常压氧联合高压氧对急性脑梗死患者血清细胞间黏附分子及基质金属蛋白酶-9的影响

目的：探讨常压氧（NBO）联合高压氧（HBO）对急性脑梗死血清细胞间黏附分子及基质金属蛋白酶-9（MMP-9）水平的影响。方法选择2011年12月至2014年3月在青岛市中心医院神经内科住院且发病24h内来院就诊的168例急性脑梗死患者为急性脑梗死组,将其随机分为常规治疗、HBO治疗及NBO联合HBO治疗3个亚组,分别在治疗前、治疗10d后采用酶联免疫吸附法（ELISA）测定各亚组血清可溶性细胞间黏附分子（sICAM-1）、可溶性E-选择素（sE-selectin,sES）及MMP-9水平,分析各亚组治疗前后神经功能缺损变化。另以50名正常人组成正常对照组。结果3个亚组治疗10d后,血清sICAM-1、sES和MMP-9水平分别较治疗前显著下降（t＝8.754-11.351,P＜0.01）;HBO亚组、NBO＋HBO亚组患者显著低于常规亚组（t＝2.237-4.162,P＜0.05或0.01）;与HBO亚组比较,NBO＋HBO亚组患者血清sICAM-1、sES和MMP-9水平均显著下降（t＝2.141-2.366,P＜0.01）;HBO亚组、NBO＋HBO亚组治疗10d后,NIHSS评分较常规亚组显著下降（t＝5.367,P＜0.01;t＝9.943,P＜0.01）,而NBO＋HBO亚组较HBO亚组治疗后NIHSS评分显著下降,差异具有统计学意义（t＝2.827,P＜0.01）。结论 NBO联合HBO治疗抑制血清sICAM-1、sES和MMP-9水平优于HBO亚组,且更能改善急性脑梗死患者临床预后。     

基质金属蛋白酶类在颅内动脉瘤中的表达

目的检测基质金属蛋白酶类(MMPs)中MMP-2、MMP-9在颅内动脉瘤中的表达情况。方法取经DSA证实为颅内动脉瘤,并经显微神经外科手术夹闭动脉瘤的17例患者的17个动脉瘤的瘤壁组织为研究标本(动脉瘤组)。17个动脉瘤中,小动脉瘤10个,大动脉瘤7个;Hunt-HessⅠ～Ⅱ级的患者为11例,≥Ⅲ级的患者为6例。对照组为同期经CT及MRI证实为非血管性疾病的外伤患者,共15例,取其颞浅动脉组织为对照标本。经HE染色及免疫组化染色,检测动脉瘤的瘤壁组织和正常血管壁的组织结构变化及其中MMP-2、MMP-9的表达情况,计算阳性指数(PI)。结果①对照组的动脉壁各层MMP-2、MMP-9的阳性表达较低。动脉瘤组瘤壁组织的内膜、中膜、外膜有MMP-2、MMP-9的阳性表达。②动脉瘤组患者MMP-2、MMP-9的阳性表达率分别为88.2%和82.4%,高于对照组的6.7%和13.3%,差异有统计学意义,P<0.01。③小动脉瘤患者MMP-2和MMP-9的PI值分别为5.1±2.2、5.1±4.2,大动脉瘤患者MMP-2和MMP-9的PI值分别为4.6±2.4、4.1±2.3,差异均无统计学意义,P>0.05。④Hunt-HessⅠ～Ⅱ级患者MMP-2和MMP-9的PI值分别为4.5±1.6、4.2±3.7,高于Ⅲ级患者的MMP-2和MMP-9的PI值(分别为5.7±3.1、5.7±3.1),差异均无统计学意义,P>0.05。⑤经Spearman相关分析,动脉瘤组MMP-2的PI值与MMP-9的PI值呈正相关,r=0.425,P<0.05。结论 MMP-2、MMP-9在动脉瘤的瘤壁组织中表达较高,其高表达可能促进了颅内动脉瘤的形成和破裂。     

