高海拔对流量-容积曲线和通气功能的影响

平原人长期移居高原环境对慢性低氧的通气适应,国内外学者研究甚多,一致认为主要是由于低氧刺激引起的过度通气来实现。而通气适应的力学机制国内研究甚少。本工作对昭觉地区(海拔2200m)从青少年到成年的世居彝族和移居汉族进行肺通气功能观察,初步探     

急性低氧对高原土生动物藏系绵羊血气的影响

为了探讨急性低氧时藏系绵羊(Ovis aries)的血气特点,揭示其低氧适应机制,将7只雄性藏系绵羊和5只雄性移居绵羊分别置于高低压氧舱内,测定模拟海拔0、2 300和4 500 m时各动物清醒状态下的血气指标。用热稀释法测定心输出量。使用血气分析仪和EG7血样板,测定动脉及混合静脉血的血气指标,按Ficks方法计算氧耗量。结果显示,随着模拟海拔高度的升高,藏羊和移居羊的动静脉血氧饱和度(So2)、氧分压(Po2)、二氧化碳分压(Pco2)都呈明显下降趋势(P<0.05),血红蛋白浓度(Hb)、血液pH、心输出量及氧耗量虽无明显的差异性改变,但它们在4 500 m处的绝对值是增加的。在相同海拔,藏羊的Hb明显低于移居羊(P<0.05),4 500 m时藏羊的动脉血氧饱和度(Sao2)及组织摄氧量显著高于移居羊(P<0.05)。表明藏羊在急性低氧时表现出的高Sao2及高组织摄氧量,低Hb、低pH是它适应高原低氧的生理基础。     

颜色明度辨别阈限的高海拔效应北大核心CSCD

高海拔低氧环境暴露广泛影响人类中枢神经系统。以往高海拔低氧环境影响人类颜色感知的研究集中于模拟高海拔环境和急性暴露于高海拔环境,鲜有对长期暴露于高海拔低氧环境的移居者和世居者的研究。本研究采用最小变化法比较汉族平原居住者(30名)、汉族移居高海拔区时间满2年者(30名)、高海拔藏族世居者(28名)的红、绿、蓝、黄4种颜色的明度差别阈限,观察其受海拔环境的影响。结果显示,长期高海拔暴露对世居者和移居者的蓝色和红色差别阈限影响最显著,对蓝色差别阈限影响显著大于红色,而对绿色差别阈限产生的影响仅发生于世居者。研究提示,血液供应量与高原环境暴露导致视觉颜色加工选择性改变有内在的关联。     

颜色明度辨别阈限的高海拔效应

高海拔低氧环境暴露广泛影响人类中枢神经系统。以往高海拔低氧环境影响人类颜色感知的研究集中于模拟高海拔环境和急性暴露于高海拔环境,鲜有对长期暴露于高海拔低氧环境的移居者和世居者的研究。本研究采用最小变化法比较汉族平原居住者(30名)、汉族移居高海拔区时间满2年者(30名)、高海拔藏族世居者(28名)的红、绿、蓝、黄4种颜色的明度差别阈限,观察其受海拔环境的影响。结果显示,长期高海拔暴露对世居者和移居者的蓝色和红色差别阈限影响最显著,对蓝色差别阈限影响显著大于红色,而对绿色差别阈限产生的影响仅发生于世居者。研究提示,血液供应量与高原环境暴露导致视觉颜色加工选择性改变有内在的关联。     

