冠脉内注射腺苷减少急性心肌梗死直接PTCA术中无再流的发生

目的 探讨冠状动脉内注射腺苷对急性心肌梗死急诊直接PTCA术中无再流现象发生的影响。方法 79例急性心肌梗死患被随机分配到腺苷组（51例）和非腺苷组（28例）,腺苷给药方法为在每次球囊扩张前及其后冠状动脉内弹丸式注射24－48μg。结果 非腺苷组有8例出现无血流（28．6％）,腺苷组有3例出现无血流（5．9％）。注射腺苷患未见明显合并症。结论 对于急性心肌梗死患,急诊TCA术中冠状动脉内注射腺苷安全有效,无再流发生率显降低,因此对改善患预后具有极为重要的意义。     

大剂量阿托伐他汀对急性ST段抬高型心肌梗死患者急诊PCI治疗后冠脉无复流现象的作用

目的探讨大剂量阿托伐他汀对急性sT段抬高型心肌梗死急诊PCI术后冠脉无复流现象的影响。方法选择诊断为急性sT段抬高型心肌梗死并行急诊PCI治疗的患者60例,术前即刻分别给予阿托伐他汀（立普妥）20mg（对照组,n=30）和80mg（负荷组,n=30）,评价TIMI心肌灌注分级（TMPG）、单导联sT段下降幅度、术前及术后超敏C反应蛋白（hs-CRP）及术后6个月超声心动图评价心脏功能情况。结果与对照组相比,负荷组的TMPG2～3级者显著多于对照组（P=0．01）,sT段回落幅度明显增大（P=0．001）,术前、术后48h血浆hs-CRP降低（P〈0．05）,心功能明显改善（P〈0．05）,围手术期CK-MB及CTn-I峰值水平。结论大剂量阿托伐他汀能够明显改善PCI术后心肌血流灌注,防止无复流的发生,并可以改善远期心脏结构和功能。     

Immunohistochemical and functional studies for M3 muscarinic receptors and cyclo‐oxygenase‐2 expressed in the mouse atrium

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Remote per‐conditioning reduces oxidative stress,downregulates cyclo‐oxygenase‐2 expression and attenuates ischaemia–reperfusion‐induced acute kidney injury

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经导管向血管远端注射三磷酸腺苷对急诊PCI术中无复流现象的疗效

目的观察急诊经皮冠状动脉介入治疗(Percutaneous coronary interventions,PCI)术中出现无复流现象后,经导管向远端血管床注射三磷酸腺苷(ATP)的临床效果。方法 2008年6月-2010年9月,接受急诊PCI手术出现无复流的46例患者,随机分为研究组(B组)24例和对照组(A组)22例。B组经导管注入ATP 200μg,A组注入维拉帕米200μg,必要时可以反复注射。观察注射药物后校正的TIMI血流帧幅数(CTFC)、术中血流动力学参数,记录术后左室射血分数(EF值)及住院期间主要不良心血管事件发生率。结果两种药物在多次给药后,均可以使90%的患者恢复TIMI 3级血流(A组:90.1%,B组:91.7%,P>0.05),A组、B组的CTFC值分别为26.5±14.6、258±10.3(P>0.05),但B组血压下降幅度明显小于A组[(8.7±5.6)mmHg vs(13.4±10.6)mmHg,P<0.05],需要IABP支持的患者数量有减少的趋势。两组的并发症及不良事件发生率差异无统计学意义。结论经导管向远端血管床注射三磷酸腺苷,可以即刻提高靶血管血流灌注和心肌组织灌注,是一种安全有效的治疗无复流的方式。     

辛伐他汀对急性心肌梗死患者血清C反应蛋白及血脂的影响

目的：探讨辛伐他汀对急性心肌梗死患者血清C反应蛋白（CRP）及血脂水平的影响,并研究不同剂量的治疗效果。方法：选择急性心肌梗死患者96例,随机分为3组,A组给予常规治疗,B组在此基础上加用辛伐他汀20mg/d,C组加用辛伐他汀40mg/d,分别在发病24h内及治疗后不同时段检测CRP及血脂水平。结果：①B组及C组患者治疗1周后,hs-CRP水平明显降低,TC、LDL-C、HDL-C略有降低（P〈0.05）,TG略有升高（P〈0.05）;治疗2周后,hs-CRP水平进一步降低（P〈0.05）,TC、LDL-C、HDL-C水平与治疗后1周比较呈升高趋势（P〈0.05）,TG进一步升高,差异具有统计学意义（P〈0.05）。②治疗后,C组患者较B组患者hs-CRP水平降低更为明显,差异具有统计学意义（P〈0.05）。结论：辛伐他汀降低hs-CRP及血脂TC、LDL-C与剂量呈正相关。     