Intraplaque MMP-8 levels are increased in asymptomatic patients with carotid plaque progression on ultrasound

Carotid atherosclerotic plaque remodelling and increased risk of symptomatic plaque rupture seem to be partially mediated by matrix metalloproteinases (MMPs). In this study, we have investigated whether different MMPs are related to carotid atherosclerosis or to recent ischaemic brain disease. Eighty-four consecutive patients undergoing carotid endarterectomy for symptomatic and asymptomatic disease were studied. Plaques were analysed by ultrasound and later by morphology. Plasma MMP-2, MMP-8 and MMP-9 levels were quantified by ELISA. MMP expression and activity in carotid plaques was analysed by Western blotting and in situ zymography. Results were analysed with respect to plaque stability, morphology, symptomatic disease, presence of vascular risk factors and plasma markers of acute inflammation as high sensitivity C-reactive protein (hsCRP), fibrinogen, D-dimer and white blood cell counts. Patients with hypoechogenic plaques on ultrasound had more plasma MMP-8 (p = 0.04) and increased MMP activity as assessed by in situ zymography. Asymptomatic patients with plaque progression had more active intraplaque MMP-8 than asymptomatic patients without plaque progression. Presence of recent intraplaque haemorrhage or past history of CAD was related to increased activity of MMPs as assessed by in situ zymography (p < 0.01, CI 95% 0.8-1.0). Plasma MMP-8 and MMP-9, but not MMP-2 levels, decrease with time after ischaemic stroke. Patients with hypertension had more intraplaque active MMP-9 than normotensive (p = 0.03, CI 95% 0.7-1.0). Hypoechogenic carotid plaques had increased MMP activity and asymptomatic patients with plaque progression show increase intraplaque MMP-8 levels.     

Adjunctive effect of hyperbaric oxygen treatment after thrombolysis on left ventricular function in patients with acute myocardial infarction

Background

The role of hyperbaric oxygen in patients with acute myocardial infarction is controversial, ranging from not beneficial to having a favorable effect. This randomized study was conducted to further assess the benefit of hyperbaric oxygen treatment after thrombolysis on left ventricular function and remodeling in patients with acute myocardial infarction.

Methods

Seventy-four consecutive patients with first acute myocardial infarction were randomly assigned to treatment with hyperbaric oxygen treatment combined with streptokinase (HBO+) or streptokinase alone (HBO−).

Results

There was a significant decrease of end-systolic volume index from the first day to the third week in HBO+ patients compared with HBO− patients (from 30.40 to 28.18 vs from 30.89 to 36.68 mL/m², P < .05) accompanied with no changes of end-diastolic volume index in HBO+ compared with increased values in HBO− (from 55.68 to 55.10 vs from 55.87 to 63.82 mL/m², P < .05). Ejection fraction significantly improved in the HBO+ group and decreased in the HBO− group of patients after 3 weeks of acute myocardial infarction (from 46.27% to 50.81% vs from 45.54% to 44.05 %, P < .05).

Conclusions

Adjunctive hyperbaric oxygen therapy after thrombolysis in acute myocardial infarction has a favorable effect on left ventricular systolic function and the remodeling process.     

Monocyte matrix and ADAM metalloproteinase expression in type 2 diabetes after aspirin therapy

