金属表面TiO2薄膜的溶胶-凝胶法制备及其血液相容性研究

通过溶胶 凝胶法制备TiO2 薄膜对 316L不锈钢和NiTi形状记忆合金进行表面改性处理。研究发现 ,经 5 0 0℃处理 1h的薄膜结构致密 ,膜层均匀平滑 ,薄膜主要由锐钛矿相TiO2 构成 ,随热处理温度的提高 ,锐钛矿相逐渐转变为金红石相。电化学腐蚀和动态凝血时间及溶血率测试表明 ,通过溶胶 凝胶法制备TiO2 膜进行表面改性的 316L不锈钢和NiTi合金的抗模拟体液腐蚀性提高 ,动态凝血时间延长 ,溶血率下降 ,说明溶胶 凝胶法制备TiO2 膜可以提高金属植入物的血液相容性     

Effects of tryptophan depletion on central and peripheral chemoreflexes in man

Klein (Arch. Gen. Psychiatry 50, 306-317, 1993) suggests that panic attacks are the result of a defective 'suffocation alarm' threshold that presents with carbon dioxide (CO(2)) hypersensitivity, exaggerated ventilatory response and panic in panic disorder (PD) patients. Serotonergic deficiencies enhance this ventilatory response in PD patients, as per 'suffocation alarm' theory predictions, suggesting that serotonin (5-HT) normalizes the ventilatory response. Other research supports a serotonin system-mediated stimulation of ventilation. Knowledge of 5-HT's role on ventilatory output and its neurophysiological sources impacts on the 'suffocation alarm' theory validity and predictive value. We used tryptophan depletion (TRP-) in concert with a modified Read rebreathing test to determine the effect of deficient serotonergic modulation on the central and peripheral chemoreflex threshold and sensitivity of response to CO(2) in 11 healthy men. TRP- did not affect central or peripheral chemoreflex threshold or sensitivity of response to CO(2). However, basal ventilation was significantly elevated during TRP-. In contrast to 'suffocation alarm' theory predictions, decreased 5-HT neurotransmission does not significantly affect the respiratory chemoreflex response to CO(2), impacting on non-chemoreflex drives to breathe. Panic associated respiratory abnormalities may be related to defective 5-HT modulation of non-chemoreflex drives to breathe, unrelated to any respiratory chemoreflex abnormality.     

Effects of carbon dioxide on preoptic thermosensitive neurons in vitro

Effects of carbon dioxide (CO₂) on the firing rates of preoptic thermosensitive neurons were examined in rat brain slice preparations. The perfusing medium was saturated with gas mixtures consisting of 90% O₂ and one of various concentrations (5%, 6.3%, 7.5%, and 10%) of CO₂ balanced with N₂. The medium containing 5% CO₂ was used as control. Most preoptic neurons were inhibited during application of a high CO₂ medium. An excitatory effect of CO₂ on a small number of neurons was also significant, although this was weak and transient compared to the inhibitory effect. Thermosensitivities of the neurons did not correlate with their CO₂ sensitivities. The influence of CO₂ tended to be more evident at higher temperatures. We conclude that the direct effect of CO₂ on PO thermosensitive neurons as well as on thermally insensitive neurons is mainly inhibitory.     

低氧对大鼠肺动脉平滑肌细胞血红素加氧酶-1 mRNA 表达及细胞增殖的影响

探讨血红素加氧酶－1（HO－1）mRNA在低氧大鼠肺动脉平滑肌细胞（PASMC0的表达及HO－1／一氧化碳（HO－1／CO）体系对PASMC增殖的影响。应用荧光定量RT－PCR法测定HO－1mRNA表达。用双波长法检测碳氧血红蛋白（HbCO)吸光值。应用免疫细胞化学方法检测细胞增殖核抗原（PCNA）及核转录因子－κB（NF-κB）的表达。发现HO－1 mRNA在常氧大鼠PASMC有低水平的表达，低氧12h HO-1mRNA水平是常氧时的1．5倍，且HbCO产量随之显著增高（P＜0．01）；低氧24h HO-1 mRNA表达呈回落趋势，HbCO产量亦有所减少，但两者仍高于常氧水平。低氧12h及24h PASMC PCNA核阳性反应颗粒表达较常氧时增强（P＜0．01，P＜0．001），使用HO抑制剂ZnPP-9，其PCNA该阳性反应颗粒表达较单纯低氧时增加更多（P＜0．001，P＜0．01）。低氧组核NF－κB阳性染色较常氧组增强（P＜0．001），使用ZnPP-9，其表达则比低氧时更多（P＜0．01）。低氧通过诱导大鼠PASMC的HO－1 mRNA基因表达，上调HO／CO体系活性，使内源性CO含量增高，抑制PASMC增殖；NF－κB参与了PASMC增殖的调控机制。     

