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Pulmonary hypertension(PH)is a chronic,progressive,high-mortality disease characterized by a continuous increase in pulmonary vascular pressure. All types of PH have the same characteristics,i.e.,the excessive proliferation,anti-apoptosis and inflammation of pulmonary artery endothelial cells and smooth muscle cells,which leads to progressive thickening of pulmonary small vessels,resulting in pulmonary vascular remodeling and increased pulmonary vascular resistance,ultimately leading to right ventricular hypertrophy,heart failure,and death. The drugs used to treat PH mainly include L-type calcium channel blockers,phosphodiesterase 5 inhibitors,guanosine cyclase activators,endothelin receptor antagonists,and synthetic prostacyclin and its analogues. These drugs reduce pulmonary artery pressure by relaxing pulmonary blood vessels but do not cure the patient,and their prognosis remains poor. Therefore,the development of drugs that can effectively improve or even reverse pulmonary vascular remodeling is the key to treating PH. In recent years,studies on pulmonary vascular remodeling mainly included(1)the synthesis of new small-molecule compounds;(2)the transformation of mature drugs,such as the use of drug combinations and dosage form transformation,etc.;(3)the pharmacodynamic evaluation of traditional Chinese medicines and derived compounds based on the theory of "lung distension";(4)research into monomers of traditional Chinese medicine; and(5)research into new targets.
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Chronic hypoxic lung diseases are major causes of disability and mortality worldwide, which are typically aggravated by hypoxic pulmonary hypertension.The pathogenesis of hypoxic pulmonary hypertension is complex, and its mechanism has not been fully elucidated.The previous studies have shown abnormally elevated levels of free Ca + in the cytoplasm of pulmonary artery smooth muscle cells to be the predominant drivers of pulmonary hypertension , causing continuous contraction and remodeling of the pulmonary vessels.This article briefly summarizes the mechanism of hypoxia-induced imbalance in calcium homeostasis in pulmonary artery smooth muscle cells, together with its related drug research, based on the existing literature.Hypoxia induces an imbalance in calcium homeostasis in pulmonary artery smooth muscle cells by regulating hypoxia-inducible factor-1, K+ , store-operated calcium channel, receptor-operated calcium channel, the Ca +-sensing myosin contractile mechanism by binding to calmodulin, leading to pulmonary vasoconstriction.Ca + can also activate PKC/ MAPKs and PI3K/Akt/mTOR pathways, leading to pulmonary vascular remodeling.
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OBJECTIVE@#To investigate the role of acetylated modification induced by coactivator p300 in lipopolysaccharide (LPS)- induced inflammatory mediator synthesis and its molecular mechanism.@*METHODS@#Agilent SurePrint G3 Mouse Gene Expression V2 microarray chip and Western blotting were used to screen the molecules whose expression levels in mouse macrophages (RAW246.7) were correlated with the stimulation intensity of LPS. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (chip-qPCR) were used to verify the binding of the molecules to the promoters of IL-6 and TNF-α genes. The effects of transfection of RAW246.7 cells with overexpression or interfering plasmids on IL-6 and TNF-α synthesis were evaluated with ELISA, and the binding level of the target molecules and acetylation level of H3K27 in the promoter region of IL-6 and TNF-α genes were analyzed by chromatin immunoprecipitation sequencing technique (chip-seq).@*RESULTS@#Gene microarray chip data and Western blotting both confirmed a strong correlation of p300 expression with the stimulation intensity of LPS. Immunocoprecipitation confirmed the binding between p300 and c-myb. The results of EMSA demonstrated that c-myb (P < 0.05), but not p300, could directly bind to the promoter region of IL-6 and TNF-α genes; p300 could bind to the promoters only in the presence of c-myb (P < 0.05). The expressions of p65, p300 and c-myb did not show interactions. Both p300 overexpression and LPS stimulation could increase the level of promoter-binding p300 and H3K27 acetylation level, thus promoting p65 binding and inflammatory gene transcription; such effects were obviously suppressed by interference of c-myb expression (P < 0.05). Interference of p65 resulted in inhibition of p65 binding to the promoters and gene transcription (P < 0.05) without affecting p300 binding or H3K27 acetylation level.@*CONCLUSION@#LPS can stimulate the synthesis of p300, whose binding to the promoter region of inflammatory genes via c-myb facilitates the cohesion of p65 by inducing H3K27 acetylation, thus promoting the expression of the inflammatory genes.