The matrix metalloproteinase system (MMP and the TIMP inhibitors), and the ADAM metalloproteinases, have roles in maintaining vascular plaque stability and the shedding of cell surface molecules, such as TNF-alpha and adhesion molecules; aspirin suppresses MMP expression and ADAM activity from some cell lines in vitro. In a randomised prospective controlled study, we examined peripheral venous monocyte MMP-9, TIMP-1 and ADAM mRNA levels, and protein expression, in subjects with type 2 diabetes (n=10) and controls (n=14) before and after oral aspirin therapy (150mg daily for 14 days) or no active intervention. Baseline monocyte TIMP-1 mRNA levels were significantly lower in the diabetes group (p=0.0014), although monocyte MMP-9 mRNA, and MMP-9 and TIMP-1 protein expression after culture did not differ significantly between groups. Plasma MMP-9 (p=0.027) and TIMP-1 (p=0.016) concentrations were significantly greater, and the ratio of plasma TIMP-1:MMP-9 concentrations significantly lower, in the diabetes group (p=0.023). ADAM mRNA levels did not differ significantly between groups and oral aspirin therapy had no significant effect on any variable. Type 2 diabetes is characterised by reduced monocyte TIMP-1 mRNA levels, and a lower plasma MMP-9 to TIMP-1 protein ratio compared to controls, a pattern that would promote coronary plaque instability if reproduced within vascular plaque. Monocyte ADAM mRNA levels do not differ between group and oral aspirin has no significant effect on these variables.     

Differential regulation of matrix metalloproteinase-9 by monocytes adherent to collagen and platelets

Circulating monocytes adhere to platelets and matrix proteins at sites of vascular injury, where engagement of specific surface tethering molecules mediates outside-in signaling and synthesis of gene products by the leukocytes. Here we demonstrate that interaction of isolated human monocytes with collagen induces matrix metalloproteinase-9 (MMP-9; gelatinase B) synthesis by monocytes, a process that is greatly enhanced in the presence of platelets. MMP-9 is a potent matrix degrading enzyme implicated in atherosclerotic plaque rupture, aneurysm formation, and other vascular syndromes. Synthesis of MMP-9 by monocytes is tightly regulated and synergistically increased following adhesion to collagen and platelets. Adhesion to control matrix proteins alone did not result in MMP-9 protein production and, similarly, adhesion of monocytes to platelets activated with thrombin in suspension was not sufficient to induce MMP-9 synthesis in the absence of monocyte adhesion to collagen. Interruption of intercellular contact between platelets and monocytes dramatically inhibited MMP-9 synthesis. These observations demonstrate that discrete adhesion-dependent signaling pathways govern MMP-9 synthesis by monocytes. The synthesis of MMP-9 by monocytes may be critical in vascular syndromes and other pathological processes that are dependent on dysregulated cell-cell and cell-matrix interactions.     

The determination of matrix metalloproteinase 9 activity and gene expression levels in Behcet’s disease patients with aneurysmal complications

The information concerning aneurysmal progress in Behcet’s disease is still insufficient, while researches in the role of matrix metalloproteinases (MMPs) in aneurysmal formation are rapidly expanding. The goal of the present study is to investigate the role of metalloproteinase 9 (MMP-9) in vascular complications which is observed in 10% of Behcet’s disease patients. Three groups have been studied; patients with Behcet’s disease, patients with Behcet’s disease who have vascular problems (vasculo-Behcet’s), and patients with abdominal aortic aneurysm (AAA). The third group was used as a control. The activity and gene expression levels of MMP-9 in plasma have been determined. We showed that compared to AAA patients there was no difference in the MMP-9 activity in Behcet’s disease patients (vascular and non-vascular). We also evaluated the gene expression level and activity of MMP-9 for every patient. The increase in the gene expression level for MMP-9 could only be detected at two patients. One of them was Behcet’s, the other was AAA patient. It is surprising that MMP levels of these patients were different. While the patient with Behcet’s had low protein level, another patient with AAA had high of MMP-9 level. This result suggested to us that the relationship between gene expression and active protein level is not correlated. It is not sufficient alone to determine MMPs levels for evaluating the pathogenesis. At the same time gene expression and the level of active protein should be assessed together.     

