高原红细胞增多症患者进入平原后肺循环的变化

对7例高原红细胞增多症患者分别在西宁和苏州进行肺动脉压直接测定以及其它有关参数的测定,发现患者进入平原后血气明显改善、血红蛋白减少、红细胞压积降低、肺动脉压和全肺阻力降低、运动5min后肺动脉压恢复时间缩短、心输出量和心脏指数增高。证实低氧是高原红细胞增多的主要病因;低氧性肺动脉高压具有可逆性,并在较短时期内就可恢复到接近正常水平;脱离低氧环境对患者是有利的。     

高原红细胞增多症患者血清促红细胞生成素活性的观察

目的 :探讨血清促红细胞生成素 (EPO)活性与西藏高原红细胞增多症 (HAPC)的关系。方法 :择藏汉两族男性 HAPC患者 (红细胞压积 >6 5 % ,血红蛋白 >2 0 0 g/ L) ,用骨髓造血细胞培养、细胞集落计数等方法测定其单位浓度血清 EPO的促骨髓造血干细胞增生活性 ,并与同族对照组进行统计学比较。结果 :1藏族 HAPC的 EPO检出率为 35 .7% ,汉族为 34 .6 % ,两组的发生率没有明显区别。2藏、汉两族 HAPC患者血浆 EPO水平的平均值较同族对照组分别增高了 148%和 2 84% ,藏族的增高差异有显著性意义。 3藏、汉两族 HAPC患者单位浓度的血清 EPO(1.0 5 IU/ L)活性均低于同族对照组 ,其中对红系集落形成单位 CFU- E的影响汉族降低了6 2 .4% ,藏族降低了 5 0 .7%。对红系爆式集落形成单位 BFU- E的影响汉族降低了 6 1.4% ,藏族降低了 2 7.3%。结论 :1藏、汉两族 HAPC组具有较高平均血浆 EPO水平 ;2藏、汉两族 HAPC组血清 EPO平均活性降低     

高原红细胞增多症合并慢性胃炎76例临床分析

高原红细胞增多症(HAPC)为慢性高原病的一种临床类型.人体长期在高原低氧环境下生活,慢性缺氧引起红细胞增生过度,血红蛋白、红细胞压积过度增高,导致各脏器及组织充血、血流淤滞及缺氧性损害,以移居高原人群的发病率居多.我们对我院76例高原红细胞增多症合并慢性胃炎患者行胃镜及胃黏膜病理学检查,并做相应的治疗.现将临床资料分析如下.     

西藏高原30例高原红细胞增多症患者临床治疗分析

高原红细胞增多症是一种高原地区常见病、多发病.我院地处海拔3700米左右,现将我院2008年1月～2012年12月收治的30例高原红细胞增多症患者的临床资料进行回顾性分析,现报告如下. 临床资料 1.一般资料:2008年1月～ 2012年12月在我院经治的30例高原红细胞增多症患者,其中男18例,女12例,年龄42～65岁,平均年龄49.5岁;藏族15例、汉族12例、其他3例.     

高原红细胞增多症动脉粥样硬化危险因素分析

目的检测高原红细胞增多症(HAPC)有关血脂、血压、体重指标并分析其与动脉粥样硬化的关系。方法在海拔2800 m青海格尔木地区选择HAPC患者86例和健康对照人群200例,清晨空腹状态下检测血压、体重、心率等生理参数及血脂指标,并进行比较分析。结果 HAPC组较对照组:(1)血TG、LDL升高,HDL、ApoA1降低,动脉硬化指数增高及ApoA1/ApoB比值降低,差异具有显著性(P<0.05);高甘油三酯血症、高胆固醇血症、混合型高脂血症、低高密度脂蛋白血症的比例较对照组明显增高,其中高甘油三酯血症的检出率高于其他血脂增高类型,差异具有显著性(P<0.05)。(2)体重、体质指数、心率较对照组明显增高,肥胖、高血压的检出率较对照组明显增高,且高血压以舒张压增高为多见,差异具有显著性(P<0.05)。结论 HAPC具有血脂紊乱、高血压、肥胖这三种重要的动脉粥样硬化高危因素,提示其发生动脉粥样硬化及其相关疾病的危险性增高。     

高压氧治疗对高原红细胞增多症患者血液流变学的影响

目的探讨高压氧(HBO)治疗对高原红细胞增多症(HAPC)血液流变学指标的影响.方法 44例HAPC患者随机分为单纯药物治疗组(对照组)和药物+高压氧治疗组(高压氧组),观察两组治疗前后血液流变学指标的变化.结果高压氧组治疗后全血低切粘度[ηb(低切比)]、全血高切粘度[ηb(高切比)]、血浆粘度(ηp)、红细胞压积(HCT)、红细胞总数(RBC)、血红蛋白(Hb)降低明显(P均<0.05),而对照组治疗前后变化不明显;高压氧组治疗后ηb 、HCT、RBC、Hb降低,与对照组比较差异有非常显著性(P<0.01).结论 HBO在纠正组织缺氧、改善微循环中起重要作用,是治疗HAPC的一种有效方法.     

