Objective: To study the protective effect of propofol precondition against glutamate (Glu) neurotoxicity to neonatal rat cerebrocortical slices.
Methods: Brain slices of Sprague-Dawley (SD) rats were cultured in vitro and observed the morphologic changes. Brain slices were randomly divided into three groups: blank control group, Glu injury group (1 mmol/L Glu for 0.5 hour), propofol precondition group (20 mg/L propofol for 24 hours), each n=12. Changes in pathological and ultra-structure of cells were observed using microscope. Lactate dehydrogenase (LDH) leakage rate was measured. Meanwhile, the expression of glial fibrillary acidic protein (GFAP) was detected by immunohistochemical technology, then the positive cell were counted.
Results: Cultured brain slices of cell were intact and survived well. Hematoxylin-eosin (HE) staining, electron microscopy and LDH test results showed that cerebral film neuron severely damage, gliosis, edema, LDH leakage rate in Glu injury group were significantly more severe compared with blank control group [(68.5±2.0)% vs. (16.0±2.5)%, P<0.01]. Reduce the brain slice of the propofol pretreatment group of neuronal cell jury, cell shape recovery significantly reduced LDH leakage rate compared with the Glu injury group [(38.5±2.4)% vs. (68.5±2.0)%, P<0.05]. Immunohistochemical detection of GFAP expression of Glu injury group glial cell body swelling, producing increase in the number of GFAP positive reaction strong, the number of positive cells compared with blank control group was significantly increased (50±5 cells/HP vs. 10±3 cells/HP, P<0.01). The recovery of propofol pretreatment group glial cell morphology, cell processes slender GFAP positive reaction decreased the number of positive cells compared with the Glu injury group was significantly decreased (30±4 cells/HP vs. 50±5 cells/HP, P<0.05).
Conclusion: Propofol pretreatment has protective effect against Glu injured rat cerebrocortical slices.
Objective: To investigate the therapeutic strategies and prognostic factors of refractory medium-severe heart failure in uremic patients.
Methods: A single center, self control clinical research was conducted, and the data consisted of 30 uremic patients with refractory medium-severe heart failure undergoing maintenance hemodialysis (MHD), who received routine combined modality therapy and Xuebijing injection (to modify micro-inflammation). The systolic function of the left ventricle was compared before and after therapy. Multiple linear regression models were established to predict the improvements of systolic function of ventricle. Relationship between the accumulated dose of Xuebijing injection and changes of C-reactive protein (ΔCRP) was observed.
Results: The values of left ventricle ejection fraction (LVEF), fractional shortening (FS), and stroke volume (SV) after therapy were improved compared with those before therapy [LVEF: 0.42±0.07 vs. 0.34±0.04, FS: (21.07±3.83)% vs. (16.33±2.43)%, SV: 66.83±7.00 ml vs. 52.20±7.62 ml, all P<0.01]. In terms of cardiac output (CO), there was no statistical difference before and after therapy (4.77±0.65 L/min vs. 4.49±0.68 L/min, P>0.05). In the multiple linear regression models of ΔLVEF, ΔFS and ΔSV, the independent variables that affect dependent variables included age, ΔCRP, changes of hemoglobin (ΔHb), accumulated dose of Xuebijing injection, changes of HCO(3)(-) (Δ HCO(3)(-)), changes of serum creatinine (ΔSCr), Hb and CRP after therapy, the factors and weights of which had slight variation on accordance with different dependent variables. There was significant positive correlation between accumulated dose of Xuebijing injection and ΔCRP (r=0.561, P=0.001).
Conclusions: Xuebijing injection can improve heart function in uremic patients by modifying micro-inflammation, whose accumulated dose and therapeutic effect show positive correlation. In addition the improvement of heart failure has something to do with age, ΔHb, Hb after therapy, the correction of acidosis and dialysis sufficiency.
Objective: To explore the role of microRNA-92a (miR-92a) in evaluating endothelium damage induced by percutaneous coronary intervention (PCI).
Methods: A case control study was prospectively conducted. Fifty-eight patients with ST-segment elevation acute myocardial infarction (STEAMI) received PCI were enrolled. MiR-92a expression in circulation was determined on the next day after PCI (reverse transcription-polymerase chain reaction). The correlation between miR-92a expression in circulation and PCI influence factors, such as inflation pressure, duration of balloon inflation and length of culprit atheromatous plaque were explored.
Results: MiR-92a was lower in inflation pressure 11-19 atm (1 atm=101.325 kPa) group [n=43, mean -0.36, 95% confidence interval (95%CI) -0.60 to -0.12] than inflation pressure ≤10 atm group (n=11, mean 1.16, 95%CI 0.80 to 1.52, P<0.01) and ≥ 20 atm group (n=4, mean 0.26, 95%CI 0.26 to 0.26, P=0.1); and also lower in duration of balloon inflation 6-7 seconds group (n=24, mean -0.42, 95%CI -0.83 to -0.01) than in duration of balloon inflation ≤ 5 seconds group (n=9, mean 0.63, 95%CI 0.49 to 0.78, P=0.03) and ≥ 8 seconds group (n=25, mean 0.45, 95%CI 0.10 to 0.80, P<0.001); lower in implanted stent length ≤30 mm (n=31, mean -0.48, 95%CI -0.80 to -0.16) than those >30 mm (n=27, mean 0.16, 95%CI 0.01 to 0.32, P<0.01). A significantly negative correlation was found between inflation pressure and duration of balloon inflation. (r=-0.48, P<0.001).
