induced activation of the MAPK pathway by suppressing the phosphorylation of p38, ERK, and JNK, suggesting that MAPK signaling mediates its protective effects. These findings suggest that LF supplementation may enhance heat tolerance and prevent HS-induced intestinal barrier damage through ferroptosis inhibition and MAPK pathway regulation.