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ObjectiveTo explore heart rate variability (HRV),cardiac troponin Ⅰ (cTnI),left ventricular ejection fraction (LVEF) and electrocardiogram (ECG) in order to clarify the function of cardiac autonomic nerve system and the incidence of potential myocardium injury in patients with severe brain injury.MethodsClinical data of 65 patients with severe brain injury admitted between June 2006 and June 2010 were reviewed.For the sake of comparison,patients were divided by different groupings as per different biomarkers or outcomes such as Glasgow coma scale (GCS) 6 - 8 group and GCS 3 - 5 group; cTnl ＞ 0.5 group,0.04 ＜ cTnl ＜ 0.5 group and CTnl ＜ 0.04 group; and survival group and death group.Another 30 healthy subjects were enrolled as control group.Heart rate variability (HRV) was analyzed with both timedomain and frequency domain methods based on data from 24-hour Holter monitoring.The level of serum cardiac troponin Ⅰ was detected. The left ventricular ejection fraction was measured by beside color ultrasonogram.The different relationships between HRV and GCS as well as prognosis,between cTnI and GCS as well as fatality,between cTnI and ECG,and between EF and GCS were analyzed.The computer statistical software SPSS version 13.0 was used for statistical analysis of data.ResultsAll of the 65 patents with severe brain injury were subjected to decrease in HRV.The patients of GCS 6 - 8 group and GCS 3 - 5 group showed significantly lowered HRV in comparison with control group ( P ＜ 0.05 ).The death group showed more obvious decrease in HRV than the survival group ( P ＜ 0.05 ).Fifty-one of the 65 patients had myocardial injury evidenced by increase in cardiac troponin Ⅰ.The patients of cTnl ＞0.5 group and 0.04 ＜cTnI ＜ 0.5 group showed significantly higher fatality compared with cTnI ＜ 0.04 group ( P ＜ 0.05 ).Compared with the GCS 6 ～ 8 group,more patients in the GCS 3 -5 group had abnormal serum CTnl level and lower EF.ConclusionsThere are cardiac autonomic nerve system disorders and different degrees of myocardial injury in patients with severe brain injury,and early intervention is essential to decrease the fatality of severe brain injury.
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The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-operated group (group S, n=8), sepsis model group (group C, n=24), diallyl trisulfide (DATS)-treated group (group D, n=24). Animals in groups C and D were further divided into three subgroups according to different observation time points, with 8 rats in each subgroup· Rats in group D and C were intravenously injected with normal saline or DATS respectively at a dose of 20 mg/kg after the establishment of sepsis model. Eight rats in groups C and D were sacrificed at 3, 6 and 24 h post-CLP and their livers were harvested for detection of interleukin (IL)-1 receptor associated kinase-4 (IRAK-4), nuclear factor-κB (NF-κB), c-fos, c-jun, malondialdehydethhe (MDA) and superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α) and for pathological examination. The results showed that the levels of serum IRAK-4, NF-κB and TNF-α in hepatic tissues were higher in group C than group S (control group) (P<0.05). After DATS treatment, the levels of IRAK-4 and NF-κB in the hepatic tissues and serum TNF-α in group D were lower than those in group C (P<0.05). The levels of c-fos and c-jun and MDA in the hepatic tissues were higher in group C than in group S (P<0.05). After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05). When compared with group S group, concentration of SOD in the hepatic tissues in group C was significantly lower (P<0.05). After DATS treatment, the concentration of SOD in the hepatic tissues was higher in group D than in group C (P<0.05). These findings suggested that treatment with DATS could ameliorate sepsis-induced liver injury in rats. The protective effect might be related to its ability to inhibit the signal pathway of IRAK-4 and NF-κB, thereby decreasing the production of oxygen free radicals and down-regulating the expression of c-fos and c-jun.
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The protective effects of diallyl trisulfide on liver were examined in rats with sepsis. Sepsis was reproduced in rats by cecum ligation and puncture (CLP). Fifty-six male Wistar rats were randomly divided into sham-operated group (group S, n=8), sepsis model group (group C, n=24), diallyl trisulfide (DATS)-treated group (group D, n=24). Animals in groups C and D were further divided into three subgroups according to different observation time points, with 8 rats in each subgroup· Rats in group D and C were intravenously injected with normal saline or DATS respectively at a dose of 20 mg/kg after the establishment of sepsis model. Eight rats in groups C and D were sacrificed at 3, 6 and 24 h post-CLP and their livers were harvested for detection of interleukin (IL)-1 receptor associated kinase-4 (IRAK-4), nuclear factor-κB (NF-κB), c-fos, c-jun, malondialdehydethhe (MDA) and superoxide dismutase (SOD), tumor necrosis factor alpha (TNF-α) and for pathological examination. The results showed that the levels of serum IRAK-4, NF-κB and TNF-α in hepatic tissues were higher in group C than group S (control group) (P<0.05). After DATS treatment, the levels of IRAK-4 and NF-κB in the hepatic tissues and serum TNF-α in group D were lower than those in group C (P<0.05). The levels of c-fos and c-jun and MDA in the hepatic tissues were higher in group C than in group S (P<0.05). After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05). When compared with group S group, concentration of SOD in the hepatic tissues in group C was significantly lower (P<0.05). After DATS treatment, the concentration of SOD in the hepatic tissues was higher in group D than in group C (P<0.05). These findings suggested that treatment with DATS could ameliorate sepsis-induced liver injury in rats. The protective effect might be related to its ability to inhibit the signal pathway of IRAK-4 and NF-κB, thereby decreasing the production of oxygen free radicals and down-regulating the expression of c-fos and c-jun.
