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1.
In anaesthetized rabbits the effects of high frequency ventilation (HFV) on breathing pattern and on stretch receptor (SR) activity were examined in order to elucidate the mechanism underlying the inhibition of respiration during HFV. An attempt was undertaken to compare the effects of HFV with those of static lung inflations.HFV applied in frequencies between 5 Hz and 25 Hz and with peak airway pressure (Paw) between 5 and 15 cm H2O led — proportionally to Paw — to a gradual prolongation of expiration up to an apnoea. Similar effects occurred during lung inflations, although at higher Paw than during HFV. HFV-induced apnoea was accompanied by a tonic phrenic and diaphragmatic activity which was absent during inflation-induced apnoea.In addition to the activity due to spontaneous breathing, during HFV the SR discharge rate increased with each positive airflow pulse particularly in the expiratory phase, whereas the inspiratory discharge rate was less affected. During static lung inflations there was a parallel increase of both inspiratory and expiratory SR activity, the expiratory discharge rate, however, remaining lower and the inspiratory discharge rate rising more than during HFV.It is concluded that the HFV-induced increase of expiratory SR discharge rate may account for the inhibition of spontaneous breathing during HFV. The persistence of phrenic and diaphragmatic activity during HFV-induced apnoea is thought to be due to activation of irritant receptors.  相似文献   

2.
The contribution of pulmonary stretch receptor (SR) activity to the changes in breathing pattern (f,V T,t I,t E,t I:t E) following inhalation of ammonia vapour has been studied in rabbits at three levels of lung distension, i.e., three levels of SR activity, and during reversible SO2-blockade of SR.The results show that the increase in breathing frequency (f) and the decrease in tidal volume (V T) due to ammonia inhalation are almost identical for animals with and without blockade of SR, whereas the duration of inspiration and expiration (t I,t E) as well as their relationship (t I:t E) vary considerably, the variations dependeing on the level of SR activity. For a givent I the expiration was longer in animals with SR intact than in animals with SR blocked.It is concluded that in rabbits the increased activity of SR after inhalation of ammonia counteracts significantly the predominant effects of irritant (deflation) receptor stimulation, thus rendering possible a longer expiration.  相似文献   

3.
We tested the hypothesis that the pattern of chest wall configuration during speech production correlates with the pattern of chest wall motion during resting breathing. Twenty-one men (age 40 ± 8 years) with ankylosing spondylitis and varied degrees of ribcage involvement participated in the study. None of the patients had an obvious speech abnormality. Ribcage and abdominal displacements during quiet breathing and during reading were measured with a respiratory plethysmograph. Measurements were taken in the sitting and standing body positions. In each body position, ribcage or abdominal displacements during quiet breathing correlated with the corresponding chest wall displacements recorded during reading (P < 0.001). In addition, linear regression analysis showed that the slope of the chest wall motion loop during quiet breathing correlated with the ratio of ribcage to abdomen contribution to lung volume displacement during reading (r = 0.78, P < 0.001 for sitting and r = 0.64, P = 0.002 for standing position). The slopes of the regression lines did not differ between the sitting and standing body position (P > 0.05). We conclude that the relative contribution of the ribcage and abdomen to lung volume displacement during speech production correlates with the relative ribcage and abdomen contribution to tidal volume during quiet breathing; our data support the notion that the pattern of chest wall configuration during quiet breathing largely predicts the pattern of ribcage and abdomen displacement during speech.  相似文献   

4.

Study Objectives:

Many patients with obstructive sleep apnea (OSA) have spontaneous periods of stable flow limited breathing during sleep without respiratory events or arousals. In addition, OSA is often more severe during REM than NREM and more severe during stage 2 than slow wave sleep (SWS). The physiological mechanisms for these observations are unknown. Thus we aimed to determine whether the activity of two upper airway dilator muscles (genioglossus and tensor palatini) or end-expiratory lung volume (EELV) differ between (1) spontaneously occurring stable and cyclical breathing and (2) different sleep stages in OSA.

Design:

Physiologic observation.

Setting:

Sleep physiology laboratory.