平原人进驻高原后凝血和纤溶功能的改变及其意义

目的:探讨高原低氧环境下凝血及纤溶功能的变化.方法:对从平原(海拔1 400 m)进驻3700 m和5 380 m高原第7 d及半年的40名健康青年血浆抗凝血酶Ⅲ(AT-M)、纤溶酶原含量(PLG)、D-二聚体含量(DD)、组织纤溶酶原激活物活性(t-PA)、纤溶酶原激活抑制物活性(PAI)、纤溶蛋白原(Fg)、α2-抗纤溶酶抑制物活性(α2-PI)进行检测,并与20名平原健康青年作对照.结果:高原低氧环境AT-Ⅲ、t-PA明显低于平原(P<0.05或P<0.01),且随海拔高度的升高而降低(P<0.01),随居住时间的延长而升高(P<0.05或P<0.01).PLG、DD、PAI、α2-PI及Fg在海拔3 700 m第7 d和海拔5 380 m第7d及半年均较平原增高显著((P<0.05或P<0.01),且随海拔高度的升高而增高,居住时间的延长而降低(P<0.05或P<0.01);3 700 m居住半年时较平原无显著性差异(P>0.05).结论:高原低氧存在凝血功能紊乱,表现为凝血与纤溶被激活的同时伴有纤溶受抑,凝血及纤溶的平衡被破坏而使血液呈高凝和低纤溶状态.     

Ca2+对根际低氧胁迫下黄瓜幼苗生长和叶片荧光特性的影响

采用营养液栽培,以根际低氧耐性不同的2个黄瓜品种为试验材料,研究了Ca2 对根际低氧胁迫下黄瓜幼苗生长和叶片荧光特性的影响。结果表明:(1)根际低氧胁迫下,黄瓜植株根长、根表面积和根尖数减少,但根径有所增大;叶片干重、鲜重和叶面积显著减小,提高营养液钙浓度可使植株叶片干、鲜重和叶面积得到部分恢复。(2)根际低氧胁迫下,叶片光合色素含量降低,提高营养液钙浓度对色素含量无明显影响。(3)根际低氧胁迫下,常钙和高钙处理黄瓜叶片Fv/Fm与通气常钙(CK)无显著差异,但低氧缺钙处理的Fv/Fm显著降低;与通气常钙相比,根际低氧胁迫处理的光化学猝灭(qP)减小、非光化学猝灭(qN)增大、光合功能相对限制值(L(PFD))升高,提高营养液钙浓度可使qP和qN恢复至近对照水平,而使L(PFD)低于对照,且‘绿霸春四号’黄瓜品种表现得更为突出;根际低氧胁迫下,光化学速率(Prate)减小,天线热耗散速率(Drate)都随钙浓度升高而降低。总之,根际低氧胁迫下黄瓜幼苗生长被显著抑制,PSⅡ反应中心受到一定程度的破坏,提高钙浓度可使PSII反应中心恢复至接近甚至高于通气对照的水平,从而有效缓解根际低氧胁迫对黄瓜幼苗造成的伤害。     

成人急性低氧通气压抑中的内啡肽作用

本工作设想,内啡肽参与了成人急性低氧通气压抑机制。受试者均为健康成年男子。6名受试者吸入中度低氧混合气(12.8％O_2)30min;7名吸入重度低氧混合气(10.8％O_2)20min,其中6名并在重度低氧下吸入三口纯氮气。吸入低氧气前先由静脉注入生理盐水(对照)或纳洛酮(中度低氧5mg,重度低氧10mg)。观察低氧时的通气反应、终末潮气二氧化碳分压(P_(ETCO2)、动脉血氧饱和度和外周低氧通气敏感性以及纳洛酮对上述测定的影响。结果表明,纳洛酮使重度低氧下的通气压抑明显减弱,低氧第3～15分钟的通气水平明显高于对照实验;而P_(ETCO2)明显低于对照值。但纳洛酮对中度低氧下的通气压抑无明显作用。此外,纳洛酮显著增强外周低氧敏感性。结果提示,在重度低氧下,内啡肽参与了成人低氧通气压抑机制,并对外周低氧敏感性有抑制作用。     