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Animals , Mice , Acetylation , Inflammation Mediators , Interleukin-6/metabolism , Lipopolysaccharides/pharmacology , Tumor Necrosis Factor-alpha/metabolismABSTRACT
Since the first edition of ISO15189"Medical laboratories: requirements for quality and competence" was published in 2003, it has been rapidly and widely used in the world under the promotion of the International Laboratory Accreditation Cooperation Organization (ILAC), and has become the basic standard for the quality management, capacity-building and capacity attestation of medical laboratories. The Mutual Recognition Arrangement (MRA) of ILAC for ISO15189 is the most authoritative international permit for examination results, which is accepted by international organizations. Since the establishment of ISO15189 medical laboratory accreditation system in 2004 in China, more than 530 medical laboratories have been accredited, which plays an important role in improving the quality and competence of medical laboratories in China, and improves the influence of Chinese medical laboratories in the world. ISO 15189:2012 is currently being revised by the International Organization for Standardization/Technical Committee on Clinical Laboratory Testing and in vitro diagnostic test systems (ISO/TC212). This revision will bring significant changes and the medical laboratory shall pay attention to these changes. In order to help medical laboratories understand the new ideas in advance, this paper summarizes and analyses the draft of the new international standards, and provides references for users.
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Patients with hypoxia pulmonary hypertension (HPH) are often accompanied by dyspnea, fatigue, and headache. With the development of the disease, the right ventricle gradually collapses and eventually leads to death. Hypoxic pulmonary vascular remodeling is an important pathological basis of HPH, and the remodeled pulmonary vessels will form permanent thickening. The mechanism of hypoxic pulmonary vascular remodeling is relatively complex. At present, there are few studies on drugs for pulmonary vascular remodeling on the market, mainly focusing on the alleviation of pulmonary vasoconstriction. It was found that hypoxia induces calcium overload in pulmonary artery smooth muscle cells (PASMCs), resulting in the proliferation of PASMCs. The main mechanisms include: ① abnormal expression of calcium pumps; ② abnormal calcium channels in the plasma membrane of pulmonary artery smooth muscle cells; ③ overexpression of calcium-sensitive receptors in cells; ④ the expression of Na+/Ca2+ exchanger type-1 was abnormal. This review summarized several mechanisms of hypoxia induced calcium overload leading to pulmonary artery remodeling, hoping to provide a new idea for the treatment of HPH.
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OBJECTIVES@#To study the association of β2-drenergic receptor (@*METHODS@#A total of 143 children with asthma who attended the hospital from October 2016 to October 2020 were enrolled as the asthma group, among whom 61 children had mild symptoms (mild group) and 82 children had moderate-to-severe symptoms (moderate-to-severe group). A total of 137 healthy children were enrolled as the control group. Peripheral venous blood samples were collected from the two groups. The SNaPshot SNP technique was used to analyze the SNP and haplotypes of the @*RESULTS@#Polymorphisms were observed in the @*CONCLUSIONS@#SNP/haplotype of the
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Child , Humans , Asthma/genetics , Case-Control Studies , Genetic Predisposition to Disease , Genotype , Haplotypes , Polymorphism, Single Nucleotide , Receptors, Adrenergic, beta-2/genetics , Regulatory Sequences, Nucleic AcidABSTRACT
OBJECTIVE@#To explore the influencing factors and countermeasures of infection in leukemia patients after allogeneic peripheral blood hematopoietic stem cell transplantation.@*METHODS@#A total of 126 patients with leukemia admitted in our hospital from August 2016 to March 2018 were selected. The number of infected patients after transplantation was recorded, and the causes of infection were analyzed.@*RESULTS@#Among the 126 patients, 43 were positive for infection, and the infection rate was 34.13%. A total of 89 pathogens were detected, of which bacteria accounted for 64.05%; virus accounted for 22.47%, and fungi accounted for 13.48%. The patient's age, donor type, pre-transplant infection, prophylactic use of antibiotics and aGVHD all were factors influencing the patient's infection (P<0.05). The follow-up results showed that the incidence of infection in the intervention group significantly decreased after intervention with prevention program (P<0.05). After reasonable nursing intervention, the incidence of infection in the intervention group after follow-up for 12 months was lower than that in the control group (P<0.05).@*CONCLUSION@#Pre-transplant infection and prophylactic use of antibiotics are factors influencing the infection after allogeneic hematopoietic stem cell transplantation. The incidence of infection can be reduced by reasonable infection prevention.
