肌电图检测膈肌疲劳

呼吸肌疲劳是呼吸衰竭的重要原因之一。膈肌是主要的呼吸肌,在呼吸衰竭中起重要作用。目前检测膈肌疲劳(DiF)的方法主要有跨膈压和膈肌肌电图(EMGdi)。EMGdi又有食道电极和体表电极两种方法。测定跨膈压和食道电极法EMGdi均需要在食道和胃内放置气囊导管或电极,较难推广。体表电极法EMGdi简便易行,但对其检测DiF的意义尚有争议。本研究对此作初步的探讨。     

人体的括约肌

括约肌是分布在人体某些管腔周缘的一种环行肌肉。括:扎,束;约:限制。“括约”即“控制”之意。靠括约肌的收缩和舒张作用,以控制物质的通过。分布于消化系统的括约肌(一)食道胃括约肌食道和胃之间,在解剖上虽并不存在括约肌,但用测压法可以观察到,在食道与胃贲门连接处以上,有一段约4-6厘米长的高压区     

泥鳅消化道过氧化物酶、三磷酸腺苷酶、琥珀酸脱氢酶、酸性磷酸酶、碱性磷酸酶及非特异性酯酶的分布与组织定位

目的研究过氧化物酶(POX)、三磷酸腺苷酶(ATPase)、琥珀酸脱氢酶(SDH)、酸性磷酸酶(ACP)、碱性磷酸酶(ALP)及非特异性酯酶(NSE)等6种酶在泥鳅消化道不同部位的分布和组织定位。方法在泥鳅食道、胃贲门、胃体、胃幽门、前肠、中肠和后肠等7个部位取样,采用冷冻切片、酶组织化学染色和光密度定量分析等技术。结果POX在食道黏膜上皮细胞中酶活性最高,在胃、前肠、中肠和后肠中酶活性均较低;SDH、ALP和ATPase在食道中酶活性最低,在消化道其他部位酶活性均较高,主要分布于胃黏膜上皮细胞顶部和肠上皮细胞的纹状缘;ACP在食道、胃贲门、胃体、前肠、中肠和后肠上皮细胞中酶活性均较高,胃幽门中酶活性显著较低;NSE在食道、胃贲门、胃幽门、前肠和中肠上皮细胞中酶活性均较高,在胃体和后肠中酶活性显著较低。结论泥鳅消化道黏膜6种酶的分布表明,泥鳅的胃分化程度低,胃和肠道都具有吸收功能;胃贲门、胃体和前肠是蛋白质的主要消化部位;胃贲门、胃幽门、前肠和中肠是脂质的主要消化部位。     

不同能量供需下雌性棕色田鼠胃运动的变化

用PowerLab/8sp生理信号采集分析系统记录哺乳雌鼠、禁食1d和3d雌鼠及正常对照雌鼠胃内压、胃收缩幅值及收缩频率,以研究在不同能量需求与供应状态下,棕色田鼠(Lasiopodomys mandarinus)胃运动的适应性变化。结果显示,禁食组和哺乳期雌鼠的胃内压及胃收缩幅值均显著高于正常对照雌鼠组(P0.05),禁食组胃内压、胃收缩幅值较哺乳组有所下降,且禁食3d组胃内压明显下降(P0.05)。说明在不同生理状态下,能量需求与供应不同,消化道活动发生适应性变化,且消化道生理功能变化与能量胁迫程度相关。     

串脉冲致兔隔肌疲劳的动物模型

本实验采用串脉冲刺激兔隔神经法复制了家兔膈肌疲劳模型。测定隔肌张力（Ｔｄｉ）、跨膈压（Ｐｄｉ）及其频率特性（Ｔｄｉ－Ｆ、Ｐｄｉ－Ｆ）、呼吸流速（Ｖ）、肺阻力（ＲＬ）、膈肌肌电图（ＥＭＧｄｉ等作为评价膈肌收缩力量的指标。结果发现：经串脉冲刺激后,Ｐｄｉ－Ｆ曲线在３０、５０和１００Ｈｚ时显著降低,Ｐｄｉ、Ｔｄｉ、Ｖ和跨肺压均显著下降。氨茶碱可增加隔肌收缩力,延缓膈肌疲劳过程。结果提示,用串脉冲刺激兔膈神经法建立的模型是一种灵敏、可靠和稳定的膈肌疲劳动物模型。     