平原入进驻高原后凝血和纤溶功能的改变及其意义

目的：探讨高原低氧环境下凝血及纤溶功能的变化。方法：对从平原（海拔1400m）进驻3700m和5380m高原第7d及半年的40名健康青年血浆抗凝血酶Ⅲ（AT－M）、纤溶酶原含量（PLG）、D－二聚体含量（DD）、组织纤溶酶原激活物活性（t-PA）、纤溶酶原激活抑制物活性（PAI）、纤溶蛋白原（Fg）、α2－抗纤溶酶抑制物活性（α2－PI）进行检测,并与20名平原健康青年作对照。结果：高原低氧环境AT－Ⅲ、t-PA明显低于平原（P＜0.05或P＜0.01）,且随海拔高度的升高而降低（P＜0.01）,随居住时间的延长而升高（P＜0.05或P＜0.01）。PLG、DD、PAI、α2－PI及Fg在海拔3700m第7d和海拔5380m第7d及半年均较平原增高显著（（P＜0.05或P＜0.01）,且随海拔高度的升高而增高,居住时间的延长而降低（P＜0.05或P＜0.01）;3700m居住半年时较平原无显著性差异（P＞0.05）。结论：高原低氧存在凝血功能紊乱,表现为凝血与纤溶被激活的同时伴有纤溶受抑,凝血及纤溶的平衡被破坏而使血液呈高凝和低纤溶状态。     

急性高山反应判别式与判别图的建立及应用

为探讨急性高山反应的生理学评价方法,以12名男性青年为受试对象,每人参加三次低压舱实验(模拟海拔高度为5000m),进行症状学调查的同时,测量f、V_E、P_AO_2、PaO_2、AaDO_2、P_ACO_2、PaCO_2和pH_a。结果表明,急性高山反应重者,PaO_2较低,AaDO_2较高,反应轻者,PaO_2较高,A_aDO_2较低。在此基础上,到青藏高原(海拔4700m)对52名受试者进行症状学调查的同时,测量PaO_2和AaDO_2,其结果同上。可见,急性高山反应程度与PaO_2和AaDO_2大小有密切关系。因此,我们用PaO_2和AaDO_2作为评价指标,并建立了判别式和判别图。为验证该判别式和判别图的准确性和实用性,又到青藏高原(海拔4700m)观察174名男性青年,用症状学和判别式两种方法评价急性高山反应,两种方法判定结果的总吻合率达89.0％。     

高原心搏量的自身调节

高原低氧坏境下,左心搏血功能及其调节尤为重要。我们应用超声心动图测定了不同海拔健康人左心泵功能指标,从而初步探讨了自身调节机制对高原心搏量的调节作用。 对象与方法 检查对象分别为平原南京(海拔20m),高原西宁(海拔2260m)与哈尔盖(海拔3232m)三     

Keratinocyte growth factor‐2 intratracheal instillation significantly attenuates ventilator‐induced lung injury in rats

Preservation or restoration of normal alveolar epithelial barrier function is crucial for pulmonary oedema resolution. Keratinocyte growth factor‐2 (KGF‐2), a potent epithelial cell mitogen, may have a role in preventing ventilator‐induced lung injury (VILI), which occurs frequently in mechanically ventilated patients. The aim of the study was to test the role of KGF‐2 in VILI in rats. Forty healthy adult male Sprague‐Dawley rats were randomly allocated into four groups, where rats in Groups HVZP (high‐volume zero positive end‐expiratory pressure) and HVZP+KGF‐2 were given intratracheally equal PBS and 5 mg/kg KGF‐2 72 hrs before 4 hrs HVZP ventilation (20 ml/kg), respectively, while PBS and KGF‐2 were administered in the same manner in Groups Control and KGF‐2, which underwent tracheotomy only with spontaneous breathing. Inflammatory cytokines (tumour necrosis factor‐α, macrophage inflammatory protein 2), neutrophil and total protein levels in bronchoalveolar lavage fluid and surfactant protein mRNA expression in lung tissue were detected; the number of alveolar type II cells, lung water content and lung morphology were also evaluated. The results indicate that pre‐treatment with KGF‐2 showed dramatic improvement in lung oedema and inflammation compared with HVZP alone, together with increased surfactant protein mRNA and alveolar type II cells. Our results suggest that KGF‐2 might be considered a promising prevention for human VILI or other acute lung injury diseases.     

