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Results: The CO pretreatment group received pre-exposure to 250 ppm of CO significantly reduced the expression of CHOP in the heart compared with I-R group; however, hypoxia pretreatment group showed no such effect.

吸入低浓度的CO(250 ppm)能明显改善心肌缺血-再灌注损伤;其机制可能为外源性CO缓解缺血-再灌注激发的过度内质网应激,抑制CHOP过表达,减轻ERS相关细胞凋亡的发生,从而减轻心肌缺血-再灌注损伤。

Methods: A total of 218 patients with ST segment elevated myocardial infarction whose blood routines were obtained at the admission were studied. All cases were divided into two groups according to the neuropil to lymphocyte ratio of small to large size. Then we analyzed the morbidity of AMI complications between the two groups.

入选急性ST段抬高心肌梗死患者218例,入院后即刻抽取静脉血查血常规,按中性粒细胞/淋巴细胞比率的大小由小到大将其分为A、B两组,对两组急性心肌梗死并发症发生率进行比较。

Background: Opening of cardiac ATP-sensitive potassium channels is a well-characterized protective mechanism against ischemia and reperfusion injury.

心肌细胞ATP敏感钾通道的开放可以保护心肌免受缺血再灌注损伤,有证据显示肌浆网和线粒体K通道与这种保护效应有关。

The lack of a well-characterized in vitro model of load-induced cardiac hypertrophy has hampered further mechanistic investigation in this area, and little is known as to how mechanical load in initially converted into intracellular signals of gene regulation.

以往对心肌肥厚的实验研究基本上采用体内实验方法,然而,在体的实验研究由于受血液动力学、激素、神经反射的影响,不能恰当地反映一些因子或激素在心肌肥厚中的意义。

CGRP content in myocardium gradually enhanced from normal group to controls group, and model group's was the highest. We found immunopositive neurons and nerve fibers of nNOS and CGRP by immunochemistry in normal myocardium. They were mainly round-shaped and oval-shaped, also tadpole-shaped、 shuttle-shaped、triangle-shaped、ring-shaped and irregular-shaped. Nv of neurons and nerve fibers in atria were more than in ventricle in some degree; Those in right part of heart were more than in left. Morphology of CGRP neurons changed in model group, the number of ring-shaped neurons increasing, while the round-shaped and oval-shaped decreasing, and Nv and Sv of model group were markedly less than normal. Expression of nNOS mRNA was overly higher than normal group, but CGRP was opposite.

心肌组织CGRP的含量由正常组、实验对照组至CHF组逐渐升高,差异显著;免疫组化研究表明心肌组织中存在nNOS和CGRP免疫阳性神经细胞及纤维,细胞形态多样,正常多以圆形和椭圆形为主,还有梭形、蝌蚪形、三角形、指环形及不规则形,细胞密度心房高于心室,右心高于左心;CHF组CGRP神经细胞形态有一定改变,淡染的指环形细胞增多,而深染圆形或椭圆形细胞减少,其面、数密度均明显低于正常组,差异显著;用RT-PCR测得CHF组nNOS mRNA极度表达,显著高于正常组,而CGRP表达明显低于正常组。

Methods: Twenty-four male SD rats were randomly divided into normal control (NC, n=6), protein C activator (PCA, n=6), lipopolysaccharide (LPS, n=6) and LPS+PCA group (n=6). NC group were given normal saline and PCA group were injected protein C activator (0.4 mg/kg) through vein of the tail. LPS group were administered lipopolysaccharide (10 mg/kg, 4h) by intraperitoneal injection method to make the model of septic shock rats. After the animal model was made, LPS+PCA group were injected protein C activator (0.4 mg/kg) through vein of the tail. 30 minutes after the injection, each rat was tested by Medlab biosignal analyzing system for observing mean arterial pressure and left ventricle function, the activity of LDH and iNOS in myocardium and the cuttings of myocardial tissues.

