支气管哮喘持续状态下豚鼠气道感觉神经生长相关蛋白43的表达

目的研究支气管哮喘(简称哮喘)过敏性刺激诱发气道感觉神经敏化机制。方法成年雄性豚鼠39只,按随机数字表法分为生理盐水致敏/激发对照组(A组,9只)、卵白蛋白(OVA)致敏/生理盐水激发对照组(B组,9只)、OVA致敏/激发实验组(C组,21只)。A组以生理盐水(0.5ml/只)致敏,B、C组以10%OVA(0.5ml/只)致敏,第10天开始雾化吸入生理盐水(A、B组)或1%OVA(C组)进行激发,每天1次,每次30min,根据实验需要又将C组21只豚鼠分为激发1d组(C1组,6只)、连续激发3d组(C2组,6只)、连续激发5d组(C3组,9只)。利用免疫荧光双标技术结合激光共聚焦扫描显微观察与Westernblot技术,研究生长相关蛋白43(GAP43)在气道神经以及结状神经节、颈静脉神经节内分布与水平及与P物质(SP)和胶质源神经生长因子(GDNF)受体c RET表达神经元关系。结果免疫荧光结果显示,C3组豚鼠气道内GAP43免疫反应阳性神经呈网状分布于大、中支气管内,以黏膜下层为主,部分GAP43阳性神经纤维向黏膜层内延伸;在结状神经节和颈静脉神经节内有大量GAP43免疫阳性神经胞体,在结状神经节内主要与SP免疫阳性胞体共存,在颈静脉神经节内主要与c RET免疫阳性胞体共存。Westernblot结果显示,A、B、C1、C2、C3组GAP43蛋白表达水平吸光度(A)值分别为0.38±0.04、0.41±0.03、0.49±0.05、0.79±0.08、0.76±0.04。C1、C2、C3组分别与A、B组比较差异均有统计学意义(P均0.05);C2组GAP43蛋白表达与C1组比较差异有统计学意义(P<0.01),但与C3组GAP43蛋白表达比较差异无统计学意义(P>0.05)。结论哮喘过敏性刺激能诱发气道感觉神经———SP肽能神经、GDNF敏感性神经纤维与胞体表达GAP43蛋白。     

Clinical features fail to distinguish respiratory infections caused by Branhamella catarrhalis from those caused by Haemophilus influenzae

Branhamella catarrhalis is being isolated with increasing frequency from patients with symptoms and signs of respiratory tract infection. Records of 77 patients were reviewed to define the spectrum of respiratory illness and to compare clinical and laboratory features with those of respiratory infection due to Haemophilus influenzae. Both B catarrhalis and H influenzae caused respiratory infection predominantly in elderly males with underlying heart or lung disease. There were no clinical or laboratory features aside from sputum Gram stain and culture which differentiated the two groups. Although fewer than one-half of each group received antibiotics, no patient developed progressive respiratory disease.     

Bronchial response to breathing dry gas at 3.7 MPa ambient pressure

In diving, pulmonary mechanical function is limited by the increased density of the gas breathed. Breathing cold and dry gas may cause an additional increase in airways resistance. We have measured forced vital capacity, forced expired volume in 1 s (FEV₁) and forced midexpiratory flow rate (FEF_25%–75%) before and after breathing dry or humid gas at 29–32°C during a standardized exercise intensity on a cycle ergometer at an ambient pressure of 3.7 MPa. The atmosphere was a helium and oxygen mixture with a density of 6.8 kg · m^–3. Six professional saturation divers aged 26–37 years participated in the study. There were no significant differences in convective respiratory heat loss between the exposures. The mean evaporative heat loss was 67 W (range 59–89) breathing dry gas and 37 W (range 32–43) breathing humid gas, corresponding to water losses of 1.7 g · min^–1 (range 1.5–2.2) and 0.9 g · min^–1 (range 0.8–1.1), respectively. There was a significant reduction in FEV₁ of 4.6 (SD 3.6)% (P<0.05), and in FEF_25%–75% of 5.8 (SD 4.7)% (P<0.05) after breathing dry gas. There were no changes after breathing humid gas. By warming and humidifying the gas breathed in deep saturation diving bronchoconstriction may be prevented.     