经食道心房调搏术及食道心电图在心律失常中的应用

目的:分析经食道心房调搏术(TEAP)及食道内心电图(EECG)在心律失常中的应用价值。方法:选取2018年6月至2019年12月于我院行食道心电图及经食道调搏的患者189例,其中男80例,女109例,年龄11~83岁。结果:54例为房室结折返性心动过速(AVNRT),34例为房室折返性心动过速(AVRT),8例为房性心动过速(AT),4例为心房扑动(AF),6例为心房颤动(Af),5例为室性心过速,78例为室早或其他。共105例心律失常患者拟行食道心房调搏终止心动过速,所有AVNRT和AVRT患者及17例AT患者经食道心房调搏S1S1成功转为窦律,50例AVNRT、32例AVRT、6例AT、3例AF及2例VT患者通过射频消融术成功根治。其中1例11岁AT患者因无法耐受食道调搏,未能转为窦律,患者经静推普罗帕酮后次日转为窦律。共97例患者拟行食道心房调搏诱发,共49例诱发出心动过速,1例左后分支型室速经静滴异丙肾上腺素后诱发心动过速,且仍需静滴异丙肾上腺素后经心房食道调博终止心动过速,后经射频消融术成功根治。结论:TEAP及EECG可用于复杂心律失常的诊断及治疗,是一种相对安全、临床容易掌握的技术,值得推广。     

小鼠经颈外静脉右心导管法测定心室压力的实验方法研究

目的：研究可行性高的测定小鼠右心室压力的实验方法。方法：通过自制PE导管,连接powerlab多通道生物信号记录系统,经颈外静脉插管,右心导管法测定小鼠右心室压力,并借以研究肺动脉压力变化。结果：用此方法对51只小鼠进行插管,46例成功进入心室并测压,成功率90．2％。其中33只正常小鼠中,成功30例,测得压力值：收缩压（23．4±5．7）mmHg,舒张压（3．7±2．6）mmHg,平均压（12．0±3．7）mmHg;18只肺动脉高压模型小鼠中,成功16例,测得压力值：收缩压：（32．2±2．8）mmng,舒张压（3．8±2．0）mmng,平均压（14．94±2．3）mmHg。共失败5例,经解剖发现2例进入下腔静脉,2例穿破心耳,1例穿破腋静脉进入胸壁。结论：使用自制的PE导管经颈外静脉插管,右心导管法测定右心室压具有成功率高、数据更准确、操作省时、方法易普及的优点。是一种较好的对小鼠进行右心室压力测定的方法。     

植物生理学研究中的压力探针技术

压力探针技术是一种用来测定微系统中压力大小和变化的新技术。其最初被设计用于直接测定巨型藻类的细胞膨压。随着操作装置的进一步微型化和精密化, 后来被应用于测定普通高等植物细胞膨压及其它水分关系参数。该技术的发展建立在一系列相应的流体物理学理论基础上。通过这些物理学公式的计算, 该技术能测定跨细胞膜或器官的水分运输速度以及它们的水力学导度; 测定溶液中水分和溶质的相对运输速度以及它们之间的相互影响; 还可以测定细胞壁的刚性等。目前压力探针技术已成为植物生理学和生态学领域研究中的多用途技术。它可以在细胞水平上原位测定水分及溶质跨膜运输及分布情况, 这对于阐明水通道功能具有极其重要的意义。此外, 木质部压力探针技术是目前唯一可以直接测定导管或管胞中负压的工具。该技术还可以用于单细胞汁液的样品采集, 结合微电极技术测定导管或其它细胞中的pH值、离子浓度以及细胞膜电位。本文重点介绍该技术使用的基本原理和相应的理论基础, 并详细地描述了操作过程中的技术和技巧。     