Lipoxin A4 ameliorates renal ischaemia–reperfusion‐induced acute lung injury in rats

Lipoxin A4 (LA4), a bioactive product of arachidonic acid, has been shown to exert strong anti‐inflammatory activity. By contrast, the anti‐inflammatory action of LA4 in a renal ischaemia–reperfusion (RIR)‐mediated acute lung inflammation (ALI) model and the potential pathogenesis of the condition is still unclear. The aim of the current research was to investigate the effect of LA4 on RIR‐induced ALI. The rat ALI model was induced by RIR. LA4 was injected via the tail vein immediately after RIR. The results indicate that LA4 markedly inhibits inflammatory cells infiltration, attenuates myeloperoxidase activity, and reduces the concentration of inflammatory mediators and Toll‐like receptor 4 (TLR4) in RIR‐induced ALI. Furthermore, LA4 suppressed nuclear factor kappa B (NF‐κB) p65 and mitogen‐activated protein kinase (MAPK) activation. The protective effect of LA4 in RIR‐stimulated ALI was reversed by BOC‐2 (an antagonist of the LA4 receptor). These results indicate that LA4 exerts powerful anti‐inflammatory functions in RIR‐induced ALI by attenuating TLR4 expression via MAPK and NF‐κB signalling. Accordingly, LA4 might be an underlying treatment drug for RIR‐induced ALI.     

Lycopene inhibits cyclic strain‐induced endothelin‐1 expression through the suppression of reactive oxygen species generation and induction of heme oxygenase‐1 in human umbilical vein endothelial cells

Lycopene is the most potent active antioxidant among the major carotenoids, and its use has been associated with a reduced risk for cardiovascular disease (CVD). Endothelin‐1 (ET‐1) is a powerful vasopressor synthesized by endothelial cells and plays a crucial role in the pathophysiology of CVD. However, the direct effects of lycopene on vascular endothelial cells have not been fully described. This study investigated the effects of lycopene on cyclic strain‐induced ET‐1 gene expression in human umbilical vein endothelial cells (HUVECs) and identified the signal transduction pathways that are involved in this process. Cultured HUVECs were exposed to cyclic strain (20% in length, 1 Hz) in the presence or absence of lycopene. Lycopene inhibited strain‐induced ET‐1 expression through the suppression of reactive oxygen species (ROS) generation through attenuation of p22^phox mRNA expression and NAD(P)H oxidase activity. Furthermore, lycopene inhibited strain‐induced ET‐1 secretion by reducing ROS‐mediated extrace‐llular signal‐regulated kinase (ERK) phosphorylation. Conversely, lycopene treatment enhanced heme oxygenase‐1 (HO‐1) gene expression through the activation of phosphoinositide 3‐kinase (PI3K)/Akt pathway, followed by induction of the nuclear factor erythroid 2‐related factor 2 (Nrf2) nuclear translocation; in addition, HO‐1 silencing partially inhibited the repressive effects of lycopene on strain‐induced ET‐1 expression. In summary, our study showed, for the first time, that lycopene inhibits cyclic strain‐induced ET‐1 gene expression through the suppression of ROS generation and induction of HO‐1 in HUVECs. Therefore, this study provides new valuable insight into the molecular pathways that may contribute to the proposed beneficial effects of lycopene on the cardiovascular system.     

阿托伐他汀联合普罗布考对急性心梗脂联素和超敏C反应蛋白的影响

目的 探讨阿托伐他汀联合普罗布考对急性心梗(AMI)血清脂联素(adiponectin,APN)及超敏C反应蛋白(hs-CRP)的影响.方法 选择AMI患者90例,随机分为常规治疗组(抗血小板药物、硝酸酯、阿托伐他汀、血管紧张素转换酶抑制剂及β受体阻滞剂)与联合普罗布考组(常规治疗基础上加用普罗布考) 各45例.检测入院后第1天和治疗1周后脂联素、hs-CRP水平,比较其在2组间的差异.结果 治疗后2组APN水平明显升高 (P<0.05),且联合普罗布考组上升程度明显高于常规治疗组(P<0.05); 而2组hs-CRP治疗后均显著下降 (P<0.05),且联合普罗布考组下降程度明显高于常规治疗组(P<0.05).结论 阿托伐他汀联合普罗布考可以增加对AMI患者的抗炎、抗氧化作用.     