Conclusions: There is a relationship between circulating miR-92a, inflation pressure and duration of balloon inflation. Circulating miR-92a could be used to evaluate the endothelium injury induced by PCI, and be used as a new target of prevention and treatment of endothelial dysfunction following revascularization.
Objective: To investigate whether D-dimer could be an early warning signal for patients with acute myocardial infarction (AMI), then may be helpful in risk assessment in emergency department.
Methods: Three thousand one hundred and thirty-four emergency AMI cases admitted to the hospital from January 1, 2009 to December 31, 2010 were retrospectively reviewed, and their age, gender, past medical history, D-dimer, MB isoenzyme of creatine kinase (CK-MB), cardiac troponin I (cTnI), the precursor of the N-terminal pro-brain natriuretic peptide (NT-proBNP), electrocardiogram (ECG) before treatment, and the CK-MB, cTnI and echocardiography left ventricular ejection fraction (LVEF) 2 hours after the treatment of percutaneous coronary intervention (PCI) or thrombolytic drugs, whether died and time from onset to death were recorded. According to the results of multivariate logistic regression analysis, draw the receiver operating characteristic curve (ROC curve) and fitting curve, and analyzed the relativity between the D-dimer before the treatment and prognosis of myocardial infarction.
Results: Multivariate logistic regression analysis showed that age [odds ratio (OR)=1.109, 95% confidence interval (95%CI) 1.073 to 1.147, P=0.000], whether undergoing emergency PCI (OR=4.162, 95%CI 1.980 to 8.748, P=0.000), D-dimer before treatment (OR=1.001, 95%CI 1.000 to 1.002, P=0.001), the LVEF values (OR=0.946, 95%CI 0.928 to 0.964, P=0.000) and cTnI after 2 hours of treatment (OR=1.011, 95%CI 1.004 to 1.018, P=0.002) were correlated to 28-day death. The ROC curves showed that age [area under curve (AUC) 0.796, P=0.000], whether undergoing emergency PCI (AUC 0.704, P=0.000), D-dimer before treatment (AUC 0.797, P=0.000) were positively correlated with the 28-day death; the LVEF values (AUC 0.261, P=0.000) were negative correlated with the 28-day death. The fitting curve of D-dimer before treatment, the time from onset to death and the LVEF showed no linear correlation.
Conclusions: D-dimer was correlated with the early prognosis of patients with myocardial infarction, but was not correlated with the time from onset to death. The rise in D-dimer at the early stage of AMI may be helpful to indicate the critical condition of the AMI patients.
Objective: To approach the changes in heart failure and dying regularity of rats with endotoxin-induced cardiomyopathy, and to offer some help for clinical diagnosing and further investigation.
Methods: Injecting refined endotoxin (10 mg/kg) via vein of Wistar rats. The first experiment: antidromic observing the endotoxic rats from death to the beginning to discover the performance of clinic heart function which could forecast death. The second experiment: setting 6 rats per group, respectively killing the rats at 4, 8, 16, 24, 32, 40, 48 and 72 hours after endotoxin injection, and killing 6 normal rats as control group, getting the tissue of left ventricle for biochemistry test, routine pathological examination, transmission electron microscope examination, expression level of α(1)-actin gene with reverse transcription-polymerase chain reaction (RT-PCR), and serum creatine kinase (CK) was test within 24 hours.
Results: The first experiment: heart rate (HR) and left ventricular end-systolic pressure (LVESP) of endotoxic rats began significant lower than normal at 4 hours before death (F(1)=22.032, P(1)=0.000; F(2)=29.420, P(2)=0.000), maximum rate of rise/drop of left ventricular pressure (±dp/dt max) began significant lower than normal at 8 hours before death (F(1)=17.272, P(1)=0.000; F(2)=19.685, P(2)=0.000), left ventricular end-diastolic pressure (LVEDP) showed no significant during the whole time (F=0.265, P=0.988). The heart function of all the rats showed no significant changes in the first 4 hours after injection. Mortality was 73.9% from injection to 24 hours later. Most of them died in 8-16 hours after injection. The one who had survived over 24 hours could have 2/3 probability to survive to 48 hours. The second experiment: CK in serum of different groups showed no significant difference (F=0.402, P=0.805), but showed obvious discreteness in each group except normal group. Electron microscopy and pathological examination showed obvious intracellular and intercellular damage since 8 hours later from injection. Pathology displayed that cells range disorder, mitochondria swelling, capillary hemorrhage, transverse striation disappearing, construction of myocardial cell loosing, and lateral dissociation phenomena. Electron microscopy discovered that the fiber direction and transverse striation became vague and disappeared, mitochondria got injury, the fiber became disordered, cell-cell junction were damaged seriously. Compared with the control group (0.637±0.160), the gene expression level of α(1)-actin decreased after endotoxin injection. The value dropped to the bottom at 8 hours (0.493±0.067) after injection and then rised slowly but dropped to the second wave trough again at 32 hours (0.875±0.128), but had no statistic significance; the expression of α(1)-actin gene eventually rised significantly at 40, 48, 72 hours after injection (2.231±0.545, 1.850±0.436, 2.0
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