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Animals , Male , Rats , Allyl Compounds , Pharmacology , Disease Models, Animal , Liver , Metabolism , Pathology , Rats, Wistar , Sepsis , Sulfides , PharmacologyABSTRACT
To explore the protective effect of sodium tanshinone IIA sulfonate (STS) on microcirculatory disturbance of small intestine in rats with sepsis, and the possible mechanism, a rat model of sepsis was induced by cecal ligation and puncture (CLP). Rats were randomly divided into 3 groups: sham operated group (S), sepsis group (CLP) and STS treatment group (STS). STS (1 mg/kg) was slowly injected through the right external jugular vein after CLP. The histopathologic changes in the intestinal tissue and changes of mesenteric microcirculation were observed. The levels of tumor necrosis factor-α (TNF-α) in the intestinal tissue were determined by using enzyme-linked immunoabsorbent assay (ELISA). The expression of intercellular adhesion molecule-1 (ICAM-1) in the intestinal tissue was detected by using immunohistochemisty and Western blot, that of nuclear factor κB (NF-κB) and tissue factor (TF) by using Western blot, and the levels of NF-κB mRNA expression by using RT-PCR respectively. The microcirculatory disturbance of the intestine was aggravated after CLP. The injury of the intestinal tissues was obviously aggravated in CLP group as compared with S group. The expression levels of NF-κB p65, ICAM-1, TF and TNF-α were upregulaed after CLP (P<0.01). STS post-treatment could ameliorate the microcirculatory disturbance, attenuate the injury of the intestinal tissues induced by CLP, and decrease the levels of NF-κB, ICAM-1, TF and TNF-α (P<0.01). It is suggested that STS can ameliorate the microcirculatory disturbance of the small intestine in rats with sepsis, and the mechanism may be associated with the inhibition of inflammatory responses and amelioration of coagulation abnormality.
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Objective To investigate the protective effects of endotoxin precondition on hepatic tissue in rats with endotoxemia.Method The models of rats with acute endotoxemia were produced by injecting LPS directly.Seventy-two male wistar rats were randomly divided into three groups:saline control group(N,n=24),lipopolysaccharide (LPS)-treated group(L,n=24),LPS pretreated group(P,n=24).Each group was divid-ed into four subgroups:saline control and lipopolysaccharide (LPS)-treated 2 h,4 h,6 h,12 h groups and LPS-pretreated 2 h,4 h,6 h,12 h groups.Rats in group P were first administered with introperitoneal injection of 0.25 mg/kg LPS,and after 24 hours,the rats were injected with 0.5 mg/kg LPS.Rats in group N and group L received with an equivalent amount of saline.After 72 hours,rats in group L and group P were intravenonsly injected with 10 mg/kg LPS,and rats in group N received with an equivalent amount of saline.Six rats were killed at 2,4,6 and 12 hours after injection of LPS in group L and P.The hvers were removed for detecting Toll like receptor-4 (TLR-4),nuclear factor-кB(NF-кB),tumor Necrosis Factor-apha(TNF-α)and malondialdehyde(MDA).The blood was drawn for detecting Alamine aminotmnsferose (ALT) and Aspartate aminotransferose (AST).The patho-logical changes of liver were also examined.Software SPSS13.0 was utilized to do ANOVA for statistical analysis.Results The rats exposed to LPS alone demonstrated an increase in TLR-4.NF-кB and TNF-α activity of the liver tissue.Incontrast.the rats exporsed 10 LPS prelreatment exhibited a significant decrease in TLT-4,NF-кB and TNF-α activity.The contents of TLR-4,NF-кB and TNF-α of LPS-treated 4 h groupwere,(38.76±0.67),170.82 ±31.40),293.16±49.49)and(6.263±0.351),significantly higher than those of the saline control group.The administration of endotoxin pretreatment reduced the indexes to(22.35±1.35),(135.55±26.44)and(234.23±44.96),respectively(P＜0.05).Conclusions TLR-4,NF-кB and TNF-α take part in the progress of hepatic injury in rats with endotoxemia.Endotoxin pretreatment can eliminate hepatic injury and protect the hepatic tissue by downmgulating the levels of TLR-4.NF-кB and TNF-α.