冠状动脉内注射替罗非班对急性ST段抬高型心肌梗死患者介入治疗后无复流现象的影响

目的评价冠状动脉内注射替罗非班对急性ST段抬高型心肌梗死（STEMI）患者急诊经皮冠状动脉介入治疗（PCI）后无复流发生率的影响。方法将120例STEMI患者分为替罗非班组（替罗非班＋直接PCI,60例）和对照组（直接PCI,60例）。PCI术中根据TIMI血流分级、TIMI计帧法（cTFC）评价冠状动脉血流。术后24h进行实时心肌声学造影检查,计算心肌灌注缺损计分指数（CSI）及室壁运动计分指数（WMSI）。分析术后1h2组患者心电图sT段偏移总和比值（sumSTR）的变化。结果替罗非班组TIM13级血流显著多于对照组（P〈0．05）,而cTFC显著低于对照组（P〈0．05）;替罗非班组与对照组相比CSI（1．23±0．33．1．38±0．43,P〈0．05）,WMSI（1．52±0．39：1．70±0．38;P〈0．05）均显著降低;与对照组比较,替罗非班组术后1hsumSTR〉70％比例更高（P〈0．05）。结论冠状动脉内注射替罗非班能改善STEMI患者PCI术后心肌血流,防止无复流的发生。     

Andrographolide inhibits hypoxia‐induced hypoxia‐inducible factor 1α and endothelin 1 expression through the heme oxygenase 1/CO/cGMP/MKP‐5 pathways in EA.hy926 cells

Andrographolide is a potent anti‐inflammatory agent found in Andrographis paniculata. Endothelin 1 (ET‐1) is an endothelium‐derived vasoconstrictor with pro‐inflammatory properties secreted in response to hypoxia. Mitogen‐activated protein kinase phosphatase 5 (MKP‐5) is a dual‐specificity phosphatase that dephosphorylates threonine and tyrosine residues of MAPKs. We showed previously that hypoxia‐induced HIF‐1α expression and ET‐1 secretion are dependent on p38 MAPK in EA.hy926 cells. Here, we investigate what role MKP‐5 plays in andrographolide's inhibition of hypoxia‐induced expression of HIF‐1α and ET‐1. Hypoxic conditions were created using the hypoxia‐mimetic agent CoCl₂. Andrographolide enhanced HO‐1 and MKP‐5 expression and cellular cGMP content in addition to inhibiting hypoxia‐induced ROS generation. Concomitantly, the HO‐1 byproduct CO and the cGMP analogue 8‐bromoguanosine 3′,5′‐cyclic monophosphate (8‐Br‐cGMP) increased MKP‐5 expression, and pretreatment with CO and 8‐Br‐cGMP inhibited hypoxia‐induced HIF‐1α and ET‐1 expression. Transfection of HO‐1 siRNA or pretreatment with the HO‐1 inhibitor ZnPP‐9 or 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one, a specific inhibitor of soluble guanylate cyclase, reduced andrographolide‐induced MKP‐5 expression. Moreover, silencing MKP‐5 or treatment with the phosphatase inhibitor vanadate abrogated andrographolide's suppressing hypoxia‐induced p38 MAPK activation and HIF‐1α expression. The inhibition of hypoxia‐induced HIF‐1α and ET‐1 expression by andrographolide is likely associated with HO‐1/CO/cGMP/MKP‐5 pathways, which is involved in inhibiting hypoxia‐induced p38 MAPK activation.     