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Humans , Graft vs Host Disease , Hematopoietic Stem Cell Transplantation , Infections , Leukemia , Peripheral Blood Stem Cell TransplantationABSTRACT
To investigate the normal structures of parotid duct by using magnetic resonance(MR)hydrography. MR three-dimensional heavy T2-weighted imaging was performed in 21 normal subjects.After taking 200 mg of vitamin C orally for 3 minutes,the subjects underwent parotid duct coronal hydro-magnetic resonance imaging.The images were transferred to the GE AW4.5 workstation,on which multi-planner reformation was performed using Functool software.The numbers of the parotid duct,accessory parotid duct,segments,and its branches was counted and the length and diameter of the intra-and extra-parotid ducts were measured. Accessory ducts were found in 24 parotid glands(57.1%,24/42),with the average length being(9.54±9.98)mm and the average diameter being(0.87±0.88)mm.The intra-parotid ducts were found to be with 3 segments were in 3 cases(7.14%,3/42),with 2 segments in 19 cases(45.23%,19/42),and with 1 segment in 20 cases(47.62%,20/42).The average number of the branches of the first,second and third segment was 2.38,0.88,and 0.1,respectively.The average length of the intra-parotid duct was(36.97±7.97)mm,with its average diameter being(2.01±0.76)mm.The average length of extra-parotid duct was(34.98±10.25)mm,with its average diameter being(2.13±0.79)mm.The average length of the whole parotid duct was(71.95±11.47)mm,with its average diameter being(2.07±0.68)mm. The parotid duct,the accessory parotid duct,and the segments and their branches of the intra-parotid duct can be accurately displayed by MR hydrography.
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Magnetic Resonance Imaging , Magnetic Resonance Spectroscopy , Parotid GlandABSTRACT
Objective To investigate the intervention effects of prunella vulgaris sulfated polysaccharide (PVSP) on carbon tetrachaloride(CCl4)-induced hepatic fibrosis in rat.Methods The 40% CCl4was used to induce hepatic fibrosis in rat model, then successful model rats were randomly divided into 3 groups, with 10 rats in each group, respectively, the model group(Model),the high dose PVSP group(PVSP-H:400 mg/kg)and the low dose PVSP group(PVSP-L:100 mg/kg). The blank group and solvent group were also established.The serum levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST)were determined by automatic biochemical analyzer.HE staining and Sirius red staining were used to examine the degree of hepatic fibrosis.The expression levels of collagen typeⅠ(Col-Ⅰ)and α-smooth muscle actin(α-SMA)mRNA were detected by qRT-PCR.Col-Ⅰand α-SMA in hepatic tissues were detected by immunohistochemistry staining.Results There were no significant changes in serum expressions of ALT and AST and mRNA proteins of Col-Ⅰand α-SMA in liver tissues between the blank group and Solvent group.Compared with the model group,the serum levels of ALT and AST were significantly decreased in the PVSP-H and PVSP-L groups (P<0.05). HE staining and Sirius red staining showed that PVSP could significantly reduce the degree of hepatic fibrosis.The expression of Col-Ⅰand α-SMA mRNA were decreased in the PVSP-H and PVSP-L groups(P<0.05).Immunohistochemistry showed that the expressions of Col-Ⅰ and α-SMA in hepatic tissues were decreased by PVSP (P<0.05), and the effect was dose-dependent. Conclusion PVSP has a protective effect on CCl4-induced hepatic fibrosis in rats, which may be related with the inhibiting expressions of Col-Ⅰand α-SMA,reducing secretion of collagen and promoting extracellular matrix degradation.
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Thalassemia laboratory diagnostic techniques include screening test and genetic test, the former diagnosis method is mainly based on the morphology of red blood cells and the physical and chemical properties, including routine analysis of blood, red blood cell morphology test, red blood cell permeability test, hemoglobin component analysis, etc. The latter is mainly based on various of molecular biology experiments developed on the basis of PCR, including gap-PCR,PCR-RDB,melting curve analysis,high resolution melting analysis,real-time PCR,gene chip and DNA sequencing, etc. This paper reviews the progress of laboratory diagnostic techniques on thalassemia, combination of comprehensive screening method with technique of genetic diagnosis, appropriately contributes to the diagnosis of thalassemia.