基质金属蛋白酶在胰腺癌的表达及其对预后的影响

目的 研究胰腺癌组织基质金属蛋白酶的表达与肿瘤侵犯血管和肝转移之间的联系，及其对预后的影响。方法 应用免疫组化方法测定36例胰腺癌患者切除标本中基质金属蛋白酶MMP-2和MMP-9的表达，结合临床病理和随访资料分析MMP-2和MMP-9表达与患者预后之间的关系。结果 胰腺癌MMP-2的阳性率为58．3％（21／36）。血管侵犯组的MMP-2表达率为81．8％（18／22），显著高于无血管侵犯组21．4％（3／14），P〈0．05。肝转移组的MMP2表达率为84．6％（11／13），显著高于无肝转移组的43．7％（10／23）。胰腺癌MMP9的阳性表达率为61．1％（22／36）。血管侵犯组MMP-9的表达率为77．3％（17／22）．显著高于无血管侵犯组的35．7％（5／14）。肝转移组的MMP-9表达率为84．6％（11／13），显著高于无肝转移组的47．8％（11／23），P〈0．05。Kaplan—Meier生存分析显示MMP-2阳性组的预后较差（尸〈0．05）。结论 MMP-2、MMP9与肿瘤血管侵犯和肝转移的发生相关，MMP2高表达提示其预后较差。     

MMP-9、HPSE和VEGF-C蛋白表达在中老年人肺癌抗血管和抗淋巴管生成治疗中的意义

目的探讨基质金属蛋白酶9(MMP9)、乙酰肝素酶(HPSE)和血管内皮生长因子C(VEGFC)蛋白表达在中老年人肺癌抗血管和抗淋巴管生成治疗中的意义。方法应用免疫组化SABC法检测MMP9、HPSE和VEGFC蛋白表达在65例肺癌组织中的表达,并与癌旁组织和正常肺组织对比,同时结合肺癌的临床病理学特征及预后进行分析。结果肺癌组织中MMP9、HPSE和VEGFC蛋白的阳性表达率明显高于正常肺组织和癌旁组织(P<005);不同类型和不同分化程度肺癌组织中MMP9、HPSE和VEGFC蛋白阳性表达率无显著性差异(P>005);Ⅲ期和Ⅳ期肺癌组织中MMP9、HPSE和VEGFC蛋白阳性表达率明显高于Ⅰ期和Ⅱ期(P<005);生存3年以下的肺癌组织中MMP9、HPSE和VEGFC蛋白阳性表达率明显高于生存3年以上者(P<005)。结论MMP9、HPSE蛋白表达在肺癌的生长、侵袭和转移以及血管生成中发挥重要作用;VEGFC是促进肺癌经淋巴转移的重要因素;肺癌的生长、侵袭和转移可能是MMP9、HPSE促血管生成和VEGFC促淋巴生成二者的协同作用;MMP9、HPSE和VEGFC蛋白可作为判断肺癌生物学行为和患者预后的一个参考指标;为人肺癌抗血管和抗淋巴管生成治疗的可行性提供了一定的实验依据。     

糖尿病患者动脉粥样硬化斑块内基质金属蛋白酶2和9与斑块稳定的关系

目的　比较糖尿病患者与非糖尿病组患者动脉粥样硬化斑块内基质金属蛋白酶 2和基质金属蛋白酶 9表达的差异 ,初步探索基质金属蛋白酶 2和基质金属蛋白酶 9与糖尿病动脉粥样硬化斑块稳定的关系。方法　从2 3例糖尿病足截肢和 17例尸检下肢动脉标本中选取晚期动脉粥样硬化病变的组织块共 12 6块 ,分为糖尿病组 (74块 )和非糖尿病组 (5 2块 ) ,从中随机选取各 4 0个组织块 ,运用免疫组织化学染色法检测基质金属蛋白酶 2和 9在两组粥样硬化斑块中的表达。结果　糖尿病组抗基质金属蛋白酶 2、抗基质金属蛋白酶 9免疫沉积物主要集中在斑块核心周围 ,特别是在斑块的肩部和纤维帽。糖尿病组动脉斑块内抗基质金属蛋白酶 2免疫沉积物表达显著高于非糖尿病组 (免疫沉淀物积分光密度值分别为 6 90 14± 14 4 5 9和 5 70 0 4± 16 171,阳性面积百分比分别为 13.0 %± 2 .7%和 11.1%± 3.3% ) ;糖尿病组斑块内基质金属蛋白酶 9表达也显著高于非糖尿病组 (免疫沉淀物积分光密度值分别为 10 2 4 85± 2 0 4 31和 75 2 80± 1310 6 ,阳性面积百分比分别为 18.4 %± 3.6 %和 13.7%± 2 .3% )。结论　基质金属蛋白酶 2和 9在糖尿病组动脉粥样硬化斑块中的表达显著高于非糖尿病组。基质金属蛋白酶 2和 9在糖尿病动脉中表达增     

