ABSTRACT
Heat stroke is the most serious type of heat-related diseases, and the induced multiple organ dysfunction syndrome (MODS) is an important cause of death for heat stroke patients. The cardiovascular system is one of the important targets of heat injury. Studies have reported that heat stress can lead to myocardial inhibition, abnormal heart conduction and blood flow redistribution, thus changing the hemodynamic state, leading to obvious abnormalities in electrocardiogram, echocardiography, myocardial injury biological markers and hemodynamic indicators of patients with heat stroke. In this article, the pathophysiological and histological changes and clinical manifestations of heatstroke-induced myocardial injury are reviewed, aiming to provide references for further understanding and research of myocardial damage caused by hyperthermia.
ABSTRACT
Heat stroke is the most serious type of heat-related diseases, and the induced multiple organ dysfunction syndrome (MODS) is an important cause of death for heat stroke patients. The cardiovascular system is one of the important targets of heat injury. Studies have reported that heat stress can lead to myocardial inhibition, abnormal heart conduction and blood flow redistribution, thus changing the hemodynamic state, leading to obvious abnormalities in electrocardiogram, echocardiography, myocardial injury biological markers and hemodynamic indicators of patients with heat stroke. In this article, the pathophysiological and histological changes and clinical manifestations of heatstroke-induced myocardial injury are reviewed, aiming to provide references for further understanding and research of myocardial damage caused by hyperthermia.
ABSTRACT
Heat stroke is the most serious type of heat-related diseases, and the induced multiple organ dysfunction syndrome (MODS) is an important cause of death for heat stroke patients. The cardiovascular system is one of the important targets of heat injury. Studies have reported that heat stress can lead to myocardial inhibition, abnormal heart conduction and blood flow redistribution, thus changing the hemodynamic state, leading to obvious abnormalities in electrocardiogram, echocardiography, myocardial injury biological markers and hemodynamic indicators of patients with heat stroke. In this article, the pathophysiological and histological changes and clinical manifestations of heatstroke-induced myocardial injury are reviewed, aiming to provide references for further understanding and research of myocardial damage caused by hyperthermia.
ABSTRACT
OBJECTIVE@#To investigate the effect of estrogen on expression of the cysteine-rich secretory protein containing LCCL domain 2 (CRISPLD2) in myocardium of lipopolysaccharide (LPS)-induced mice model of sepsis.@*METHODS@#Totally 12 female and 12 male Balb/c mice of specific pathogen-free (SPF) level with 7 weeks were served as objectives. The female and male mice were randomly divided into model groups and control groups, respectively, with 6 mice in each group. The model of sepsis was reproduced by intraperitoneal injection of 10% LPS (5 mg/kg), and the mice in control groups were injected with the same volume of normal saline. The general condition of mice during experiment was observed at 24 hours after injection. All the mice were sacrificed and the heart was harvested after collecting the whole blood. The concentration of estrogen in serum was determined by double antibody sandwich enzyme linked immunosorbent assay (ELISA). The myocardial tissue homogenate was prepared at the same time, and the total protein was extracted. The expression level of CRISPLD2 was determined by Western Blot. Pearson correlation analysis was used to analyze the bivariate correlation.@*RESULTS@#All of the experimental mice survived at 24 hours after injection. The mice in the model groups showed disorder and gray signs of body hair, with diarrhea and decreased appetite. No significant abnormality was observed in the control groups. There was no significant difference in the body weight or concentration of estrogen in serum between model and control group of both female and male mice [body weight (g): 24.6±1.8 vs. 24.5±1.3 in male mice, 18.0±0.8 vs. 17.5±1.1 in female mice; estrogen (ng/L): 11.93±2.59 vs. 12.17±3.87 in male mice, 28.20±5.75 vs. 29.82±6.10 in female mice, all P > 0.05]. There was no statistical difference in the expression of CRISPLD2 in myocardium between male control mice and female control mice (gray value: 1.02±0.19 vs. 1.00±0.11, P > 0.05). No significant difference in the expression of CRISPLD2 in myocardium was found between female sepsis mice and female control mice (gray value: 1.05±0.13 vs. 1.00±0.11, P > 0.05). The expression of CRISPLD2 in myocardium of male sepsis mice was significantly lower than that of male control mice (gray value: 0.29±0.08 vs. 1.02±0.19, P < 0.01), and it was significantly lower than that of female sepsis mice (P < 0.01). It was shown by correlation analysis that the expression level of CRISPLD2 in myocardium of sepsis mice was significantly correlated with serum estrogen concentration [R2 = 0.736, 95% confidence interval (95%CI) = 0.560-0.960, P < 0.001].@*CONCLUSIONS@#In female mice with sepsis, the expression of CRISPLD2 is comparable to that of female healthy mice. It is suggested that estrogen can maintain the expression of CRISPLD2 in LPS-induced septic mice at the normal level.