黑斑侧褶蛙消化道重量及长度的性别和季节差异

消化道是联系脊椎动物能量摄入和能量支出之间关系的纽带,其重量和长度对外界环境具有高度的敏感性和弹性(flexibility)。以黑斑侧褶蛙(Pelophylax nigromaculata)为研究对象,测定了山东聊城地区2012年夏季(16只,8♀/8♂)、秋季(19只,9♀/10♂)及翌年春季(17只,8♀/9♂)其体重、体长、胴体湿重和干重系数、总消化道及各段(食道、胃、小肠和大肠)的湿重、干重和长度系数的性别和季节差异(双因素方差分析),对有性别差异的指标,用单因素方差分析分别比较了雌、雄蛙的季节差异。结果显示,1)雌蛙的体重、体长均高于雄蛙,都在秋季最高,春季或夏季最低;雄蛙的胴体湿重系数高于雌蛙,夏季高于秋季;胴体干重系数既无性别差异,也无季节差异。2)除食道湿重系数无性别差异外,雌蛙总消化道及各段的湿重系数均高于雄蛙;除胃湿重系数无季节差异外,春季或秋季的总消化道及各段的湿重系数都高于夏季;雌蛙的总消化道干重和胃干重系数高于雄蛙,食道、小肠和大肠的干重系数无性别差异,所有的干重系数均无季节性差异。3)除雌蛙的大肠长系数高于雄蛙外,总消化道及各段的长度系数均无性别差异,春季和秋季的总消化道长、食道长及胃长系数均高于夏季,小肠长和大肠长系数均无季节性差异。结果表明,随着季节更替,黑斑侧褶蛙消化道各段的重量和长度表现出一定的弹性特征,这与各器官的功能及其生活环境的多样性是相适应的。     

植物生理学研究中的压力探针技术

压力探针技术是一种用来测定微系统中压力大小和变化的新技术。其最初被设计用于直接测定巨型藻类的细胞膨压。随着操作装置的进一步微型化和精密化,后来被应用于测定普通高等植物细胞膨压及其它水分关系参数。该技术的发展建立在一系列相应的流体物理学理论基础上。通过这些物理学公式的计算,该技术能测定跨细胞膜或器官的水分运输速度以及它们的水力学导度;测定溶液中水分和溶质的相对运输速度以及它们之间的相互影响;还可以测定细胞壁的刚性等。目前压力探针技术已成为植物生理学和生态学领域研究中的多用途技术。它可以在细胞水平上原位测定水分及溶质跨膜运输及分布情况,这对于阐明水通道功能具有极其重要的意义。此外,木质部压力探针技术是目前唯一可以直接测定导管或管胞中负压的工具。该技术还可以用于单细胞汁液的样品采集,结合微电极技术测定导管或其它细胞中的pH值、离子浓度以及细胞膜电位。本文重点介绍该技术使用的基本原理和相应的理论基础,并详细地描述了操作过程中的技术和技巧。     

Factors affecting the accuracy of esophageal balloon measurement of pleural pressure in dogs.

Simultaneous measurement of esophageal and tracheal pressures during an occluded inspiratory effort was used to assess the accuracy of the esophageal balloon for measuring pleural pressure in dogs. Esophageal balloons were inserted in five mongrel dogs, and an occlusion test was performed with the balloon tip 5, 10, 15, 20, and 25 cm above the esophageal sphincter; at lung volumes of functional residual capacity (FRC) and FRC + 600 ml; and in supine and right- and left-side lying postures. The protocol was repeated in paralyzed animals. This time the occlusion test was performed by injecting air into a plethysmograph to change the body surface pressure, simulating pressure changes produced by respiratory efforts in spontaneously breathing animals. In 47% of the tests in spontaneously breathing dogs, the slope of esophageal vs. tracheal pressure varied greater than 10% from unity. After paralysis the slope did not vary greater than 5% from unity under any circumstance. These data indicate that the poorer performance of the occlusion test in nonparalyzed dogs is due to active tension in the walls of the esophagus and stress induced in the intrathoracic soft tissues by the descent of the diaphragm during a breathing effort.     