Tissue influx of neutrophils and monocytes is delayed during development of trovafloxacin‐induced tumor necrosis factor‐dependent liver injury in mice

Idiosyncratic drug‐induced liver injury (iDILI) has a poorly understood pathogenesis. However, iDILI is often associated with inflammatory stress signals in human patients as well as animal models. Tumor necrosis factor (TNF) and neutrophils play a key role in onset of trovafloxacin (TVX)‐induced iDILI, but the exact role of neutrophils and other leukocytes remains to be defined. We therefore set out to study the kinetics of immunological changes during the development of TVX‐induced iDILI in the established murine model of acute liver injury induced by administration of TVX and TNF. Initially, TNF stimulated the appearance of leukocytes, in particular neutrophils, into the liver of TVX‐treated mice, but even more so in control mice treated with the non‐DILI inducing analogue levofloxacin (LVX) or saline as vehicle (Veh). This difference was apparent at 2 hours after TNF administration, but at 4 hours, the relative neutrophil amounts were reduced again in Veh‐ and LVX‐treated mice whereas the amounts in TVX‐treated mice remained at the same increased level as at 2 hours. The influx of monocytes/macrophages, which was unaffected in Veh‐ and LVX‐treated mice was markedly reduced or even absent in TVX‐treated mice. Unlike controls, mice receiving TVX + TNF display severe hepatotoxicity with clear pathology and apoptosis, coagulated hepatic vessels and increased alanine aminotransferase levels and interleukin 6/10 ratios. Findings indicate that TVX delays the acute influx of neutrophils and monocytes/macrophages. Considering their known anti‐inflammatory functions, the disruption of influx of these innate immune cells may hamper the resolution of initial cytotoxic effects of TVX and thus contribute to liver injury development.     

血糖控制对急性心肌梗死患者C反应蛋白及近期预后的影响

目的探讨伴2型糖尿病的急性心肌梗死患者血糖控制情况对高敏c反应蛋白（hs—CRP）水平及住院期间不良心血管事件产生的影响。方法110例急性心肌梗死患者分为3组,I组为不伴糖尿病组,Ⅱ组为伴2型糖尿病且血糖控制良好组,Ⅲ组为伴2型糖尿病且血糖控制不良组。观察3组患者既往糖化血红蛋白水平、入院后hs—CRP水平及不良心血管事件发生。结果Ⅱ组和Ⅲ组患者hs-CRP水平分别为（7．21±1．37）mg／L、（9．48±1．10）mg／L,明显高于I组（3．56±1．72）mg／L,差异有统计学意义（均P〈0．01）。I组、Ⅱ组和Ⅲ组不良心血管事件发生概率分别为13．5％（7／52）、31．6％（12／38）和60．0％（12／20）,Ⅱ组与I组比较P〈0．05,Ⅲ组与Ⅰ组比较P〈0．01。结论血糖控制不良可抬高伴2型糖尿病的心肌梗死患者hs—CRP水平,伴2型糖尿病的冠心病患者控制血糖可改善发生心肌梗死后的近期预后。     

急性脑梗死患者血清胱抑素C和C反应蛋白水平变化的研究

目的：探讨急性脑梗死患者血清胱抑素C（cystatin C,Cys-C）和C反应蛋白（CRP）水平对病情变化及预后判断的意义。方法选择颈动脉系统进展性脑梗死70例为进展组,非进展性脑梗死168例为非进展组,分别于入院次日（第1天）、第3、7和14天检测血清Cys-C和CRP浓度,行颈部血管超声和经颅多普勒超声（ transcranial Doppler sonography ,TCD）检查,以及卒中量表（ National Institutes of Health Stroke Scale ,NIHSS）和Barthel 指数（ Barthel index ,BI）评分。结果进展组患者入院时颅／颈动脉狭窄率高于非进展组（44．3％ vs 29．8％,P＜0．05）,非进展组患者血清Cys-C浓度在第7、14天下降,血清CRP浓度在第3、7、14天下降,进展组患者Cys-C和CRP浓度在第3天明显增加,Cys-C浓度在第14天下降,CRP浓度在第7、14天下降,明显高于非进展组（P＜0．01）。进展组NIHSS和BI评分在入院后进行性增高,非进展组NIHSS和BI评分呈下降趋势（ P＜0．01）。结论观察血清Cys-C及CRP浓度的变化有助于早期发现和及时处理进展性脑梗死。     