吸入不同浓度 CO_2对肺通气功能影响的实验观察

本实验在10名健康男性青年中观察了吸入0.5—7%CO_2对肺通气功能的影响。实验结果表明,呼吸频率、潮气量、肺通气量、肺泡 CO_2分压以及肺通气对 CO_2的反应性均与吸入气CO_2浓度成线性关系。被试者吸入 CO_2后,CO_2排出量减少;但浓度不超过5%时,3—5min 内CO_2排出量即可基本恢复到正常水平。本文根据人体 CO_2反应的这些特点提出了三个代偿区的意见。     

全口义齿修复后造成松软牙槽嵴和／或牙槽嵴粘膜增生的原因初探

目的:研究松软牙槽嵴和/或牙槽嵴粘膜增生形成的原因,探讨预防和治疗措施。方法:对180例戴用全口义齿一年以上的患者进行临床调查研究。研究内容包括缺牙原因,义齿戴用的时间,牙槽嵴粘膜情况,松软牙槽嵴和/或牙槽嵴粘膜增生发生的部位,人工牙的类型等。结果:①180例全口义齿病例中,有松软牙槽嵴者20例,占22％,男:女=6:4,其中下牙槽嵴占60％,上牙槽嵴占,20％,上下牙槽嵴均有者占20％。患牙槽嵴粘膜增生者共8例,占4.4％,最多发生在下舌侧,其次为下唇沟。同时患有松软牙槽嵴和牙槽嵴粘膜增生的有4例,占患牙槽嵴粘膜增生病例的一半。②在患松软牙槽嵴的病例中,人工牙为塑料牙和瓷牙各占50％。缺牙原因为牙周病者共12例,占60％,龋病2例,占10％,龋病-牙周病者8例,占30％。③在患松软牙槽嵴的病例中,下颌牙槽嵴条件均为差,上颌牙槽嵴条件均为中或差。在患增生的粘膜组织的病例中,75％病例义齿固位为中或差,25％义齿固位为较好。结论:发病原因与患者缺牙原因,牙槽嵴部位,牙槽嵴条件,人工牙类型等有关。因此可以认为,牙槽嵴粘膜松软是戴用全口义齿后出现的不可忽视的问题,而牙槽嵴粘膜松软和/或增生的粘膜组织是相辅相成的。所以一副全口义齿不是一劳永逸的,使用一定的时间后需要更换,特别对牙槽嵴条件较差的患者     

Lipidomic characterization and localization of phospholipids in the human lung

Lipids play a central role in lung physiology and pathology; however, a comprehensive lipidomic characterization of human pulmonary cells relevant to disease has not been performed. The cells involved in lung host defense, including alveolar macrophages (AMs), bronchial epithelial cells (BECs), and alveolar type II cells (ATIIs), were isolated from human subjects and lipidomic analysis by LC-MS and LC-MS/MS was performed. Additionally, pieces of lung tissue from the same donors were analyzed by MALDI imaging MS in order to determine lipid localization in the tissue. The unique distribution of phospholipids in ATIIs, BECs, and AMs from human subjects was accomplished by subjecting the large number of identified phospholipid molecular species to univariant statistical analysis. Specific MALDI images were generated based on the univariant statistical analysis data to reveal the location of specific cell types within the human lung slice. While the complex composition and function of the lipidome in various disease states is currently poorly understood, this method could be useful for the characterization of lipid alterations in pulmonary disease and may aid in a better understanding of disease pathogenesis.     