Subject(s)
Animals , Female , Male , Mice , Cysteine , Estrogens , Lipopolysaccharides , Myocardium , SepsisABSTRACT
Objective@#To investigate the effect of estrogen on expression of the cysteine-rich secretory protein containing LCCL domain 2 (CRISPLD2) in myocardium of lipopolysaccharide (LPS)-induced mice model of sepsis.@*Methods@#Totally 12 female and 12 male Balb/c mice of specific pathogen-free (SPF) level with 7 weeks were served as objectives. The female and male mice were randomly divided into model groups and control groups, respectively, with 6 mice in each group. The model of sepsis was reproduced by intraperitoneal injection of 10% LPS (5 mg/kg), and the mice in control groups were injected with the same volume of normal saline. The general condition of mice during experiment was observed at 24 hours after injection. All the mice were sacrificed and the heart was harvested after collecting the whole blood. The concentration of estrogen in serum was determined by double antibody sandwich enzyme linked immunosorbent assay (ELISA). The myocardial tissue homogenate was prepared at the same time, and the total protein was extracted. The expression level of CRISPLD2 was determined by Western Blot. Pearson correlation analysis was used to analyze the bivariate correlation.@*Results@#All of the experimental mice survived at 24 hours after injection. The mice in the model groups showed disorder and gray signs of body hair, with diarrhea and decreased appetite. No significant abnormality was observed in the control groups. There was no significant difference in the body weight or concentration of estrogen in serum between model and control group of both female and male mice [body weight (g): 24.6±1.8 vs. 24.5±1.3 in male mice, 18.0±0.8 vs. 17.5±1.1 in female mice; estrogen (ng/L): 11.93±2.59 vs. 12.17±3.87 in male mice, 28.20±5.75 vs. 29.82±6.10 in female mice, all P > 0.05]. There was no statistical difference in the expression of CRISPLD2 in myocardium between male control mice and female control mice (gray value: 1.02±0.19 vs. 1.00±0.11, P > 0.05). No significant difference in the expression of CRISPLD2 in myocardium was found between female sepsis mice and female control mice (gray value: 1.05±0.13 vs. 1.00±0.11, P > 0.05). The expression of CRISPLD2 in myocardium of male sepsis mice was significantly lower than that of male control mice (gray value: 0.29±0.08 vs. 1.02±0.19, P < 0.01), and it was significantly lower than that of female sepsis mice (P < 0.01). It was shown by correlation analysis that the expression level of CRISPLD2 in myocardium of sepsis mice was significantly correlated with serum estrogen concentration [R2 = 0.736, 95% confidence interval (95%CI) = 0.560-0.960, P < 0.001].@*Conclusions@#In female mice with sepsis, the expression of CRISPLD2 is comparable to that of female healthy mice. It is suggested that estrogen can maintain the expression of CRISPLD2 in LPS-induced septic mice at the normal level.