Relationship among EMG and contractile responses of the diaphragm elicited by hypotension

In a canine model, we investigated the effects of severe hypotension on the indexes of diaphragmatic failure. We measured 1) the transdiaphragmatic pressure obtained in response to 20- and 100-Hz stimulation of phrenic nerves (Pdi20 and Pdi100), 2) the power spectrum of diaphragmatic electromyogram (EMG), 3) the ratio of integrated diaphragmatic EMG to Pdi (Edi/Pdi), and 4) the rate of relaxation of Pdi100 and Pdi20. Arterial blood pressure (Pa) was reduced to 40-50 mmHg by a balloon inflated in the inferior vena cava and was maintained at this level until Pdi100 declined to 75% of the control value (100% shock time, ST). A recovery period of 60 min at normal Pa was allowed. During hypotension, Pdi100 and Pdi20 declined only at 100% ST [95.0 +/- 13.0 (SE) min]; however, only Pdi100 recovered within 15 min. The power spectrum shifted to low frequencies early and progressively during shock period. Edi/Pdi rose significantly at 80 and 100% ST and recovered within 15 min. The relaxation rate of Pdi20 and Pdi100 increased significantly at 100% ST only. We conclude that 1) diaphragmatic contractility is depressed during severe hypotension, 2) changes in the power spectrum occurred first in the shock state, followed by alterations in Edi/Pdi, and subsequently both changes in the frequency-pressure curve and relaxation rate occurred last.     

The impact of continuous positive airway pressure on the lower esophageal sphincter

The lower esophageal sphincter (LES) is the primary barrier to gastroesophageal reflux. Reflux is associated with periods of LES relaxation, as occurs during swallowing. Continuous positive airway pressure (CPAP) has been shown to reduce reflux in individuals with and without sleep apnea, by an unknown mechanism. The aim of this study was to determine the effect of CPAP on swallow-induced LES relaxation. Measurements were made in 10 healthy, awake, supine individuals. Esophageal (Pes), LES (Ples), gastric (Pg), and barrier pressure to reflux (Pb = Ples - Pg) were recorded using a sleeve catheter during five swallows of 5 ml of water. This was repeated at four levels of CPAP (0, 5, 10, and 15 cmH(2)O). Pressures were measured during quiet breathing and during the LES relaxation associated with a swallow. Duration of LES relaxation was also recorded. During quiet breathing, CPAP significantly increased end-expiratory Pes, Ples, Pg, and Pb (P < 0.05). The increase in Pb was due to a disproportionate increase in Ples compared with Pg (P < 0.05). During a swallow, CPAP increased nadir Ples, Pg, and Pb and decreased the duration of LES relaxation (4.1 s with 0-cmH(2)O CPAP to 1.6 s on 15-cmH(2)O CPAP, P < 0.001). Pb increased with CPAP by virtue of a disproportionate increase in Ples compared with Pg. This may be due to either reflex activation of LES smooth muscle, or nonspecific transmission of pressure to the LES. The findings suggest CPAP may make the LES less susceptible to reflux by increasing Pb and decreasing the duration of LES relaxation.     

Lung and chest wall mechanics in microgravity.

We studied the effect of 15-20 s of weightlessness on lung, chest wall, and abdominal mechanics in five normal subjects inside an aircraft flying repeated parabolic trajectories. We measured flow at the mouth, thoracoabdominal and compartmental volume changes, and gastric pressure (Pga). In two subjects, esophageal pressures were measured as well, allowing for estimates of transdiaphragmatic pressure (Pdi). In all subjects functional residual capacity at 0 Gz decreased by 244 +/- 31 ml as a result of the inward displacement of the abdomen. End-expiratory Pga decreased from 6.8 +/- 0.8 cmH2O at 1 Gz to 2.5 +/- 0.3 cmH2O at Gz (P less than 0.005). Abdominal contribution to tidal volume increased from 0.33 +/- 0.05 to 0.51 +/- 0.04 at 0 Gz (P less than 0.001) but delta Pga showed no consistent change. Hence abdominal compliance increased from 43 +/- 9 to 70 +/- 10 ml/cmH2O (P less than 0.05). There was no consistent effect of Gz on tidal swings of Pdi, on pulmonary resistance and dynamic compliance, or on any of the timing parameters determining the temporal pattern of breathing. The results indicate that at 0 G respiratory mechanics are intermediate between those in the upright and supine postures at 1 G. In addition, analysis of end-expiratory pressures suggests that during weightlessness intra-abdominal pressure is zero, the diaphragm is passively tensed, and a residual small pleural pressure gradient may be present.     