真性红细胞增多症2例误诊报告

例1:男,64岁。因头痛、头晕2a,呕血黑便1a,加重2d,血常规检查示血红蛋白异常升高,诊断为慢性支气管炎、肺气肿、肺心病、肺心病合并消化道出血。查体:面部赤红色,口唇紫绀。心肺听诊未见异常。肝脏未触及肿大,脾左肋下2cm。血常规:血红蛋白205g/L,红细胞660×1012/L,红细胞比积0.57,血小板360×109/L,白细胞31×109/L,中性粒细胞0.75,淋巴细胞0.23,单核细胞0.02。骨髓象:骨髓各系增生极度活跃,各阶段比例、形态大致正常,红细胞集堆分布。血氧饱和度94.5%。B超示肝肋下1.5cm,脾肋下3cm,脾厚4.5cm。确诊为真性红细胞增多症(PV),给予羟基脲2…     

高原红细胞增多症患者行下肢骨折内固定术后并发脑栓塞1例报告

1病例介绍患者,男,29岁,因车祸致左下肢疼痛、流血、活动受限4h入院。患者于2012—10-04骑坐助动车不慎与小轿车相撞,即感左下肢疼痛、流血、活动受限,不能行走,急诊x线检查示“左股骨中上段骨折,左胫腓骨骨折”,收住人院。     

Dual granule localization of the dormant NADPH oxidase and cytochrome b559 in human neutrophils

The subcellular localization of the microbicidal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and associated b-cytochrome was investigated in human neutrophils. In unperturbed neutrophils 85% of b-cytochrome and the major part of membrane-bound components of the NADPH oxidase co-sedimented with markers for specific granules and gelatinase. Using cytochrome b559 as a marker for membrane-bound components of the NADPH oxidase in quantitative studies we observed that, of the remaining 15%, the vast majority co-sedimented with latent alkaline phosphatase, a marker for a newly identified mobilizable intracellular compartment. Only a small fraction co-localized with the plasma membranes. Azurophil granules contained a protease activity which rapidly inactivated the NADPH oxidase components present in other membranes. Stimulation of the neutrophils with formyl-methionyl-leucyl-phenyl-alanine and leukotriene B4 which caused minimal degranulation of specific granules, resulted in translocation of b-cytochrome to the plasma membrane, concomitant with incorporation of alkaline phosphatase into the plasma membrane.     

[Ca2+]i oscillations in ASM: Relationship with persistent airflow obstruction in asthma

The cause of airway smooth muscle (ASM) hypercontractility in asthma is not fully understood. The relationship of spontaneous intracellular calcium oscillation frequency in ASM to asthma severity was investigated. Oscillations were increased in subjects with impaired lung function abolished by extracellular calcium removal, attenuated by caffeine and unaffected by verapamil or nitrendipine. Whether modulation of increased spontaneous intracellular calcium oscillations in ASM from patients with impaired lung function represents a therapeutic target warrants further investigation.     

Changes of cytosolic [Ca^2＋]i in neutrophils in pancreatic microcirculation of rats with caerulein-induced acute pancreatitis under fluid shear stress

AIM: To investigate the fluid shear stress induced changes of (Ca(2+))i in neutrophils in pancreatic microcirculation of experimental acute pancreatitis (AP). METHODS: Wistar rats (n = 36) were randomized into three groups. A model of AP was established by subcutaneous injection of caerulein. Low-shear 30 viscometer was used to provide steady fluid shear stress on separated neutrophils. The mean fluorescent intensity tested by flow cytometry was used as the indication of [Ca(2+)]i quantity. RESULTS: Under steady shear, cytosolic [Ca(2+)]i showed biphasic changes. The shear rate changed from low to high, [(Ca(2+)]i in different groups decreased slightly and then increased gradually to a high level (P<0.05). A close correlation was observed between the cytosolic [Ca(2+)]i level and the alteration of fluid shear stress in regional microcirculation of AP. CONCLUSION: The increase of [Ca(2+)]i is highly related to the activation of neutrophils, which contributes to neutrophil adhesion to endothelium in the early phase of AP. The effect of fluid shear stress on [Ca(2+)]i may play a crucial role in pancreatic microcirculatory failure of AP.     