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Humans , Genetic Testing , Oligonucleotide Array Sequence Analysis , Polymerase Chain Reaction , Sequence Analysis, DNA , ThalassemiaABSTRACT
<p><b>OBJECTIVE</b>To evaluate the role of microparticle (MP) derived from acute promyelocytic leukemia (APL) cells and tissue factor (TF) carried by the MP in hypercoagulable state, and the effect of treatment with cytotoxic chemotherapy/differentiating agents on procoagulant activity (PCA) of these MP.</p><p><b>METHODS</b>Bone marrow mononuclear cells (BMMNC) were extracted from 5 APL patients and 5 sex- and age- matched patients with iron deficiency anemia as controls. The cells were cultured in vitro for 48 h, then MP-rich culture medium and MP-free culture medium were harvested and MP was further obtained from certain volume of MP-rich culture medium. Subsequently, TF expression on MP was measured by ELISA. PCA of MP-rich culture medium or MP-free culture medium was assessed with thrombin generation assay. The role of TF on MP-related PCA was evaluated using anti-human TF antibody. In addition, APL cells were treated with all-trans retinoic acid (ATRA), arsenic trioxide (ATO) or daunorubicin (DNR) for 48 h, then MP-rich culture medium were harvested and the PCA was determined.</p><p><b>RESULTS</b>No TF expression was found in the MP released from bone marrow MNC in control group, whereas the obvious TF expression was found in the MP originated from BMMNC of APL. MP from both APL and control BM-MNC had obvious PCA. However, compared with the MP derived from control MNC, the MP from APL BM-MNC induced significantly higher PCA. TF played a crucial role in the PCA of APL BM-MNC derived MP, while played no role in that of MP from control MNCs. DNR-treating APL BM-MNC resulted in an increase in the PCA of MP, whereas ATO or ATRA exposure lead to exactly the opposite results.</p><p><b>CONCLUSION</b>MP derived from APL BM-MNC posseses obvious PCA. TF plays a crucial role in the MP-related PCA. The PCA of MP increases after treating APL BM-MNC with chemotherapy agent DNR and decreases following exposure of APL BM-MNC to differentiating agents ATRA or ATO.</p>
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Objective: Numerous studies have shown that bone marrow-derived mesenchymal stem cells (MSCs) enhance neurological recovery after cerebral ischemia. However, the mechanisms are still not clear. The present study aimed to investigate the beneficial effects of MSCs on global cerebral ischemia induced by cardiac arrest (CA) and the underlying mechanisms. Methods: Rats subjected to asphyxial CA were injected intravenously with MSCs (5×106 ) at 2 hours after resuscitation. Whole brain histopathologic damage scores (HDS) were assessed by histopathology at 3 and 7 days after resuscitation. The distribution of donor MSCs in the brain was evaluated. The expression of tumor necrosis factor-α-induced protein 6 (TSG-6) and pro-inflammatory cytokines in cerebral cortex was assayed. After intravenous infusion of TSG-6 siRNA-MSCs, HDS and pro-inflammatory cytokines were reevaluated at 7 days after resuscitation. Results: Intravenously administered MSCs significantly reduced whole brain HDS after global cerebral ischemia. Immunofluorescence microscopy revealed that donor MSCs were primarily found in cerebral cortex and expressed TSG-6. MSCs treatment significantly increased the expression of TSG-6 and reduced the expression of pro-inflammatory cytokines in cerebral cortex. In addition, intravenous infusion of TSG-6 siRNA-MSCs failed to attenuate brain inflammation. Conclusion: Systemically administered MSCs reduced inflammatory damage to brain in rats with global cerebral ischemia via secretion of TSG-6.