Aminophylline and human diaphragm strength in vivo

The transdiaphragmatic pressure (Pdi) twitch response to single shocks from supramaximal bilateral phrenic nerve stimulation was studied before and after acute intravenous infusions of aminophylline [14.9 +/- 3.1 (SD) micrograms/ml] in nine normal subjects. Stimulation was performed with subjects in the sitting position against an occluded airway from end expiration. Baseline gastric pressure and abdominal and rib cage configuration were kept constant. There was no significant difference in peak twitch Pdi from the relaxed diaphragm between control (38.8 +/- 3.3 cmH2O) and aminophylline (40.2 +/- 5.2 cmH2O) experiments. Other twitch characteristics including contraction time, half-relaxation time, and maximum relaxation rate were also unchanged. The Pdi-twitch amplitude at different levels of voluntary Pdi was measured with the twitch occlusion technique, and this relationship was found to be similar under control conditions and after aminophylline. With this technique, maximum Pdi (Pdimax) was calculated as the Pdi at which stimulation would result in no Pdi twitch because all motor units are already maximally activated. No significant change was found in mean calculated Pdimax between control (146.9 +/- 27.0 cmH2O) and aminophylline (149.2 +/- 26.0 cmH2O) experiments. We conclude from this study that the acute administration of aminophylline at therapeutic concentrations does not significantly affect contractility or maximum strength of the normal human diaphragm in vivo.     

Diaphragmatic contractility after upper abdominal surgery

Postoperative dysfunction of the diaphragm has been reported after upper abdominal surgery. This study was designed to determine whether an impairment in diaphragmatic contractility was involved in the genesis of the diaphragmatic dysfunction observed after upper abdominal surgery. Five patients undergoing upper abdominal surgery were studied. The following measurements were performed before and 4 h after surgery: vital capacity (VC), functional residual capacity (FRC), and forced expiratory volume in 1 s. Diaphragmatic function was also assessed using the ratio of changes in gastric pressure (delta Pga) over changes in transdiaphragmatic pressure (delta Pdi). Finally contractility of the diaphragm was determined by measuring the change in delta Pdi generated during bilateral electrical stimulation of the phrenic nerves (Pdi stim). Diaphragmatic dysfunction occurred in all the patients after upper abdominal surgery as assessed by a marked decrease in delta Pga/delta Pdi from 0.480 +/- 0.040 to -0.097 +/- 0.152 (P less than 0.01) 4 h after surgery compared with preoperative values. VC also markedly decreased after upper abdominal surgery from 3,900 +/- 630 to 2,060 +/- 520 ml (P less than 0.01) 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after surgery. In contrast, no change in FRC and Pdi stim was observed 4 h after upper abdominal surgery compared with the preoperative values. We conclude that contractility of the diaphragm is not altered after upper abdominal surgery, and diaphragmatic dysfunction is secondary to other mechanisms such as possible reflexes arising from the periphery (chest wall and/or peritoneum), which could inhibit the phrenic nerve output.     

Arterial CO2 partial pressure affects diaphragmatic function

The purpose of this study was to examine in an in vivo preparation acute variations of PCO2 on diaphragmatic contractility. Plaster casts were snugly fit around the abdomen of six open-chested dogs, moving the abdominal contents rostrally. Diaphragmatic contractions against this very fixed load in response to phrenic nerve stimulation (supramaximal voltage at 1, 20, 50, and 80 Hz) or during spontaneous inspiratory efforts were virtually isometric (quasi-isometric). Transdiaphragmatic pressure (Pdi) measured by an abdominal balloon was used as an index of diaphragmatic contractility. Arterial PCO2 (PaCO2) was reduced by hyperventilation and raised by increasing PICO2. Pdi values in response to stimulation at 1, 20, 50, and 80 Hz in ranges I (PaCO2 = 0-19 Torr) and II (PaCO2 = 20-34 Torr) did not differ statistically from the control Pdi values (range III; PaCO2 = 35-45 Torr). In range IV (PaCO2 = 46-70 Torr) Pdi values for stimulations of 20, 50, and 80 Hz were significantly lower than control. In range V (PaCO2 = 71-90 Torr), VI (PaCO2 = 91-101 Torr), and VII (PaCO2 greater than or equal to 102 Torr) Pdi values were significantly less than those in range IV at all frequencies of stimulation. In the four dogs measured during spontaneous inspiratory efforts the integrated diaphragmatic electromyogram (Edi) was correlated with the Pdi. As PaCO2 rose (range III to VII), the Pdi values observed at 25, 50, 75, 100% of the maximum Edi (of range III) were significantly lower than the Pdi value of range III.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dose effect of pentobarbital sodium on control of breathing in cats