瑞舒伐他汀对急性心肌梗死大鼠心肌组织中蛋白表达的影响研究

目的探讨瑞舒伐他汀对急性心肌梗死大鼠心肌组织蛋白表达的影响.方法选取雌性健康SD大鼠,通过结扎左冠状动脉前降支建立急性心肌梗死模型54只,随机分为瑞舒伐他汀10、6 mg/kg组和模型组各18只,另选择18只作为假手术组.瑞舒伐他汀组根据临床常用剂量分别采用瑞舒伐他汀按照10、6 mg/kg剂量溶于蒸馏水中ig给药,模型组、假手术组均采用等量生理盐水ig给药,1次/d,持续4周.采用免疫组化法检测大鼠心肌组织中Periostin、调控机制核因子κB (NF-κB)、白细胞介素-6(IL-6)蛋白的表达差异,采用RT-PCR技术检测转化生长因子(TGF-β1)、Periostin、NF-κB及IL-6的mRNA表达差异,比较各组大鼠的胶原容积分数(CVF).结果与模型组比较,瑞舒伐他汀10、6 mg/kg组大鼠Periostin蛋白灰度值以及NF-κB、IL-6蛋白阳性表达指数(PI)均显著下降(P<0.05); Periostin、NF-κB、IL-6及TGF-β1 mRNA表达均显著下降(P<0.05);CVF灰度值均显著下降(P<0.05).结论 瑞舒伐他汀可通过调节急性心肌梗死大鼠心肌组织中Periostin、NF-κB、IL-6、TGF-β1 mRNA及蛋白的表达来改善心肌重构.     

Esculetin inhibits histamine‐induced expression of inflammatory cytokines and mucin in nasal epithelial cells

Allergic rhinitis (AR) is a type of respiratory disease closely associated with chronic inflammation. Esculetin is a natural coumarin derivative and has been reported to possess anti‐allergic and anti‐inflammatory effects. However, the roles of esculetin in AR have not been studied. In this study, we aimed to examine the effect of esculetin on AR using an in vitro model. The human nasal epithelial cells (HNEpC) were stimulated by histamine for 24 hours with or without the pretreatment of esculetin. The mRNA levels and production of inflammatory cytokines including IL‐6 and IL‐8, as well as mucin 5AC (MUC5AC) were measured using qRT‐PCR and ELISA, respectively. The results showed that esculetin suppressed histamine‐induced expression and secretion of IL‐6, IL‐8, and MUC5AC in HNEpCs. Furthermore, we examined the effect of esculetin on NF‐κB pathway by detecting the expression levels of NF‐κB p65, p‐p65 and IκBα using western blot analysis. Esculetin treatment suppressed the histamine‐induced p‐p65 expression and p‐IκBα degradation. Inhibiting NF‐κB pathway suppressed histamine‐induced production of IL‐6, IL‐8, and MUC5AC in HNEpCs. These findings suggested that esculetin suppressed histamine‐induced production of inflammatory cytokines and mucin in HNEpCs, which were partly mediated by the inhibition of NF‐κB pathway.     

The role of Krüppel‐like factor 4 in transforming growth factor‐β–induced inflammatory and fibrotic responses in human proximal tubule cells

Krüppel‐like factor 4 (KLF4) is known to mitigate inflammation in several cell types. Using human proximal tubule cells, the present study aimed to investigate the role of KLF4 in regulating transforming growth factor (TGF)‐β₁ induced inflammatory and fibrotic responses. Human kidney proximal tubular cells were exposed to high glucose, or TGF‐β₁ and KLF4 expressions were determined. Cells were then transfected with empty vector or KLF4 and exposed to 2‐ng/mL TGF‐β₁ for up to 72 h. Inflammatory proteins (macrophage migration inhibitory factor and monocyte chemoattractant protein‐1) and pro‐fibrotic proteins (fibronectin and collagen IV) were measured after 72 h by enzyme‐linked immunosorbent assay and western blot, respectively. To determine the relevance to in vivo models of chronic kidney disease, KLF4 protein expression in streptozotocin‐induced diabetic mice was determined. Krüppel‐like factor 4 messenger RNA (mRNA) levels were significantly reduced in high glucose‐treated human kidney proximal tubular cells. High glucose increased TGF‐β₁ mRNA expression, which significantly increased migration inhibitory factor and monocyte chemoattractant protein‐1 protein secretion. Transforming growth factor‐β₁ significantly increased fibronectin and collagen IV protein expression. The overexpression of KLF4 significantly reduced TGF‐β–mediated increases in migration inhibitory factor and monocyte chemoattractant protein‐1 but had no effect on TGF‐β–mediated fibronectin and collagen IV mRNA and protein expression. The levels of KLF4 mRNA were significantly reduced in the diabetic kidney, and diabetic animals had a significant reduction in renal tubular expression of KLF4 proteins. This data suggest that KLF4 reduces inflammation induced by TGF‐β₁, suggesting a therapeutic role for KLF4 in diabetic nephropathy.