Hyperbaric oxygen therapy in the treatment of refractory peripancreatic abscess associated with severe acute pancreatitis

Five patients with peripancreatic abscesses associated with severe acute pancreatitis were treated by hyperbaric oxygen therapy (HBO). In 3 patients, the course after surgical mobilization of the pancreas and drainage of the pancreas bed was complicated by peripancreatic abscesses. HBO was conducted under a pressure of 2.8 atmospheres for two hours dialy. Four of the 5 patients showed a progressive improvement in their condition. In one patient who failed to respond despite seven sessions of HBO, Pseudomonas aeruginosa was isolated from the discharge, and resection of necrotic tissue and drainage were performed. The main effects of HBO were the alleviation of high spiking fever, the improvement of white blood cell count and serum amylase levels, and the reduction of the abscess size. We recognized HBO to be a successful treatment for peripancreatic abscess associated with severe acute pancreatitis and better results were obtained than in cases that did not receive HBO.     

Risk Model and Nomogram for Dysphagia and Xerostomia Prediction in Head and Neck Cancer Patients Treated by Radiotherapy and/or Chemotherapy

In our randomized trial on hyperbaric oxygen (HBO), it was shown that HBO could reduce dysphagia and xerostomia, which are frequently encountered after (chemo-) radiotherapy (RT) and/or surgery for head and neck cancer (HNC). A risk model and nomogram are developed to select those patients who most likely will respond to HBO treatment. A total of 434 HNC patients treated from 2000 to 2008 were analyzed and filled out the EORTC QLQC-30 and H&N35 questionnaires. Age, gender, chemotherapy, T and N stages, site, radiotherapy technique, RT boost, surgery of the primary tumor and neck, bilateral RT, and dose were analyzed in a statistical model. The discriminative value of the model was evaluated based on receiver operating characteristics (ROC), the area under the curve (AUC), sensitivity, specificity, and proportion of correctly classified measures. Significant factors in predicting swallowing problems are age, follow-up duration, tumor site, chemotherapy, surgery of the primary tumor and neck, and dose. For dry mouth, the significant factors are age, gender, tumor site, N stage, chemotherapy, and bilateral irradiation. For dysphagia and xerostomia, the area under the ROC curve is 0.7034 and 0.7224, respectively, with a specificity of 89/77 %, sensitivity of 27/58 %, and a positive predictive value of 83/67 % for dysphagia and xerostomia, respectively. The developed predictive risk model could be used to select patients for costly hyperbaric oxygen treatment to prevent or reduce severe late side effects of HNC treatment. Our model serves as a guideline for the Department of Radiation Oncology to reduce costs by excluding patients not amenable to hyperbaric oxygen protocols. The nomogram presented is a useful tool for clinicians in assessing patient risks when deciding on follow-up strategies (e.g., hyperbaric oxygen treatment) after RT or surgery for HNC.     

