慢阻肺患者吸氧时通气量及血气变化与通气应答关系的研究

目的：通过慢阻肺（ＣＯＰＤ）患者低氧及高二氧化碳通气应答检测，探究ＣＯＰＤ患者吸氧时通气量及血气变化的机理。方法：１１例ＣＯＰＤ患者，采用Ｒｅｂｕｃｋ和Ｃａｍｐｂｅｌｌ及Ｒｅａｄ重复呼吸法检测低氧和高二氧化碳通气应答斜率，并随机让患者室内空气呼吸和吸氧（１００％Ｏ２）呼吸各１５ｍｉｎ，观测每分通气量（ＶＥ），二氧化碳产生量（ＶＣＤ２）生理死腔／潮气量（ＶＤ／ＶＴ）及动脉血气变化。结果：吸氧时ＰａＣ     

一种适用于生物信号数据采集的鼠标器

文章介绍了鼠标驱动程度的通信方式及部分初始值的修改方法，说明了数据采集鼠标器的软硬件的工作原理，提供了数据采集鼠标器的完整电路图及软件流程图，系统的特点是使用现有成熟的通信接口及绘图软件。     

呼气末二氧化碳分压水平对慢性阻塞性肺疾病患者中枢驱动和呼吸应答的影响

目的 探讨不同呼气末二氧化碳分压(PETCO2)水平对慢性阻塞性肺疾病(COPD)患者巾枢驱动和呼吸应答的影响.方法 13例稳定期COPD患者和10例健康志愿者常规测定肺通气功能后,采用二氧化碳(CO2)重复呼吸方法 ,增加PETCO2,从45 mm Hg上升至70 mm Hg.连续记录并计算在不同PETCO2水甲时中枢驱动和呼吸应答的各项生理参数.结果 PETCO2达到70mm Hg的实验时间在COPD组为(8.5±1.6)min,正常组为(16.3±3.2)min,差异有统计学意义(P＜0.05).两组的呼吸频牢(RR)均呈线性增加,正常组稍高于COPD组.COPD组潮气量(VT和分钟通气量(VE)在PETCO2=45～55 mm Hg时,呈显著的线性增加,VT山(0.68±0.25)L 上升到(1.04±0.44)L,VE由(10.59±3.36)L/min上升到(20.13±4.52)L/min.在PETCO2=55～70 mm Hg时VT和VE出现平台.正常组VT和VE呈线性增加,高于COPD组.正常组的吸气时间占呼吸周期比值(T1/Ttot)高于COPD组,差异有统计学意义(P＜0.05).COPD组的呼吸困难评分高于正常组,差异有统计学意义(P＜0.05).两组的平均吸气流量(VT/Ti)和膈肌电电压的均方根(RMS)均呈线性增加,COPD组VT/T1在PETCO2=65～70mm Hg时低于正常组,差异有统计学意义(P＜0.05),而不同PETCO2水平时RMS高于正常组,差异有统计学意义(P＜0.05).COPD组VE/RMS呈抛物线样变化,明显低于正常组,差异有统计学意义(P＜0.05).结论在CO2重复呼吸过程中,COPD患者的呼吸应答和中枢驱动在早期表现为线性递增,后期通气量出现平台,通气-中枢耦联显著异常.正常组的呼吸应答和中枢驱动均表现为线性递增,呼吸应答高于COPD组,而中枢驱动低于COPD组.     

Maintenance of Atrial Fibrillation in Anesthetized and Unanesthetized Sheep Using Cholinergic Drive

Atrial fibrillation (AF) was induced electrically and the duration of AF was measured in six isoflurane-anesthetized sheep (weight range 54.5–72.7 kg), and in five Unanesthetized sheep (weight range 60–75 kg). In the anesthetized sheep, AF was induced by direct electrical stimulation of the right atrium with a catheter electrode and the duration of AF was determined. Intravenous neostig- mine (10 fig/kg IV) was administered and the duration of AF was again measured. Then cholinergic drive was increased by bilateral electrical vagal stimulation; AF was induced and the duration of AF was measured. In the anesthetized animals with no neostigmine or vagal stimulation, 34% of the episodes of AF lasted 10 seconds, 11% lasted 20 seconds, and only 1 % lasted 200 seconds. However, in one anesthetized animal AF was sustained for 4,800 seconds with no drug or vagal support. The administration of neostigmine alone in 3 anesthetized animals more than doubled the average duration of AF. In the animals with vagal stimulation (after neostigmine), AF persisted throughout stimulation, but ceased shortly after vagal stimulation was terminated at 2,220, 4,500, and 3,840 seconds. The AF frequency ranged from 325–750/min. The Unanesthetized sheep were lightly sedated with a small dose (200 fig/kg IM) of xylazine to make them less sensitive to environmental noise; then AF was induced and its duration was timed. After these measurements, neostigmine was administered (30 μg/kg IM) and cholinergic drive was produced reflexly by intravenous injection of 60–2,000 fig of phenylephrine. AF was electrically induced at the time of maximum reflex slowing in heart rate. For the control (no drug! studies, 64% of the AF episodes lasted 10 seconds, 20% lasted 20 seconds, and only 2% of the episodes lasted as long as 140 seconds. When phenylephrine was injected after neostigmine to provide increased cholinergic drive, the duration of fibrillation depended on the dose of phenylephrine. In a 60-kg sheep, the duration of AF increased from 1 second with an intravenous dose of 60 μg to 700 seconds with an intravenous dose of 2,000 μg. However, there was a considerable range in responsiveness to the reflex cholinergic drive provided by the intravenous phenylephrine; for example a single intravenous 500-μg dose produced AF ranging from 190–540 seconds among the sheep. The duration of AF was most controllable in the anesthetized sheep, following neostigmine administration and with bilateral vagal stimulation. In the Unanesthetized sheep, AF could generally be sustained for more than the duration of the half-life (about 4 minutes) of phenylephrine following neostigmine. However, there was a large variation in the duration of AF among the animals for the same dose of phenylephrine. This study identifies two methods (direct vagal stimulation and reflex vagal stimulation) for providing the cholinergic drive needed to sustain AF in the adult sheep. The duration of AF is sufficiently long to enable the measurement of electrical atrial defibriilation threshold.     