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Heart Arrest , Mesenchymal Stem CellsABSTRACT
Objective To evaluate the effect of controlling cost by introducing hand hygiene products with lower price on promoting hand hygiene compliance.Methods The application status and cost of hand hygiene products in 2012 was as pre-intervention group,2013 was as post-intervention group.Effective and lower price hand hygiene products were introduced in 2013,consumption and cost of hand hygiene products before and after the intervention was compared.Results Consumption of hand hygiene products per patient-day before and after the intervention was significantly different ([10.56±16.46]mL vs [13.79 ± 16.93 ]mL,Z=4.14,P 0.05).Conclusion Introduction of hand hygiene products with lower price in this hospital can improve hand hygiene compliance to certain degree without increasing the cost of hand hygiene.
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BACKGROUND:Partial pressure of end-tidal carbon dioxide (PETCO2) has been used to monitor the effectiveness of precordial compression (PC) and regarded as a prognostic value of outcomes in cardiopulmonary resuscitation (CPR). This study was to investigate changes of PETCO2 during CPR in rats with ventricular fibrillation (VF) versus asphyxial cardiac arrest. METHODS:Sixty-two male Sprague-Dawley (SD) rats were randomly divided into an asphyxial group (n=32) and a VF group (n=30). PETCO2 was measured during CPR from a 6-minute period of VF or asphyxial cardiac arrest. RESULTS:The initial values of PETCO2 immediately after PC in the VF group were significantly lower than those in the asphyxial group (12.8±4.87 mmHg vs. 49.2±8.13 mmHg,P=0.000). In the VF group, the values of PETCO2 after 6 minutes of PC were significantly higher in rats with return of spontaneous circulation (ROSC), compared with those in rats without ROSC (16.5±3.07 mmHg vs. 13.2±2.62 mmHg,P=0.004). In the asphyxial group, the values of PETCO2 after 2 minutes of PC in rats with ROSC were significantly higher than those in rats without ROSC (20.8±3.24 mmHg vs. 13.9±1.50 mmHg,P=0.000). Receiver operator characteristic (ROC) curves of PETCO2 showed significant sensitivity and specificity for predicting ROSC in VF versus asphyxial cardiac arrest. CONCLUSIONS:The initial values of PETCO2 immediately after CPR may be helpful in differentiating the causes of cardiac arrest. Changes of PETCO2 during CPR can predict outcomes of CPR.
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<p><b>OBJECTIVE</b>To investigate the inhibitory effect of resveratrol on interleukin-1β (IL-1β) production in mesenchymal stem cells (MSCs) exposed to radiation and the action mechanism of resveratrol.</p><p><b>METHODS</b>MSCs were divided into blank control group, radiation group, shRNA interference group, and resveratrol groups. The resveratrol groups were given different doses of resveratrol (50, 100, and 200 µmol/L) before radiation. The secretion and expression of IL-1β was measured by enzyme-linked immunosorbent assay, Western blot, and RT-PCR.</p><p><b>RESULTS</b>Compared with the radiation group, the resveratrol groups had significantly decreased extracellular secretion of IL-1β (t = 83.34, 24.48, and 12.52, P < 0.05 for all) and significantly decreased intracellular expression of IL-1β protein and mRNA (t = 8.695, 14.77, and 13.9, P < 0.05 for all). Compared with those given 200 µmol/L resveratrol alone before radiation, the MSCs treated by SIRT1 silencing and given 200 µmol/L resveratrol before radiation had significantly increased extracellular secretion of IL-1β (t = 18.57, P < 0.05) and significantly increased intracellular expression of IL-1β protein and mRNA (t = 10.24, P < 0.05).</p><p><b>CONCLUSION</b>Resveratrol can significantly inhibit the production of IL-1β in MSCs exposed to radiation, and SIRT1 may play a key regulatory role in the process of inflammation induced by radiation.</p>
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Humans , Cells, Cultured , Interleukin-1beta , Metabolism , Mesenchymal Stem Cells , Metabolism , Radiation Effects , Radiation , Radiation Dosage , Stilbenes , PharmacologyABSTRACT
Objective To investigate the effects of bone marrow mesenchymal stem cells (MSCs)treatment on TSG-6 in a rat model of cardiopulmonary resuscitation (CPR).Methods Sprague Dawley (SD) rats were randomly (random number) divided into sham group,phosphate buffer solution (PBS)-treated group and MSCs-treated group.Animals were subjected to asphyxial cardiac arrest followed by CPR.In PBS-treated group or MSCs-treated group,animals were injected intravenously with PBS or MSCs at 2h after resuscitation.Neurological deficit scores (NDS) were assessed at 1,3 and 7 d after CPR.Serum S-100B was assayed using enzyme linked immunosorbent assay (ELISA).Immunofluorescence was performed to detect donor MSCs and the expression of TSG-6 in brain.TSG-6 and proinflammatory cytokines in brain were assayed using real time reverse transcription-polymerase chain reaction (RT-PCR).Western blot analysis was performed to measure the levels of neutrophil elastase (NE) in brain.Multiple comparisons were made by analysis of variance.Results At 3d and 7d,MSCs-treated group demonstrated higher NDS than PBS-treated group (P < 0.01),and serum S-100B levels significantly reduced in MSCs-treated group compared with PBS-treated group (P < 0.01).DAPI-labeled MSCs migrated into the ischemic brain and some DAPI + cells colocalized with TSG-6.Compared with PBS-treated group,MSCs treatment significantly up-regulated the expression of TSG-6 and reduced the expression of NE and proinflammatory cytokines in brain at 3 d and 7 d after CPR (P < 0.05).Conclusion Systemically administered MSCs suppressed inflammatory responses in brain after CPR and improved neurological function in rats possibly via induction of TSG-6.