Reproducibility of the parameters of the on-transient cardiopulmonary responses during moderate exercise in patients with chronic obstructive pulmonary disease

To be clinically useful as indices reflective of altered physiological function consequent to interventions in patients with chronic obstructive pulmonary disease (COPD), the time constant (τ) and steady-state amplitude of the kinetic responses for oxygen uptake ( ) carbon dioxide output ( ) ventilation ( ) and heart rate (HR) have to be appropriately differentiable and reproducible. We therefore assessed the reproducibility of τ and steady state amplitude values in 41 patients with severe COPD [mean (SD)] [forced expiratory volume in 1 s=41 (7)% predicted], aged 64 (5) years. Of the total, 6 of the patients (15%) did not produce breath-by-breath data of sufficient quality to warrant kinetic analysis. The remaining 35 patients completed two moderate-intensity 10 min square-wave exercise tests separated by 2 h, both before and after an endurance training programme. Tests were conducted on an electromagnetically-braked cycle ergometer at an exercise intensity corresponding to 80% of the estimated lactate threshold (θ_La) or 50% of peak oxygen uptake if θ_La was insufficiently differentiable. Breath-by-breath measurements of , , and HR were averaged into 10 s bins and the on-transient response kinetics were estimated using a mono-exponential model. Analysing the pre-training and the post-training test 1 and test 2 comparisons together, the test 1 –test 2 differences were not significantly different from 0 for either τ or A. The standard deviation of the test 1 –test 2 differences allowed us to define the magnitude of change that would reach statistical significance. For τ, this averaged some 8, 10, 11 and 8 s, for , , and HR, respectively, for a one-tailed paired-comparisons test (i.e. appropriate for assessing hypothesised improvements resulting from an intervention); for a two-tailed comparison, the differences were approximately 2 s greater. The corresponding one-tailed values for A were 100 ml·min^–1, 95 ml·min^–1, 2.5 1·min^–1 and 4 beats·min^–1, respectively; the two-tailed values were 10%–15% greater. We therefore conclude that both τ and A for moderate-intensity exercise can be reproducibly estimated in patients with COPD when the data set provides a sufficiently large amplitude of response and sufficiently low sample variability to allow appropriate parameter estimation. Electronic Publication     

不同类型心脏患者心内直视手术期间呼气末CO2分压与动脉血CO2分压及其差值的变化

目的探讨不同类型心脏患者心内直视手术期间呼气末二氧化碳分压（PETCO2）与动脉血二氧化碳分压（PaCO2）的相关性及二者差值[P（a-ET）、CO2]的临床意义。方法45例患者分成3组，每组15例。A组：左向右分流组；B组：无分流组；C组：右向左分流组。3组分别于术前（T0）、插管后15min（T1）、手术开始时（T2）、转流前（T3）、转流停止后15min（T4）、术毕时（T5）共6个时点，用旁气流法监测PETCO2，同时抽动脉血测定PaCO2，应用直线回归分析3组各时点PETCO2与PaCO2的相关性，同时计算并分析各组不同时点的P（a-ET）CO2。结果（1）A组、B组各时点PETCO2与PaCO2呈正相关，A组r为0．70—0．85（P〈0．01），B组r为0．71—0．79（P〈0．01）；C组麻醉开始至转停后PETCO2与PaCO2均无相关（0．46—0．54，P〉0．05），而到术毕时则呈正相关（r=0．66，P〈0．05）。（2）3组患者转流前的P（a-ET）CO2变化不大，停转流后A组、B组P[a-ET）CO2增加，其中以A组增加较明显（P〈0．01），而C组P（a-ET）CO2显著减少（P〈0．05）。结论无分流或左向右分流心脏患者在体外循环转流前后PETCO2与PaCO2的相关性较好；右向左分流心脏患者转流前的相关性较差，心内畸形纠正后其相关性可发生变化。P（a-ET）CO2在不同的心脏患者之间差异较大，必须与PaCO2相结合，才能正确指导临床。     