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阻塞性睡眠呼吸暂停综合征(OSAS)是以睡眠时上呼吸道反复塌陷为特征的疾病,常伴日间嗜睡和心脑血管疾病。虽然上气道解剖异常可能与这一疾病的发生有关,但其发生机制尚不完全清楚。最近的一些研究显示,OSAS的发生与呼吸中枢驱动异常有关。文章将介绍呼吸中枢驱动评价方法包括用多导食管电极记录膈肌肌电。研究显示,OSAS事件发生时呼吸中枢驱动事实上是下降而不是增高。     

Neurobehavioral Dynamics Following Chronic Sleep Restriction: Dose-Response Effects of One Night for Recovery

Objective:

Establish the dose-response relationship between increasing sleep durations in a single night and recovery of neurobehavioral functions following chronic sleep restriction.

Design:

Intent-to-treat design in which subjects were randomized to 1 of 6 recovery sleep doses (0, 2, 4, 6, 8, or 10 h TIB) for 1 night following 5 nights of sleep restriction to 4 h TIB.

Setting:

Twelve consecutive days in a controlled laboratory environment.

Participants:

N = 159 healthy adults (aged 22-45 y), median = 29 y).

Interventions:

Following a week of home monitoring with actigraphy and 2 baseline nights of 10 h TIB, subjects were randomized to either sleep restriction to 4 h TIB per night for 5 nights followed by randomization to 1 of 6 nocturnal acute recovery sleep conditions (N = 142), or to a control condition involving 10 h TIB on all nights (N = 17).

Measurements and Results:

Primary neurobehavioral outcomes included lapses on the Psychomotor Vigilance Test (PVT), subjective sleepiness from the Karolinska Sleepiness Scale (KSS), and physiological sleepiness from a modified Maintenance of Wakefulness Test (MWT). Secondary outcomes included psychomotor and cognitive speed as measured by PVT fastest RTs and number correct on the Digit Symbol Substitution Task (DSST), respectively, and subjective fatigue from the Profile of Mood States (POMS). The dynamics of neurobehavioral outcomes following acute recovery sleep were statistically modeled across the 0 h-10 h recovery sleep doses. While TST, stage 2, REM sleep and NREM slow wave energy (SWE) increased linearly across recovery sleep doses, best-fitting neurobehavioral recovery functions were exponential across recovery sleep doses for PVT and KSS outcomes, and linear for the MWT. Analyses based on return to baseline and on estimated intersection with control condition means revealed recovery was incomplete at the 10 h TIB (8.96 h TST) for PVT performance, KSS sleepiness, and POMS fatigue. Both TST and SWE were elevated above baseline at the maximum recovery dose of 10 h TIB.

Conclusions:

Neurobehavioral deficits induced by 5 nights of sleep restricted to 4 h improved monotonically as acute recovery sleep dose increased, but some deficits remained after 10 h TIB for recovery. Complete recovery from such sleep restriction may require a longer sleep period during 1 night, and/or multiple nights of recovery sleep. It appears that acute recovery from chronic sleep restriction occurs as a result of elevated sleep pressure evident in both increased SWE and TST.

Citation:

Banks S; Van Dongen HPA; Maislin G; Dinges DF. Neurobehavioral dynamics following chronic sleep restriction: dose-response effects of one night for recovery. SLEEP 2010;33(8):1013–1026.     

Assessment of electrical impedance endotomography for hardware specification

Purpose

The purpose of the study is the quantitative assessment of Electrical Impedance Endotomography (EIE) for the specification of hardware systems. EIE is a modality of Electrical Impedance Tomography (EIT) where the electrodes are located on a probe placed in the middle of the region of interest. The absence of material boundary to the explored volume and the decrease in sensitivity away from the probe requires specific study.