活化淋巴细胞诱导人血管平滑肌细胞基质金属蛋白酶表达

为探讨活化的淋巴细胞直接接触对血管平滑肌细胞基质金属蛋白酶表达的影响 ,用乙酸肉豆蔻佛波醇活化并经 1%多聚甲醛固定的人外周血淋巴细胞 ,与培养的人类胚胎血管平滑肌细胞共同孵育 ,用聚丙烯酰胺凝胶电泳法测定细胞培养上清液中基质金属蛋白酶的活性。结果发现 ,基础状态下的体外培养人血管平滑肌细胞合成基质金属蛋白酶 2的酶原形式 ,有少量基质金属蛋白酶 2的活性形式存在。经佛波醇活化淋巴细胞组上清液中可检测到基质金属蛋白酶 1、基质金属蛋白酶 3和基质金属蛋白酶 9活性 ,并且基质金属蛋白酶 2活性形式较对照组增加 198%± 2 7% (P <0 .0 1) ,未经佛波醇活化的淋巴细胞不影响血管平滑肌细胞基质金属蛋白酶的合成和分泌。以上结果提示 ,活化固定的淋巴细胞可以通过细胞直接接触诱导血管平滑肌细胞基质金属蛋白酶表达增加及活化 ,在动脉粥样硬化的斑块破裂过程中可能起重要作用     

匹伐他汀对血管平滑肌细胞金属基质蛋白酶9表达的影响

目的 观察金属基质蛋白酶9(MMP-9)在动脉粥样硬化组织中的分布及匹伐他汀对TNF-α刺激血管平滑肌细胞MMP-9 蛋白和mRNA 表达的影响.方法 病理标本取自外科择期手术病例,行常规病理和免疫组织化学检查;对照组动脉标本取自非正常死亡健康成人尸体及非血管病变切除标本;血管平滑肌细胞取自开放手术切除的主动脉中膜.实验为5 组,对照组和4 个实验组.实验各组平滑肌细胞在给予TNF-α刺激前预先加入不同浓度的匹伐他汀(分别为1 ng/ml、10 ng/ml、100 ng/ml、500 ng/ml),测定其MMP-9 蛋白和mRNA 表达.结果 免疫组化检测显示,实验组动脉硬化组织TNF-α和MMP-9 蛋白分布明显增加,主要集中在炎性细胞聚集处,与对照组比较差异有统计学意义;MMP-9 的分布与TNF-α明显相关.匹伐他汀呈浓度依赖方式抑制TNF-α诱导平滑肌细胞MMP-9 蛋白和mRNA 表达;MMP-9 蛋白表达分别减少10.5%、24.1%、46.0%和61.0%,mRNA 表达分别减少9%、21%、35%和46%,差异有统计学意义.结论 动脉硬化组织中MMP-9 分布与TNF-α明显相关,提示动脉粥样硬化组织中MMP-9 增加与其他细胞因子相互影响有关.预先给予匹伐他汀可以呈现浓度依赖方式显示抑制TNF-α诱导的血管平滑肌细胞MMP-9 蛋白和mRNA 表达,提示他汀类药物可以通过抑制MMP-9 表达,延缓、稳定动脉粥样硬化病变,早期干预效果更好.     

Relationship of Matrix Metalloproteinases 2 and 9 in the Wall of Abdominal Aortic Aneurysms