类金刚石薄膜的碳相成分对其血小板黏附特性的影响

对不同工艺和条件制备的 7个类金刚石薄膜 (Diamondlikecarbon ,DLC)试样 ,经X光电子能谱 (XPS)碳相成分分析后 ,分别进行了血小板黏附实验、黏附血小板的形貌观察、分类计数和形态指数计算 ,并通过灰色关联分析 ,研究了碳相成分对血小板黏附量、黏附血小板的形态指数的影响。结果显示 :来自全方位离子注入离子束增强沉积工艺的DLC ,其血小板黏附量和形态指数明显小于等离子体化学气相沉积工艺制备的样品 ;在DLC的 5种碳相成分中 ,DLC碳相与血小板黏附量和形态指数的 (负 )关联度远大于其它碳相成分 ,除此之外只有C H和C O碳相与血小板形态指数的 (正 )关联度较大。表明 :(1)DLC碳相对血小板黏附的影响远较其它碳相成分为大 ,增加DLC碳相的含量是优化DLC血液相容性的关键所在 ;(2 )C H和C O碳相对黏附血小板的变形有促进作用 ,须从工艺上抑制其产生或尽可能降低其含量 ;(3)采用全方位离子注入离子束增强沉积工艺有助于改善DLC的血液相容性。这些结论对设计与改进DLC的制备工艺具有重要的指导意义。     

Near‐infrared spectroscopy determined brain and muscle oxygenation during exercise with normal and resistive breathing

To elevate effects of carbon dioxide (CO₂) retention by way of an increased respiratory load during submaximal exercise (150 W), the concentration changes of oxy‐ (ΔHbO₂) and deoxy‐haemoglobin (ΔHb) of active muscles and the brain were determined by near‐infrared spectroscopy (NIRS) in eight healthy males. During exercise, pulmonary ventilation increased to 33 (28–40) L min^–1 (median with range) with no effect of a moderate breathing resistance (reduction of the pneumotach diameter from 30 to 14 and 10 mm). The end‐tidal CO₂ pressure (P_ETCO ₂) increased from 45 (42–48) to 48 (46–58) mmHg with a reduction of only 1% in the arterial haemoglobin O₂ saturation (S_aO ₂). During control exercise (normal breathing resistance), muscle and brain ΔHbO₂ were not different from the resting levels, and only the leg muscle ΔHb increased (4 (–2–10) μM , P < 0.05). Moderate resistive breathing increased ΔHbO₂ of the intercostal and vastus lateralis muscles to 6 ± (–5–14) and 1 (–7–9) μM (P < 0.05), respectively, while muscle ΔHb was not affected. Cerebral ΔHbO₂ and ΔHb became elevated to 6 (1–15) and 1 (–1–6) μM by resistive breathing (P < 0.05). Resistive breathing caused an increased concentration of oxygenated haemoglobin in active muscles and in the brain. The results indicate that CO₂ influences blood flow to active skeletal muscle although its effect appears to be smaller than for the brain.     

Ventilatory and upper-airway resistance responses to upper-airway cooling and CO2 in anaesthetised rats

The effects of upper airway (UA) cool air and CO₂ on breathing and on laryngeal and supraglottic resistances were studied in anaesthetised rats breathing spontaneously through a tracheostomy. Warm, humidified air containing 0, 5 and 9–10% CO₂ and cool, room-humidity air were delivered at constant flow to either the isolated larynx to exit through a pharyngotomy or to the supraglottic UA to exit through the mouth and/or nose (nose open or sealed). Spontaneous tracheal airflow and UA airflows, temperatures and pressures were recorded. CO₂ had no effect on breathing but caused a slight increase in laryngeal resistance which was abolished by cutting the superior laryngeal nerves (SLN). Cool air caused a decrease in respiratory frequency and/or peak inspiratory flow when applied to the isolated larynx or to the supraglottic airway with the nose closed. These effects were abolished by SLN section. With the nose open, the ventilatory inhibition was not abolished by SLN section. Cool air also caused substantial decreases in laryngeal and supraglottic resistances which were attenuated by SLN section and which persisted following recurrent laryngeal nerve section. In conclusion, whilst UA cooling inhibits breathing and decreases UA resistances, UA CO₂ has minimal effects.