Acupuncture Therapy ; Adult ; Heat Stroke ; complications ; therapy ; Humans ; Male

Gastrointestinal Hemorrhage ; etiology ; Heat Stroke ; complications ; Humans ; Male ; Middle Aged ; Shock, Hemorrhagic ; etiology

OBJECTIVETo establish a rat model of heatstroke complicated by endotoxemia for studying the pathogenesis of severe heatstroke.

METHODSMale specific pathogen-free Wistar rats were randomly assigned into 4 groups, namely normothermic saline group (group C), heat exposure saline group (group H), normothermic LPS group (group L), and heat exposure LPS group (group HL). The rectal temperature (Tr), heart rate (HR), mean arterial pressure (MAP), and respiratory rate (RR) of the rats receiving different treatments were continually monitored and their white blood cell count (WBC) and histology of the lungs were observed at 0, 40, 80 and 120 min after the treatments.

RESULTSThe rats in HL-Group displayed significantly higher Tr (43.04+/-0.11 degrees C), HR (660+/-42 beats/min), and RR (150+/-11/min) but lower MAP (49.0+/-3.5 mmHg) as compared with the C Group. There were significant differences in the values of Tr, HR, RR and MAP between HL and group L and in HR and MAP between H groups HL and. The rats in group H displayed significantly higher WBC than group C. In contrast, the rats in L groups HL and had significantly lower WBC. LPS injection and heat stress induced pulmonary edema and features characteristic of acute microvascular lung injury in the rats.

CONCLUSIONThe rat model established by LPS injection and heat stress can successfully mimic the development of severe heatstroke after LPS challenge and heat stress, and provides a suitable model for studying the primordial role of the lungs in the pathogenesis of severe heatstroke.

Animals ; Disease Models, Animal ; Endotoxemia ; chemically induced ; complications ; Heat Stroke ; complications ; Lipopolysaccharides ; Male ; Random Allocation ; Rats ; Rats, Wistar

Brain Diseases ; etiology ; therapy ; Heat Stroke ; complications ; therapy ; Humans ; Hyperbaric Oxygenation ; Male ; Middle Aged ; Occupational Diseases ; complications ; therapy

Heat stroke is a potentially fatal disorder that's caused by an extreme elevation in body temperature. We report here an unusual case of multiple organ failure that was caused by classical, nonexertional heat stroke due to taking a warm bath at home. A 68 year old diabetic man was hospitalized for loss of consciousness. He was presumed to have been in a warm bath for 3 hrs and his body temperature was 41 degrees C. Despite cooling and supportive care, he developed acute renal failure, disseminated intravascular coagulation (DIC) and fulminant liver failure. Continuous venovenous hemofiltration was started on day 3 because of the progressive oligouria and severe metabolic acidosis. On day 15, septic ascites was developed and Acinetobacter baumanii and Enterococcus faecium were isolated on the blood cultures. In spite of the best supportive care, the hepatic failure and DIC combined with septic peritonitis progressed; the patient succumbed on day 25.
Multiple Organ Failure/*etiology ; Male ; Liver Failure/*etiology ; Kidney Failure/*etiology ; Humans ; Heat Stroke/*complications/etiology ; Fatal Outcome ; Baths/*adverse effects ; Aged

OBJECTIVE: To analyze the clinical characteristics and risk factors of early acute liver injury in patients with heat stroke (HS), and to provide basis for early identification of HS-related liver injury and its pathogenesis in clinical practice. METHODS: The clinical data of patients with HS admitted to the department of critical care medicine of Haian People's Hospital from June 2015 to August 2022 were retrospectively analyzed. The patients with HS were divided into early liver injury group and early non-liver injury group according to the occurrence of acute liver injury within 24 hours of admission. The differences of basic data, clinical data, laboratory indexes and clinical outcomes of the two groups were analyzed. Logistic regression was used to analyze the risk factors for early HS-related acute liver injury, and receiver operator characteristic (ROC) curves were drawn to evaluate their value in predicting the occurrence of early HS-related acute liver injury. RESULTS: A total of 76 patients with HS were enrolled, and 46 patients with acute liver injury, accounting for 60.53%. In the early liver injury group, 14 patients (30.43%) had elevated aminotransferase alone, 9 patients (19.57%) had elevated total bilirubin (TBil) alone, and 23 patients (50.00%) had elevated both aminotransferase and TBil. Among the patients with elevated aminotransferases, 24 patients (64.87%) had mild elevation, 5 patients (13.51%) had moderate elevation, 8 patients (21.62%) had severe elevation. Compared with the early non-liver injury group, acute physiology and chronic health evaluation II (APACHE II), sequential organ failure assessment (SOFA), arterial blood lactate (Lac), interleukin-6 (IL-6), procalcitonin (PCT), alanine aminotransferase (ALT), aspartate aminotransferase (AST), TBil, γ-gamma glutamyl transferase (γ-GGT), lactate dehydrogenase (LDH), creatine kinase (CK), MB isoenzyme of creatine kinase (CK-MB), cardiac troponin I (cTnI), myoglobin (MYO), N-terminal B-type pro-brain natriuretic peptide (NT-proBNP), prothrombin time (PT), activated partial thromboplastin time (APTT), D-dimer in the early liver injury group were significantly increased, while platelet count (PLT) were significantly decreased within 24 hours after admission, the 28-day mortality was significantly increased [28.26% (13/46) vs. 6.67% (2/30)], and the differences were statistically significant (all P < 0.05). Univariate Logistic regression analysis showed that APACHE II score, SOFA score, PLT, Lac, IL-6, PCT, γ-GGT, LDH, CK, CK-MB, cTnI, MYO, PT, APTT, D-dimer were risk factors of early HS-related acute liver injury (all P < 0.05). Multivariate Logistic regression analysis showed that PLT, IL-6, and LDH were independent risk factors of early HS-related acute liver injury [odds ratio (OR) and 95% confidence interval (95%CI) were 0.986 (0.974-0.998), 1.027 (1.012-1.041), and 1.002 (1.000-1.004), all P < 0.05]. The ROC curve analysis showed that the area under the ROC curve (AUC) of PLT, IL-6 and LDH for predicting the occurrence of early HS-related acute liver injury was 0.672 (95%CI was 0.548-0.797), 0.897 (95%CI was 0.824-0.971) and 0.833 (95%CI was 0.739-0.927), respectively. IL-6 had the highest predictive value for early HS-related liver injury. When the optimal diagnostic threshold of IL-6 was 48.25 ng/L, the sensitivity was 95.7%, the specificity was 73.3%, and the predictive value of PLT was the lowest. CONCLUSIONS The early HS-related liver injury is mainly manifested as the simultaneous elevation of aminotransferase and TBil, and most of cases are mild liver injury. PLT, IL-6 and LDH are independent risk factors of early HS-related acute liver injury.
Humans ; Prognosis ; Retrospective Studies ; Interleukin-6 ; ROC Curve ; Sepsis/diagnosis* ; Heat Stroke/complications* ; Risk Factors ; Alanine Transaminase ; Creatine Kinase, MB Form ; Lactic Acid ; Creatine Kinase