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Objective To explore the protective effects of Caspase inhibitor on in vitro hippocampal neurons of rats with oxygen glucose deprivation (OGD) injury.Methods The primary hippocampal neurons from newborn Sprague-Dawley rats were cultured for 7 days,and then,divided into control group,OGD/re-OG treatment group,Caspase inhibitor (Z-VAD-FMK) treatment group and DMSO treatment group; and OGD/re-OG was performed in the later three groups for OGD duration of 6 h.Through the experimental process,20 μmol/L Z-VAD-FMK was given to the Z-VAD-FMK treatment group,while 1‰ DMSO was added into culture medium in the DMSO group.The morphology of the neurons was observed 24 hours after re-OG under light microscopy and electron microscopy.MTT assay was used to determine the rate of survived cells and lactate dehydrogenase (LDH) content in culture medium.The neurons apoptosis rate was measured by using flow cytometry (Annexin V-FITC/PI).Caspase-3 activity of neurons was analyzed by colorimetry.The protein expression of Caspase-3 wasassessed by Western blotting.Results Cells in the OGD/re-OG treatment group showed swelled body,some having ruptured membrane,cell integrity being damaged,cell nucleus edema,mitochondrial swelling and cristae ordered chaos; cells in the Z-VAD-FMK treatment group showed decreased injury as compared with the OGD/re-OG treatment group,having cell integrity; as compared with the OGD/re-OG treatment group,Z-VAD-FMK treatment group had significantly higher absorbance value (0.204±0.019 vs.0.303±0.018) and cell survivalrate (0.481%±0.045%vs.0.704%±0.040%),obviously decreased lactate dehydrogenase (LDH) content ([406.500±21.286] U/L vs.[326.000±20.278] U/L),apoptosis rate (49.700%±3.100% vs.29.820%±2.839%),absorbance value of the Caspase-3 active area and Caspase-3 protein expression (1.070±0.077 vs.0.785±0.058),with statistically differences (P<0.05).Conclusions Caspase inhibitor may protect rat hippocampal neurons from oxygen glucose deprivation injury by inhibiting Caspase-3 activity.
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Objective To study the establishment of rat model of asphyxia-cardiac arrest and efficacy of CPR in order to find the length of optimum time of asphyxia to cause injury.Methods One hundred and twenty-six male Sprague-Dawley rats were randomly (random number) divided into sham operation group and experimental groups.Cardiac arrest was induced by asphyxiation after intravenous injection of vecuronium bromide.The experimental groups were assigned into AP4 (four-minute asphyxia period),AP6 and AP8 subgroups in accordance with different lengths of time of asphyxia subjected to.In these groups,CPR,including pre-cordial compression and synchronized mechanical ventilation,was initiated 4,6 and 8 min after asphyxia-induced cardiac arrest,respectively.The successful ratio of resuscitation and hemodynamic variables were recorded.Brain water content,neural deficit scores (NDS),imaging changes on MR,pathological changes of brain tissue and neuronal apoptosis were evaluated at 1 d,3 d and 7 days after ROSC.All the data were analyzed by single-factor analysis of variance or Chi-square test.P < 0.05 was considered statistically significant.Result The lowest NDS occurred at 1 d after ROSC,brain water content and imaging changes on MR were most obvious at 3 d after ROSC,while pathological changes of brain tissue and neuronal apoptosis increased and reached the peak at 7d after ROSC.The survival rates after 24 hours of AP4,AP6 and AP8 groups were 85%,75% and 45%,respectively.The rate of ROSC and survival rate of AP8 group were significantly lower than those of other groups (P <0.01).The longer time of asphyxia the severer pathological changes of brain tissue,brain edema,neural deficit,and magnetic resonance imaging changes in all experimental groups.As compared to other groups,the brain damage index of AP8 group was most serious,while that of AP6 group was moderate.Conclusions The rat model following asphyxia-induced cardiac arrest and cardiopulmonary resuscitation was established successfully.From the evidence of survival rate and damage grade of brain tissue,asphyxia for 6 min may be the rational length of ischemic time in this model.