取SD雄性大鼠24只随机分成对照组、PCA组、LPS组和LPS+PCA组四组,对照组尾静脉注射生理盐水,PCA组尾静脉注射蝮蛇毒蛋白C激活物,LPS组腹腔注射LPS (10 mg/kg, 4h)的方法建立败血症休克的实验动物模型,在建立败血症的实验动物模型的基础上,尾静脉注射PCA (0.4 mg/kg)为LPS+PCA组,每只大鼠均于药后30 min时运用Medlab生物信号采集处理系统记录平均动脉压和左心室功能指标,并测定心肌中乳酸脱氢酶活性、诱导性一氧化氮合酶活性及心肌病理切片。

Comparing with crystalloid and blood cardioplegic solution, self-blood cardioplegic solution is a good cardioprotection for infants in cardiopulmonary bypass and could provide satisfactory protection for the immature myocardium.

自体冷血停搏液对婴幼儿心内直视手术心肌保护优于冷血和晶体停搏液,对未成熟心肌具有良好的保护作用。

RESULTS: Both HPC and treatment with ruthenium red (5μmol/L) during the first 10 min reoxygenation improved recovery of LVDP±dp/dt and decreased LVEDP, which was associated with reduced infarct size and lactate dyhydrogenase release.

用TTC染色法测心肌梗死面积。结果:低氧预处理和低氧后复氧期的前10min用钌红(5μmol/L)处理均可促进LVDP、±dp/dt,和LVEDP的恢复,减小心肌梗死面积,减少LDH释放。

RESULTS: Both HPC and treatment with ruthenium red (5 μmol/L) during the first 10 min reoxygenation improved recovery of LVDP,±dp/dtmax and decreased LVEDP, which was associated with reduced infarct size and lactate dyhydrogenase release.

用TTC染色法测心肌梗死面积。结果:低氧预处理和低氧后复氧期的前10 min用钌红(5 μmol/L)处理均可促进LVDP、±dp/dtmax和LVEDP的恢复,减小心肌梗死面积,减少LDH释放。复氧期的前10 min用精胺(20 μmol/L)处理可减弱低氧预处理的心脏作用。

The 4th left rib was cut and a model of left coronary artery occlusion/release was carried outo Rats were divided randomly into 4 groups: control group without LCA occlusion (group A, n=6);I/R group(group B, n=6); ketamine(5mg.kg-1)+I/R group (group C, n=6); ketamine(10mg.kg-1)+I/R group(group D,n=6)o All rats in groups B, C , D were subjected to 30 minutes of LCA occlusion followed by 120minutes of reperfusion. Rats in group C and D were injected with 5mg.kg-1 and 10mg.kg-1 of ketamine before reperfusion, respectively. Significant electrocardiogram and color changes at the area at risk were considered indicative of successful coronary occlusion and reperfusionc Serum was exampled from left jugular vein at 30 minutes and 120 minutes during reperfusion to measure IL-6 and TNF- level by ELISA measurements. After reperfusion of 120 minutes, the heart was removed and the cardiac apex was exampled with snap-frozen in liquid nitrogen and stored at -70 C .

采用左冠状动脉前降支结扎开放建立心肌缺血/再灌注模型,健康SD大鼠24只,随机分为心包打开假手术组(A组,n=6),缺血/再灌注对照组(B组,n=6),5 mg·kg~(-1)氯胺酮+缺血/再灌注组C组,n=6,缺血30min后右腹股静脉注入5 mg·kg~(-1氯胺酮,10mg·kg~(-1)KTM+I/R组D组,n=6,缺血30min后右腹股静脉注入10 mg·kg~(-1氯胺酮。10%水合氯醛40 mg·kg~(-1)腹腔注射麻醉,气管切开,连接多功能监护仪记录心电图;小动物呼吸机人工呼吸,呼吸频率60次/分,潮气量2ml/100g,于左胸第四肋间打开胸腔暴露心脏,在左心耳下1mm左冠状动脉处,用丝线,眼科外用不锈钢小圆针穿过心肌浅层,稳定10min后将U型含有铜丝的胶管置于冠状动脉表面一起结扎(A组不结扎,B、C、D组结扎);结扎开始左心室心尖部即由红色变暗,30 min后呈暗红色,心电图中出现S-T段抬高,说明缺血形成。

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