OBJECTIVETo investigate whether Chinese medicine (CM) syndrome is associated with particular molecular mechanism, we explored the correlation between CM syndrome and changes of intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase 9 (MMP-9) and heat shock protein 70 (HSP70) in patients with ischemic stroke, which were reported to play an important role in the inflammatory and apoptosis cascade.

METHODSCM syndrome factors of 175 patients with ischemic stroke were assessed using Ischemic Stroke CM Syndrome Factor Diagnostic Scale (ISTSFDS). The patients were grouped according to the main syndrome factor combinations at different time points based on distribution probability of syndrome factor combinations. Blood levels of ICAM-1, MMP-9 and HSP70 were quantified by enzyme-linked immunosorbent assay.

RESULTSICAM-1 expression was significantly higher in the internal-wind+phlegm-dampness+blood-stasis, phlegmdampness+ blood-stasis, internal-fire+phlegm-dampness+blood-stasis group than that in the blood-stasis+qideficiency group within 72 h from stroke onset (P <0.05); HSP70 expression was significantly lower in the phlegm-dampness+blood-stasis, internal-fire+phlegm-dampness+blood-stasis, blood-stasis group than that in the phlegm-dampness+blood-stasis+qi-deficiency group on the 7th day from stroke onset (P<0.05).

CONCLUSIONSPhlegm-dampness and blood-stasis exist through the whole process of ischemic stroke. An increased level of ICAM-1 and a reduced level of HSP70 reflect the pathological state of phlegm-stasis mutual binding. These results suggest that inflammation and apoptosis induced by cerebral vascular injury in the pathological processes of ischemic stroke are more prominent in the excess syndrome state like phlegm-dampness and blood-stasis.

Biomarkers ; blood ; Brain Ischemia ; blood ; complications ; Female ; HSP70 Heat-Shock Proteins ; blood ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; Male ; Matrix Metalloproteinase 9 ; blood ; Medicine, Chinese Traditional ; Middle Aged ; Probability ; Stroke ; blood ; complications ; Syndrome ; Time Factors

OBJECTIVETo observe the effect of Gingerol on endotoxemia mouse induced by heatstroke.

METHODSForty mice were randomly divided into five groups, the endotoxemia model group (A), the normal temperature group (B), the Gingerol treated group (C), the solvent control group (D), and the saline control group (E), 8 mice in each group. Group B to E was administered with saline, Gingerol, solvent and saline respectively. Mice in group B were placed at room temperature 25 +/- 0.5 degrees C , relative humidity 43 +/- 5 % for 2 hrs, while mice in the other groups were exposed under 35 +/- 0.5 degrees C and relative humidity 65 +/- 5 % for 2 hrs in an artificial hot-climate mimic cabin to establish heatstroke endotoxemia model. The energy metabolic level of celiomacrophage was detected with MTT; the phagocytic ability was examined with neutral red chromometry; the hepatocyte ultrastructure was observed with transmission electron microscopy, as well as the activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in plasma was tested.

RESULTSAs compared with Group A, D and E, in Group C, energy metabolic levels of macrophage, phagocytic ability, and activity of SOD were significantly higher (P < 0.01), and the level of MDA was significantly lower respectively (P < 0.01), with the levels of SOD and MDA approaching to those in Group B (P >0.05). The pathologic changes of hepatocyte ultrastructure in group C were less than those in the other three endotoxemia groups.

CONCLUSIONGingerol could raise the energy metabolic level of celio-macrophage to enhance its phagocytic ability, increase the activity of SOD and reduce the production of MDA in mouse with heatstroke endotoxemia, so as to alleviate the liver damage.

Animals ; Catechols ; Endotoxemia ; drug therapy ; etiology ; Fatty Alcohols ; isolation & purification ; pharmacology ; therapeutic use ; Female ; Ginger ; chemistry ; Heat Stroke ; complications ; Macrophages ; immunology ; Male ; Mice ; Phagocytosis ; drug effects ; Phytotherapy ; Random Allocation