This study examines the pathogenesis of abdominal aortic aneurysms (AAAs) with respect to pathological characteristics and expressions of matrix metalloproteinases (MMP)-2, MMP-9 and tissue inhibitor of metalloproteinases (TIMP)-1, in Tottori University Hospital, Japan. Thirty-four consecutive patients were operated on for (AAAs). During surgery, the anterior wall of the aneurysmal aorta was resected from the site of maximal diameter throughout the wall. AAA specimens consisted of the aneurysmal aortas, while control specimens consisted of the undulated aortas of autopsy cases. The expression of MMP-2, MMP-9 and TIMP-1 was evaluated by immunohistochemistry, Western blotting and competitive polymerase chain reaction (C-PCR). Immunohistochemistry showed MMP-2-positive cells and TIMP-1 positive cells mainly in the intima, and MMP-9-positive cells in the intima and adventitia. Western blotting revealed the expression of MMPs and TIMP-l variably in all the cases examined. C-PCR showed significantly higher elevation of MMP-2 mRNA in the small-diameter AAAs (30–45 mm), plus higher MMP-9 mRNA expression in both the small-diameter and the medium-large-diameter AAAs (45 < mm), than in controls. The ratio of MMP-2 to TIMP-1 mRNA levels in the small-diameter AAAs, and the ratio of MMP-9 to TIMP-1 mRNA levels in both the small-diameter and medium-large-diameter AAAs were significantly higher than in controls. The mRNA levels were significantly correlated between MMP-2 and MMP-9, between MMP-2 and TIMP-1, and between MMP-9 and TIMP-1 in the AAAs. This study demonstrates that increases in mRNA imbalanced expression of MMPs/TIMP, as well as increases of MMP-2 and MMP-9 expression, may play crucial roles in the development and growth of AAAs, and TIMP-1 may play an important rule of preventing the aortic expansion.     

Aggregated low density lipoproteins decrease metalloproteinase-9 expression and activity in human coronary smooth muscle cells

Plaque stability largely depends on vascular smooth muscle cell (VSMC) function. VSMC secrete metalloproteinases (MMPs), matrix degrading endopeptidases, that regulate VSMC migration and function. Among them, gelatinase B or MMP-9 seems to have a protective effect by promoting a stable plaque phenotype. In macrophage foam cells oxidized LDL (oxLDL) uptake regulates MMP-9 expression. However, it is unknown whether VSMC-lipid loading by aggregated LDL (agLDL) internalization produces any effect on MMP-9 production by human resident vascular cells. In the present study, we analyzed the effect of lipid-internalization in MMP-9 and MMP-2 expression and activity and its consequences in VSMC migration. Our results show that agLDL-internalization down-regulates MMP-9 activity in a time-dependent manner up to 42% at 48h and in a dose-dependent manner up to 87% at 300 microg/mL. nLDL induced similar but not sustained decrease on MMP-9 activity. However, neither agLDL nor nLDL exerted any significant effect on MMP-2 and TIMP-1. VSMC regrowth after a scratch injury was significantly reduced by exposure to agLDL. We conclude that agLDL-lipid loading reduces MMP-9 activity and this effect is associated to inhibition of VSMC migration. Thus, agLDL internalization may have consequences on vascular remodeling after injury, and the stability of lipid-rich atherosclerotic plaques.     

Hyperbaric oxygen therapy: from the nineteenth to the twenty-first century

Hyperbaric oxygen technology now occupies a legitimate place in modern medical practice, and the number of clinically active hyperbaric facilities has grown. We estimate that more than 200 monoplace (single-patient) chambers and over two dozen multiplace facilities are presently active in the United States. Nevertheless, the majority of patients suffering from syndromes amenable to HBO therapy are treated in hospitals devoid of such modalities. This situation stems in part from the significant cost of appropriate facilities, the relative scarcity of trained personnel, and the difficulties in obtaining appropriate compensation in an era of rapidly changing reimbursement paradigms. Frequently, patients undergoing HBO therapy require mechanical ventilation, vasoactive drug infusions, sophisticated monitoring, and accurate fluid and electrolyte therapy during treatment. The demonstrated efficacy of HBO as an important part of the treatment of certain acute disease processes, however, justifies the facilities and skilled personnel necessary for the care of critically ill patients in a hyperbaric environment.     

Myocardial hibernation identified by hyperbaric oxygen treatment and echocardiography in postinfarction patients: comparison with exercise thallium scintigraphy.