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Objective: Asphyxia and ventricular fibrillation are the two most prevalent causes of cardiac arrest. The study investigated the differences in brain damage after cardiac arrest between asphyxial and ventricular fibrillation cardiac arrests in rats. Methods: Male healthy Sprague-Dawley rats were randomly assigned to the asphyxial group (cardiac arrest of 6 min, n=15), ventricular fibrillation group (cardiac arrest of 6 min, n=15) and sham group (n=5). Neurologic deficit scores and tape removal test were evaluated at 1, 3 and 7 days after cardiopulmonary resuscitation from three groups. Serum S-100B and brain histopathologic damage scores were also examined. Results: There were no differences in neurologic performance at 1, 3 and 7 days after cardiopulmonary resuscitation between the asphyxial group and ventricular fibrillation group (P>0.05, respectively). Serum S-100B level was higher in the asphyxial group at 1, 3 and 7 days, compared with the ventricular fibrillation group (P<0.05, respectively). There were significantly higher histopathologic damage scores at 1, 3 and 7 days in the asphyxial group compared with the ventricular fibrillation group (P<0.05, respectively). Conclusion: Asphyxial cardiac arrest has worse morphologic brain damage compared with ventricular fibrillation cardiac arrest, but the functional brain damage caused by asphyxial cardiac arrest is similar to that caused by ventricular fibrillation cardiac arrest.
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<p><b>OBJECTIVE</b>To evaluate the effectiveness and safty of tranexamic acid in patients receiving on-pump coronary artery bypass grafting (CABG) without clopidogrel and aspirin cessation.</p><p><b>METHODS</b>The current study is a prospective, randomized and placebo-control trial. A total of 116 patients receiving selective on-pump CABG with their last ingestion of clopidogrle and aspirin within 7 days preoperatively were recruited. Despite 6 patients withdrawal their consent, the rest 110 were randomized to receive tranexamic acid or placebo. The tranexamic acid regimen was a bolus of 10 mg/kg followed by a maintenance of 10 mg·kg(-1)·h(-1) throughout the surgery. The primary outcome was the volume of allogeneic erythrocyte transfused perioperatively.</p><p><b>RESULTS</b>Baseline characteristics were comparable between the groups. In patients receiving tranexamic acid and placebo respectively, the volume of allogeneic erythrocyte transfused was 4.0 (7.5) units and 6.0(6.0) units (W = 1021, P < 0.01). In these 2 groups respectively, blood loss was 930 (750) ml and 1210 (910) ml (W = 1042, P < 0.01), the incidence of major bleeding was 50.9% and 76.4% (χ(2) = 7.70, P < 0.01), the incidence of reoperation was 0 and 9.1% (χ(2) = 5.24, P = 0.02); the volume of plasma transfused was 400 (600) ml and 600 (650) ml (W = 1072, P = 0.01), the exposure of plasma was 60.0% and 85.5% (χ(2) = 8.98, P < 0.01) and the exposure to any allogeneic blood products was 85.5% and 98.2% (χ(2) = 5.93, P = 0.01). Perioperative mortality, morbidity and the incidence of adverse events were balanced between the groups without statistical significance.</p><p><b>CONCLUSION</b>Tranexamic acid reduced significantly postoperative bleeding and transfusion in patients receiving on-pump CABG without clopidogrel and aspirin cessation.</p>