The dose effect of pentobarbital sodium on integrated ("moving time average") phrenic activity (EPHR), transdiaphragmatic pressure (Pdi), gastric pressure (Pga), changes in lung volume (V), and mechanical properties of the respiratory system was studied in six cats breathing room air. Increased pentobarbital dose from an initial value of 35 mg/kg ip, had no substantial effect on the relationship between EPHR and Pdi during both unoccluded and occluded inspirations, indicating that the diaphragmatic excitation-contraction coupling was not affected. Similarly, increased anesthetic dose had no effect on the relationship between EPHR and delta Pga during both occluded and unoccluded breaths, suggesting that the contribution of the diaphragm to the breathing movements did not change with increasing depth of anesthesia. Although the time course of phrenic activity showed substantial interanimal differences, the shape of the phrenic neurogram did not change substantially with increased pentobarbital dose in any of the cats studied. Increased anesthetic dose depressed, in the same proportion, the rate of rise of EPHR, Pdi, and V, but the mechanical properties of the respiratory system remained unchanged. The depression of ventilation with increased anesthetic dose was not proportional to the drop in central inspiratory activity, as quantified in terms of rate of rise of EPHR.     

Changes in rate of relaxation of sniffs with diaphragmatic fatigue in humans

The rate of relaxation of the diaphragm after stimulated (4 subjects) and voluntary (8 subjects) contractions was compared in normal young men. Stimulated contractions were induced by supramaximal unilateral phrenic nerve stimulation and voluntary contractions by short, sharp sniffs of varying tensions against an occluded airway. The rate of relaxation of the diaphragm was calculated from the rate of decline of transdiaphragmatic pressure (Pdi). In both conditions the maximum relaxation rate (MRR) was proportional to the peak transdiaphragmatic pressure (Pdi), whereas the time constant (tau) of the later exponential decline in Pdi was independent of Pdi. The mean +/- SE rate constant of relaxation (MRR/Pdi) was 0.0078 +/- 0.0002 ms-1 and the mean tau was 57 +/- 3.8 ms for stimulated contractions. The rate of relaxation after sniffs was not different, and it was not affected by either the lung volume at which occluded sniffs were performed (in the range of residual volume to functional residual capacity + 1 liter) or by the relative contribution gastric pressure made to Pdi. After diaphragmatic fatigue was induced by inspiring against a high alinear resistance there was a decrease in relaxation rate. In the 1st min postfatigue MRR/Pdi decreased (0.0063 +/- 0.0003 ms-1; P less than 0.005) and tau increased (83 +/- 5 ms; P less than 0.005). Both values returned to prefatigue levels within 5 min of the end of the studies. We conclude that the sniff may prove to be clinically useful in the detection of diaphragmatic fatigue.     

Respiratory sensation and pattern of respiratory muscle activation during diaphragm fatigue

We have examined the relationship between respiratory effort sensation (modified Borg scale) and amplitude of the integrated surface electromyogram of the diaphragm (Edi, esophageal electrode), rib cage muscles (Erc), and sternomastoid muscle (Esm) during the development of diaphragm fatigue in five normal subjects. Three conditions were studied: run A: transdiaphragmatic pressure (Pdi), 65% Pdimax; esophageal pressure (Pes), 60% Pesmax; run B: Pdi, 50% Pdimax; Pes, 60% Pesmax; and run C: Pdi, 50% Pdimax; Pes, 20% Pesmax. During all runs there was a progressive rise in sensation, which was greater in runs A and B than in run C (P less than 0.05, analysis of variance). There was no difference between runs A and B. At the end of run C subjects did not report a maximal Borg score despite their inability to generate the target Pdi. The increase in sensory score with fatigue correlated highly with Esm/Esmmax and with Erc/Ercmax. There was no correlation between sensory score and Edi/Edimax. We conclude that the increase in respiratory effort sensation that accompanies diaphragm fatigue is not due to perception of increased diaphragmatic activation. It may reflect increased overall respiratory motor output not directed to the diaphragm.