肺炎衣原体感染小鼠肺组织免疫组化表现

目的 :通过研究小鼠肺组织免疫组化 ,对肺炎衣原体肺炎的发病机制进行初步的探讨。　方法 :以肺炎衣原体鼻内或静脉接种Icr小鼠 ,在不同时间点处死动物 ,用免疫组化的方法检测小鼠肺炎衣原体肺炎急性期肺组织的病理改变。　结果 :小鼠吸入肺炎衣原体后第 3、7、14天 ,肺组织中肺炎衣原体的免疫过氧化酶染色呈阳性。炎性肺组织阳性染色呈不均一性 ,为局限性分布。肺炎衣原体抗原阳性表达主要在肺泡巨噬细胞、间质细胞以及支气管周围淋巴组织等部位。静脉接种组引起上述类似改变 ,但程度轻 ,肺炎衣原体抗原阳性表达主要集中在肺泡巨噬细胞及间质细胞中。　结论 :免疫组化法检测小鼠肺炎衣原体肺炎急性期肺组织的病理改变 ,有助于肺炎衣原体肺炎急性期的诊断。肺炎衣原体呼吸道局部感染比血行感染的病理改变更为严重     

Physiological consequences of a high work of breathing during heavy exercise in humans

The healthy respiratory system has a remarkable capacity for meeting the metabolic demands placed upon it during strenuous exercise. For example, in order to regulate alveolar partial pressure of oxygen and carbon dioxide during heavy workloads, a 20-fold increase in alveolar ventilation can occur. The high metabolic costs and subsequent increased work of breathing associated with this ventilatory increase can result in a number of limitations to the healthy respiratory system. Two examples of respiratory system limitations that are associated with a high work of breathing are expiratory flow limitation and exercise-induced diaphragmatic fatigue. Expiratory flow limitation can lead to an inability to increase alveolar ventilation () in the face of increasing metabolic demands, resulting in gas exchange impairment and diminished endurance exercise performance. Furthermore, the high ventilatory requirements of endurance athletes and the inherent anatomical differences in females could make these groups more susceptible to expiratory flow limitation. Fatigue of the diaphragm has also been documented after strenuous exercise and may be related to a mechanism which increases sympathetic vasoconstrictor outflow and reduces limb blood flow during prolonged exercise. This competition between the muscles of respiration and locomotion for a limited cardiac output may have dramatic consequences for exercise performance. This brief review summarizes the literature as it pertains to the work of breathing, expiratory flow limitation, and exercise-induced diaphragmatic fatigue in healthy humans.     

Damage mechanics and load failure of fiber-reinforced composite fixed partial dentures

OBJECTIVES: Damage mechanics has been defined as the study of the initiation (initial failure) and accumulation of damage to and including rupture (final failure). This study was designed to evaluate the effect of increasing fiber-reinforced composite (FRC) substructure within a standardized fixed partial denture (FPD) model on the failure performance, in terms of damage mechanics. METHODS: The two FRC restorative systems, Targis/Vectris (TV) (Ivoclar Vivadent) and EverStick (ES) (Stick Tech with Gradia, GC Corp.), were used to restore the molar FPD model (1.5 mm axial and 2.0 mm occlusal reduction). Templates were used to standardize substructure designs with 0, 18, 43, and 66% cross-sectional FRC volume fraction (V(FRC)) of fiber substructure. Specimens (n = 5) were homogenized at 29 points and stored for 1 week at 37 degrees C in distilled water. Specimens were luted with calcium hydroxide, then statically loaded until failure. Initial failure (IF), final failure (FF) and the mode of failure were recorded. RESULTS: The lowest mean load to initial failure was 530 N (TV 18%) and the highest was 1208 N (ES 66%). Linear regression analysis calculated the Pearson's correlation coefficient (r) for the interactions between V(FRC) and IF (ES: r = 0.7879, TV: r = 0.6184), V(FRC) and FF (ES: r = 0.912, TV: r = 0.8152), and between IF and FF (ES: r = 0.892, TV: r = 0.7237). Unreinforced specimens universally fractured instantaneously. SIGNIFICANCE: The highest loads to initial and final failure were yielded by specimens with the highest cross-sectional V(FRC).     

呼吸电刺激训练对肺功能康复的作用

通过电流和声、光信号刺激，对２０例慢性阻塞性肺疾患（ＣＯＰＤ）患者进行呼吸电刺激训练（ＲＥＴ），结果在ＲＥＴ时呼吸频率和平均吸气流速明显下降，潮气量和吸气间期明显增加，跨膈压增大，氧耗量和能量代谢无明显变化；于ＲＥＴ１５天后ＰａＣＯ２明显下降，ＰａＯ２和运动能力明显增高，肺勇气功能明显改善。表明ＲＥＴ１５天后ＰａＣＯ２明显下降，ＰａＯ２和运动能力明显增高，肺通气功能明显改善。表明ＲＥＴ能使ＣＯＰＤ     

Effects of amino acids on the excitability of respiratory bulbospinal neurons in solitary and para-ambigual regions of medulla in cat