Material and methods

The method is the derivation of the equation linking explored medium’s conductivity, the sensitivity distribution of the electrode patterns used for data collection and measuring system’s noise and bandwidth. The assessment of EIE was achieved by means of simulations based on realistic data of conductivity and noise level.

Results

The derived equation enabled the estimation of the current needed under realistic operating conditions corresponding to prostate imaging. The generalisation to other organs is straightforward. The image reconstructed from the simulated data and from bench experiments were in agreement and showed that the two selected drive patterns, fan3 and adjacent, gave images of similar quality in absence of noise and that adjacent drive requires significantly higher measurement current.

Conclusion

The study confirmed the feasibility of EIE with achievable hardware specifications. The derived equation enabled the determination of design parameters for the specification of hardware systems corresponding to any given application. The study also showed that EIE is more appropriate for tissue characterisation than for high speed imaging.     

呼吸中枢驱动增加时呼吸力学改变以及对吸气开始信号的影响

目的探讨呼吸中枢增加所造成的呼吸力学改变及其对吸气开始信号的影响。方法以10例正常志愿者为研究对象,采用CO2重复呼吸的方法,使呼气末CO2分压(PCO2-ET)增高到最大耐受水平,观察呼吸中枢驱动增加时的呼吸力学和吸气开始时相关信号的动态变化。结果正常志愿者重复呼吸试验最大可以耐受的PCO2-ET值为(81.2±6.6)mm Hg。随着PCO2-ET逐渐升高,膈肌肌电图的均方根(RMSdi)、跨膈压(Pdi)和潮气量(VT)进行性增高,而呼吸周期(Ttot)逐渐缩短,PCO2-ET水平从基础值[PCO2-ET(level-0)]到最大值[PCO2-ET(level-4)],RMSdi从(17.17±12.41)μV增加到(147.99±161.64)μV,Pdi和VT分别由(7.5±1.7)cm H2O和(0.68±0.27)L增加到(26.13±11.51)cm H2O和(2.21±0.37)L,而Ttot从(2.91±0.85)s减少到(1.92±0.39)s,RMSdi、Pdi、VT和Ttot与PCO2-ET的动态变化呈高度线性相关(r值分别为0.956、0.973、0.956和0.89,P均<0.001)。吸气开始时,最早出现吸气信号改变为RMSdi,其次为口腔压(Pm),再次为吸气流量(Flow);随着PCO2-ET增加,Pm和Flow滞后于RMSdi的时间逐渐延长,而Flow滞后于Pm的时间不变。结论膈肌肌电图信号的出现先于其他吸气相关信号,随着呼吸中枢驱动的增加,传统的吸气同步信号口腔压和吸气流量滞后于膈肌肌电图时间延长,提示膈肌肌电图可作为更加敏感的吸气开始的信号,可以用于呼吸机的人机同步触发,改善同步性,尤其是适合在中枢驱动异常增高的条件下。     

肺鳞癌驱动基因及其靶向治疗的研究进展

应用分子靶向药物治疗晚期肺腺癌已逐渐成为当今临床研究的主流,其中EGFR基因突变患者可从靶向治疗中获益。肺鳞癌驱动基因的研究相对较少,近期多种检测技术对肺鳞癌标本进行基因检测,结果发现多数标本存在多个可测靶点,针对这些靶点已开发出一系列药物,其疗效仍待观察。     

Characteristics of the respiratory mechanical and muscle function of competitive breath-hold divers

Competitive breath-hold divers (BHD) employ glossopharyngeal insufflation (GI) to increase intrapulmonary oxygen stores and prevent the lungs from dangerous compressions at great depths. Glossopharyngeal insufflation is associated with inflation of the lungs beyond total lung capacity (TLC). It is currently unknown whether GI transiently over-distends the lungs or adversely affects lung elastic properties in the long-term. Resting lung function, ventilatory drive, muscle strength, and lung compliance were measured in eight BHD who performed GI since 5.5 (range 2–6) years on average, eight scuba divers, and eight control subjects. In five BHD subsequent measures of static lung compliance (Cstat) were obtained after 1 and 3 min following GI. Breath-hold divers had higher than predicted ventilatory flows and volumes and did not differ from control groups with regard to gas transfer, inspiratory muscle strength, and lung compliance. A blunted response to CO₂ was obtained in BHD as compared to control groups. Upon GI there was an increase in mean vital capacity (VC_GI) by 1.75 ± 0.85 (SD) L compared to baseline (p < 0.001). In five BHD Cstat raised from 3.7 (range 2.9–6.8) L/kPa at baseline to 8.1 (range 3.4–21.2) L/kPa after maximal GI and thereafter gradually decreased to 5.6 (range 3.3–8.1) L/kPa after 1 min and 4.2 (range 2.7–6.6) L/kPa after 3 min (p < 0.01). We conclude that in experienced BHD there is a transient alteration in lung elastic recoil. Resting lung function did not reveal a pattern indicative of altered lung ventilatory or muscle function.