肺泡II型上皮细胞转分化

哺乳动物肺泡上皮细胞主要由肺泡II型上皮细胞(AECII)和肺泡I型上皮细胞(AECI)组成。在肺发育和肺损伤修复过程中,AECII可转分化为AECI,体外原代培养的AECII有这种转分化的特性。现对AECII转分化的标志、影响及调控因素及其在肺损伤中的作用进行综述。     

Extracellular signal-regulated kinase (ERK) participates in the hypercapnia-induced Na,K-ATPase downregulation

Hypercapnia has been shown to impair alveolar fluid reabsorption (AFR) by decreasing Na,K-ATPase activity. Extracellular signal-regulated kinase pathway (ERK) is activated under conditions of cellular stress and has been known to regulate the Na,K-ATPase. Here, we show that hypercapnia leads to ERK activation in a time-dependent manner in alveolar epithelial cells (AEC). Inhibition of ERK by U0126 or siRNA prevented both the hypercapnia-induced Na,K-ATPase endocytosis and impairment of AFR. Moreover, ERK inhibition prevented AMPK activation, a known modulator of hypercapnia-induced Na,K-ATPase endocytosis. Accordingly, these data suggest that hypercapnia-induced Na,K-ATPase endocytosis is dependent on ERK activation in AEC and that ERK plays an important role in hypercapnia-induced impairment of AFR in rat lungs.     

牙周病摄片数字化分析用于临床诊断的探讨

本文探讨了牙周病摄片数字化分析,即纹理分析技术,应用于牙周病诊断的可能性。数字化分析能提供牙槽骨图象的细部特征特征描述和定量表达的形式,将为牙周病提供一种新的诊断方法。     

Induction of interleukin 8 (IL-8) production by Pseudomonas nitrite reductase in human alveolar macrophages and epithelial cells.

Interleukin-8 (IL-8) participates in the generation of dense neutrophil accumulations in bronchopulmonary infections caused by Pseudomonas aeruginosa (P. aeruginosa). We have recently reported that nitrite reductase, a bifunctional enzyme located in the periplasmic space of P. aeruginosa, induces IL-8 generation in bronchial epithelial cells (K. Oishi et al. Infect. Immun. 65: 2648-2655, 1997). We examined whether or not Pseudomonas nitrite reductase (PNR) could also stimulate human alveolar macrophages (AM) and pulmonary type II epithelial-like cells (A549) to induce IL-8 production and mRNA expression as well as the production of TNF alpha and IL-1beta. We demonstrated a time- and dose-dependent IL-8 protein synthesis and IL-8 mRNA expression, but no TNF alpha or IL-1beta production, by A549 cells in response to PNR. New protein translation was not required for PNR-mediated IL-8 mRNA expression in the same cells. Furthermore, simultaneous stimulation of PNR with serial doses of TNF alpha or IL-1beta resulted in additive IL-8 production in A549 cells. In adherent AM, PNR enhanced IL-8 protein synthesis and IL-8 mRNA expression in a time-dependent fashion. PNR similarly induced a time-dependent production of TNF alpha and IL-1beta by human adherent AM. Neutralization of TNF alpha or IL-1beta did not influence the levels of IL-8 production in adherent AM culture. We also evaluated whether the culture supernatants of the A549 cells or AM stimulated with PNR could similarly mediate neutrophil migration in vitro. When anti-human IL-8 immunoglobulin G was used for neutralizing neutrophil chemotactic factor (NCF) activities in the culture supernatants of these cells stimulated with 5 microg/ml of PNR, the mean percent reduction of NCF activities were 49-59% in A549 cells and 24-34% in AM. Our present data support that PNR directly stimulates AM and pulmonary epithelial cells to produce IL-8. PNR also mediates neutrophil migration, in part, through IL-8 production from AM and pulmonary epithelial cells. These data suggest the contribution of PNR to the pathogenesis of bronchopulmonary infections due to P. aeruginosa.     

In vitro assessment of environmental toxicology using alveolar cells astarget

Biphasic culture of alveolar cells (alveolar macrophages and type II cells) has been widely developed and permits a precise evaluation of the toxic effects of air pollutants. Clearly, in vitro exposure of alveolar cells to high concentrations of oxidant gases is responsible for a loss of cell viability. In contrast, when exposed to realistic concentrations of gases (NO₂, O₃), cell viability is not altered and various proinflammatory mediators are released. This in vitro model has proved to be sensitive at levels of gas exposure of ambient air quality standards and appears a sensitive biological indicator of air pollutant cell toxicity.Abbreviations AM alveolar macrophages