The effects of inhibitory (gamma-aminobutyric acid (GABA) and glycine) and excitatory (L-glutamate and DL-homocysteate, DLH) amino acids on the excitability of respiratory bulbospinal neurons were studied in decerebrate, paralyzed, bilaterally vagotomized, artificially ventilated cats. Unit activities were recorded extracellularly in the medulla in both the ventrolateral portion of the nucleus tractus solitarius and the para-ambigual region in the vicinity of the nucleus ambiguus (dorsal and ventral respiratory groups, respectively). All neurons were bulbospinal since they could be antidromically activated by electrical stimuli to the spinal cord. We used variations in antidromic latency (ADL) as a measure of changes in excitability of the soma. All neurons exhibited variations in ADL related to the respiratory cycle, being shortest (minimum ADL) during neural activity and longest (maximum ADL) in the silent period. Neurons whose discharge frequencies fell during application of putative inhibitory amino acids showed an increase of minimum ADL compared to control, indicating hyperpolarization. Minimum ADL, in some cells, became shorter during application of excitatory amino acids, indicating depolarization; in others, mechanisms secondary to increased neuronal firing likely obscured their effects. The transient maximum ADL usually present at the onset of the silent period was increased by excitatory amino acids and, in some units, was reduced or eliminated by inhibitory amino acids. These effects are discussed in terms of a modulation by synaptic inputs and neurotransmitters of the cumulative afterhyperpolarization which follows bursts of action potentials.     

An Intrapleural Lung Prosthesis: Rationale, Design, and Testing

Abstract: Extracorporeal life support (ECLS or ECMO) is standard treatment for severe respiratory failure but poses many contraindications to future lung transplantation. The solution to this dilemma is the implantable gas exchange device (IGED) or artificial lung. Preliminary efforts to create such an artificial lung have been made since 1970 and include designs involving single devices, intravascular devices (i. e., IVOX), and combination heart–lung devices, Stringent requirements govern the design of such a device, the most important of which are high gas exchange efficiency, low resistance to blood flow, and size. This paper describes such a device. It incorporates large diameter inflow and outflow ports in close proximity and a low resistance wound hollow fiber core encapsulated in a compliant outer shell which conserves the work of the right ventricle. In a large animal model (adult sheep) this device was connected in line with the main pulmonary artery in series with the native lungs. This configuration has the advantages of using the lungs as an embolic filter, perfusing the lungs with fully oxygenated blood, and maintaining the integrity of the anatomy necessary for transplant. Laboratory experiments have run >8 h. Preliminary data show that the animals have remained hemodynamically stable while the devices have supported the animals completely by supplying 100% O₂ saturation with PO₂ values ranging from 250–350 mm Hg. Additionally, this model makes possible the study of respiratory failure without introducing other variables such as extracorporeal circuits or pumps. The other metabolic, endocrine, and reticuloendothelial functions of normal and injured lungs can now be studied more precisely by excluding these variables. Further studies are needed to evaluate this device in chronic (long–term implantation) experiments before clinical application.     

A follow-up study of respiratory function in workers exposed to acid aerosols in a food-processing industry

A follow-up investigation was performed on 49 female workers studied 2 years earlier in a vegetable-pickling plant. Acute and chronic respiratory symptoms and ventilatory capacity measurements were recorded during the original and the follow-up studies. Maximal expiratory flow-volume (MEFV) curves were recorded during the Monday morning work shift. The forced vital capacity (FVC), 1-s forced expiratory volume (FEV1), and flow rates at 50% and the last 25% of the FVC (FEF50, FEF25) were measured. There were small increases in the prevalence of chronic symptoms between the two studies for both smokers and nonsmokers, but these did not reach statistical significance. Five workers at the time of the initial study had a diagnosis of occupational asthma; only one of these was still working at the time of follow-up. Workers lost to the follow-up had lower lung function than those seen at follow-up. In workers who were followed, larger than expected mean annual declines were noted for all ventilatory capacity parameters in both smokers (FVC 0.070 l, FEV1 0.070 l; FEF50 0.355 l/s, FEF25 0.270 l/s) and nonsmokers (FVC 0.045 l, FEV1 0.045 l, FEF50 0.285 l/s; FEF25 0.130 l/s). The decrease was particularly pronounced for FEF50 and FEF25. The accelerated decline in ventilatory capacity tests noted in the female nonsmokers suggests an independent effect on lung function of work exposure in this environment. Our data confirm that work in the pickling industry, particularly in small, poorly regulated plants, has deleterious effects on respiratory function. Received: 24 September 1996 / Accepted: 19 June 1997