To evaluate the potential for hyperbaric oxygen (HBO) to produce transient improvement in function in areas of myocardium ischemic at rest (hibernating myocardium), 24 patients were studied within 1 week of acute myocardial infarction. Results were compared with single-photon emission computed tomography (SPECT) thallium-201 exercise scintigraphy. Echocardiography demonstrated improved contraction following HBO in 20 of 62 damaged left ventricular segments in 12 of 24 patients. Thirteen of the 28 segments and 9 of the 14 patients showing reversible ischemia on SPECT imaging showed improvement with HBO. There were eight segments with apparently normal resting contraction that showed a reversible thallium defect. Of 42 segments with fixed contraction abnormalities following HBO, eight had reversible thallium defects, four had normal thallium kinetics, and 30 had fixed thallium defects. Thus hyperbaric oxygen can demonstrate improvement in function in some segments of left ventricle after infarction. There is some overlap with viability as determined by thallium studies, but the two techniques may be complementary in describing myocardial ischemia.     

急性冠状动脉综合征患者颈动脉斑块与血浆基质金属蛋白酶的相关性

目的研究急性冠状动脉综合征患者颈动脉斑块与血浆基质金属蛋白酶的相关性。方法采用高分辨率超声，测定30例急性冠状动脉综合征患者、29例稳定型心绞痛患者和17例正常对照者的颈动脉内膜中膜厚度及斑块积分，同时采用夹心酶联免疫分析法测定血浆基质金属蛋白酶9和组织型金属蛋白酶抑制因子1的变化。结果三组间的年龄、性别、总胆固醇、甘油三酯、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇无显著性差异。急性冠状动脉综合征组血浆基质金属蛋白酶9、组织型金属蛋白酶抑制剂、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1及颈动脉内膜中膜厚度、总斑块积分、软斑块积分和硬斑块积分显著高于稳定型心绞痛组和正常对照组。基质金属蛋白酶9与颈动脉内膜中膜厚度、总斑块积分、软斑块积分呈正相关（r=0．468，P〈0．01；r=0．592，P〈0．01；r=0．677，P〈0．01）；组织型金属蛋白酶抑制剂与颈动脉内膜中膜厚度、总斑块积分、软斑块积分、硬斑块积分呈正相关（r=0．449，P〈0．01；r=0．493，P〈0．01；r=0．435，P〈0．01；r=0．227，P〈0.05）；基质金属蛋白酶9，组织型金属蛋白酶抑制剂1与颈动脉内膜中膜厚度、总斑块积分、软斑块积分呈正相关（r=0．253，P〈0．05；r=0．431，P〈0．01；r=0．547，P〈0．01）。去除年龄因素后，偏相关分析显示颈动脉内膜中膜厚度与基质金属蛋白酶9（r=0．461，P〈0．001）、组织型金属蛋白酶抑制剂1（r=0．441，P〈0.001）、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1（r=0．241，P〈0．01）呈正相关关系。结论急性冠状动脉综合征患者血浆基质金属蛋白酶9、组织型金属蛋白酶抑制剂1、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1及颈动脉内膜中膜厚度、总斑块积分、软斑块积分和硬斑块积分显著高于稳定型心绞痛患者和正常对照。血浆基质金属蛋白酶9、组织型金属蛋白酶抑制剂1、基质金属蛋白酶9，组织型金属蛋白酶抑制剂1与颈动脉内膜中膜厚度、总斑块积分、软斑块积分呈正相关关系。     

Influence of hyperbaric oxygen on tumor necrosis factor-alpha and nitric oxide production in endotoxin-induced acute lung injury in rats

We previously demonstrated that hyperbaric oxygen (HBO) treatment alleviated lipopolysaccharide (LPS)-induced acute lung injury in rats. However, the mechanisms responsible for the protective effect are still not fully understood. To obtain further information on the protective effect of HBO, in this study we investigated the role of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) in intratracheal spraying LPS-induced acute lung injury in rats after HBO or hyperoxia treatment. The results showed that HBO but not hyperoxia attenuated the TNF-alpha level in plasma and bronchoalveolar lavage (BAL) fluid, NO concentration in BAL and plasma, and inducible NO synthase protein expression in lung tissue based on the Western blotting and immunohistochemical staining.