ABSTRACT
Sepsis is a common disease in intensive care units (ICU), and the resulted multi-organ dysfunction syndrome (MODS) is the main cause of death in patients with severe sepsis. The cardiovascular system is one of the most important target organ for sepsis. The severity of cardiac dysfunction is closely related to the clinical prognosis of patients with sepsis. Studies have reported that various cytokines are expressed during sepsis. They have influence on myocardial contractile function, mitochondrial function and self-regulation. Where after, it will induce cardiomyocyte apoptosis, which can lead to myocardial dysfunction. In this article, the pathogenesis of sepsis-induced myocardial dysfunction (SIMD) were reviewed to further clarify the pathogenesis of SIMD, and provide theoretical basis for subsequent research.
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Objective To investigate N-terminal pro-B-type natriuretic peptide (NT-proBNP) cutoff value for the mortality in different age groups in critically ill patients.Methods A retrospective study was conducted.295 patients admitted to the intensive care unit (ICU) of 401st Hospital of PLA from January 2011 to October 2012 were divided into two groups according to age [group with age＜65 years old (n=105) and group with age≥ 65 years old (n =190)].The concentrations of serum NT-proBNP,hematocrit (HCT),procalcitonin (PCT),C-reactive protein (CRP),serum creatinine (SCr),estimated glomerular filtration rate (eGFR),acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score and probability of survival (PS) were recorded within 24 hours.The primary outcome was ICU mortality.Receiver operator characteristic curve (ROC curve) was used to evaluate the value of NT-proBNP for predicting the mortality.Results ① There were no significant differences in the length of stay in ICU,mechanical ventilation rate,the mortality,the incidence of cardiovascular disease,digestive disease,neurologic disease,and the number of patients having received operation,HCT,PCT and CRP between the two groups (all P＞0.05).The percentage of the male,the APACHE Ⅱ score,the percentage of respiratory disease,and NT-proBNP in group with age ≥ 65 years old were higher than those of the group with age ＜ 65 years old [the percentage of the male:51.6％ vs.33.0％,x2=9.093,P=0.003; APACHE Ⅱ score:22.94 ±8.10 vs.19.44 ±8.51,Z=-3.259,P=0.001; the percentage of respiratory disease:29.47％ vs.17.14％,x2=5.472,P=0.024; NT-proBNP(ng/L):5 859.00(2 050.75,23 802.75) vs.2 882.00 (275.15,6 236.00),Z=-5.514,P=0.000]; PS,the percentage of patients having multiple injuries and other diseases and eGFR in group with age ≥65 years old were lower than those of the group with age ＜65 years old [PS:59.0 (31.5,79.0)％ vs.70.0 (40.0,84.0),Z=-3.431,P=0.001; the percentage of multiple injuries:0.53％ vs.17.14％,x2=30.987,P=0.000; the percentage of other disease:5.79％ vs.13.33％,x2=4.962,P=0.030; eGFR (ml·min-1· 1.73 m-2):81.07 (45.77,131.80) vs.95.54 (33.64,165.55),Z=-2.214,P=0.027].② The area under the ROC curve (AUC) [95％ confidence interval (95％ CI)] of NT-proBNP in patients with age＜65 years old was significantly higher than that of group with age≥65 years old and the entire group [0.825(0.738-0.892) vs.0.664 (0.592-0.731) and 0.725 (0.670-0.775),Z1 =-2.835,P1 =0.005; Z2=-1.995,P2=0.046].③ The sensitivity (76.]0％ vs.64.10％),specificity (82.35％ vs.67.12％),positive predictive value (90.0％ vs.75.8％),and negative predictive value (62.2％ vs.53.8％) with cutoff value of NT-proBNP (2 882 ng/L) in group with age ＜65 years old were significantly higher than those with NT-proBNP cutoff value (6 062 ng/L) in group with age ≥ 65 years old.Conclusion NT-proBNP cutoff value in different age groups for the prediction of mortahty in the critically ill patients maybe more objective and accurate.