Distinct modulation of myocardial performance,energy metabolism,and [Ca2+]i transients by positive inotropic drugs in normal and severely failing hamster hearts

Summary The present study compared the effects of amrinone, dobutamine, dibutyryl cAMP, digoxin, and isoproterenol on mechanical performance, the high energy phosphate metabolites, and the [Ca²⁺]_i transients in normal and cardiomyopathic hamster hearts with severe heart failure. In normal hearts dobutamine, dibutyryl cAMP, and isoproterenol increased left ventricular developed pressure, while amrinone and digoxin did not. However, the amplitude of [Ca²⁺]_i transients was augmented with all drugs. Diastolic [Ca²⁺]_i level was increased with dobutamine and lowered with dibutyryl cAMP and isoproterenol. In cardiomyopathic hearts with severe heart failure, left ventricular developed pressure, the amplitude of [Ca²⁺]_i transients, the phosphorylation potential, and [cAMP]_i were significantly depressed and left ventricular end-diastolic pressure and diastolic [Ca²⁺]_i were significantly elevated when compared with normal hearts. Amrinone, dibutyryl cAMP, and isoproterenol improved mechanical performance while increasing [cAMP]_i and the amplitude of [Ca²⁺]_i transients, and decreasing diastolic [Ca²⁺]_i. On the other hand, with dobutamine and digoxin diastolic [Ca²⁺]_i was further increased and mechanical performance deteriorated with digoxin. Thus, distinct differences exist in modulation of mechanical performance, high-energy phosphate metabolism, and [Ca²⁺]_i transients by positive inotropic drugs between normal and cardiomyopathic hearts with severe heart failure.Supported in part by the George D. Smith Foundation and NIH grant AA 07413-01. Peter Buser is a recipient of a Career Development Grant (SCORE # 32-29340,90) from the Swiss National Science Foundation.     

地塞米松快速抑制气道平滑肌内游离钙升高实验初探

目的 通过对平滑肌细胞行地塞米松快速预处理,拟证实糖皮质激素对平滑肌细胞内游离钙离子浓度[Ca2+]i升高有快速抑制作用.方法 原代培养的大鼠平滑肌细胞,比较不同浓度地塞米松预处理后10 min与对照组之间游离钙上升情况的区别.利用Fura-2/AM显微荧光检测技术,检测肌细胞内[Ca2+]i在受到激动剂刺激后的浓度变化;同时设立RU486及CHX对照组,排除基因组作用在该反应中的影响.结果 地塞米松温浴10 min,能够明显降低Ach引起的气道平滑肌细胞内[Ca2+]i峰值.以上反应均不能被RU486和CHX影响或者逆转.结果 地塞米松能够通过非基因组作用快速抑制Ach引起的气道平滑肌细胞内[Ca2+]i浓度升高.     

Augmented NADPH oxidase activity and p22phox expression in monocytes underlie oxidative stress of patients with type 2 diabetes mellitus

Background

This study was to test the hypothesis that enhanced oxidative stress is induced in monocytes with over-activated NADPH oxidase during the development of type 2 diabetes mellitus.

Methods

Levels of glucose and lipids were analyzed in 73 diabetic patients and 36 controls. Superoxide dismutase (SOD), malondialdehyde (MDA), reactive oxygen species (ROS) and protein carbonylation were tested. Expression of NADPH oxidase was examined and p47phox translocation was assessed.

Results

With the abnormality of glucose and lipid metabolism, diabetic patients showed a higher oxidative stress state indicated by decreased SOD activity but elevated MDA and protein carbonylation level. Monocytes in diabetes also showed elevated ROS generation and protein carbonylation level. Furthermore, NADPH oxidase was highly activated in monocytes represented by p22phox up-regulation and p47phox translocation. Significant positive bivariate correlation was found between glucose and MDA level as well as p22phox expression. In vitro experiments also indicated that glucose could stimulate ROS generation in a NADPH oxidase dependent manner. Moreover, we carried out same measurement in 40 diabetic patients with anti-diabetic intervention and obtained the reinforced results.

Conclusions

Hyperglycemia is the main factor which induces oxidative stress mainly by activation of NADPH oxidase in monocytes of diabetic patients.     

Imaging of Ca2+ Transients in Endothelial Cells of Single Perfused Capillaries: Correlation of Peak [Ca2+]i with Sites of Macromolecule Leakage

Objective: To investigate the mechanisms responsible for variation in the macromolecular leakage (formation of localized leaky sites) in venular microvessels with increased permeability, we examined the hypothesis that cytoplasmic calcium concentration [Ca²⁺]_i, does not increase uniformly within microvessel endothelial cells. Methods: We loaded the endothelial cells forming the walls of venular microvessels in frog mesentery with fura-2, and imaged [Ca²⁺]_i using a cooled CCD camera. Results: Control [Ca²⁺]_i was close to 60 nM in all regions. Control permeability was uniformly low in all microvessels. Exposure to ionomycin (5 mM) increased [Ca²⁺]_i in a biphasic manner, but not uniformly. There was variation in both time to peak (bimodal distribution) and peak [Ca²⁺]_i (274 ± 13 nM; mean variation above or below the peak value was 110 nM). Raising extracellular calcium from 1.1 to 5 mM increased the mean variation of [Ca²⁺]_i about peak values. Extravascular leakage of fluorescently labeled albumin or low-density lipoproteins was most prominent at sites where increases in [Ca²⁺]_i were largest. Conclusions: These data indicate that variation in [Ca²⁺]_i within individual endothelial cells or groups of cells could account, at least in part, for the distribution of localized leakage sites for macromolecules in venular microvessels in the high-permeability state.