Study Participants:

15 OSA patients with documented periods of spontaneous stable breathing.

Intervention:

Subjects were instrumented with intramuscular electrodes for genioglossus and tensor palatini electromyograms (EMGGG and EMGTP), chest and abdominal magnetometers (EELV measurement), an epiglottic pressure catheter (respiratory effort), and a mask and pneumotachograph (airflow/ventilation). Patients slept supine overnight without CPAP.

Measurements and Results:

Peak and Tonic EMGGG were significantly lower during cyclical (85.4 ± 2.7 and 94.6 ± 4.7 % total activity) than stable breathing (109.4 ± 0.4 and 103 ± 0.8 % total activity, respectively). During respiratory events in REM, tonic EMGGG activity was lower than during respiratory events in stage 2 (71.9 ± 5.1 and 119.6 ± 5.6 % total activity). EMGGG did not differ between stable stage 2 and stable SWS (98.9 ± 3.2 versus 109.7 ± 4.4 % total activity), nor did EMGTP or EELV differ in any breathing condition/sleep stage.

Conclusions:

Increased genioglossus muscle tone is associated with spontaneous periods of stable flow limited breathing in the OSA subjects studied. Reductions in genioglossus activity during REM may explain the higher severity of OSA in that stage. Increased lung volume and tensor palatini activity do not appear to be major mechanisms enabling spontaneous stable flow limited breathing periods.

Citation:

Jordan AS; White DP; Lo YL; Wellman A; Eckert DJ; Yim-Yeh S; Eikermann M; Smith SA; Stevenson KE; Malhotra A. Airway dilator muscle activity and lung volume during stable breathing in obstructive sleep apnea. SLEEP 2009;32(3):361–368.  相似文献   

5.
A mathematical model of non-obstructive human periodic breathing (Cheyne–Stokes respiration) or central sleep apnea (CSA) is described which focused on explaining recently reported non-linear behavior. Evidence was presented that CHF (chronic heart failure)–CSA and ICSA (idiopathic central sleep apnea) both involved limit cycle oscillations. The validity of applying linear control theory for stabilization must then be re-examined. Critical threshold values and ranges of parameters were predicted which caused a change (bifurcation) from limit cycle periodic breathing to stable breathing. Changes in lung volume were predicted to form a bifurcation during CHF–CSA where stability and instability can involve a lung volume change as small as 0.1 l. CSA therapy based on reducing control loop gain was predicted to be relatively ineffective during stable limit cycle oscillation. The relative ratios of durations of ventilation to apnea (T v/T a) during periodic breathing were primarily determined by peripheral chemoreceptor dynamics during crescendo, de-crescendo, and apnea phases of CSA.  相似文献   

6.
The effects of changes in static airway pressure (P aw) and arterial PCO2 (P aCO2) on phrenic nerve activity were studied in unanesthetized, decerebrate dogs and compared with previous results from chloralose/urethane anestetized dogs using the same experimental preparation (Mitchell et al. 1982; Mitchell and Selby 1987). In ten mid-collicular decerebrate dogs, the lungs were independently ventilated while the left pulmonary artery was occluded and the right vagus nerve was transected. Changes in left lung P aw, therefore, exerted effects on pulmonary stretch receptors without altering blood gases; changes in the inspired gas ventilating the right lung controlled blood gas composition, without altering lung volume feedback. Phrenic burst frequency (f) and integrated amplitude (Phr) were monitored while P aw was varied between 2 and 12 cmH2O at various constant levels of P aCO2 between 31 and 69 mmHg. The major findings of this study are: (1) hypercapnia decreases the slope of the relationship between expiratory duration (t E) and P aw in both decerebrated and anesthetized dogs; (2) hypercapnia increases the inspiratory duration (t I) in decerebrated, but not anesthetized dogs; and (3) hypercapnia decreases the slope of the relationship between f and P aw due to these effects on t E and t I. These results support previous studies indicating that vagal and suprapontine mechanisms exert independent effects on respiratory timing. It is concluded that neither suprapontine influences nor anesthesia are necessary in the mechanism underlying interactions between stretch receptors and CO2-chemoreceptors in modulating t E. Furthermore, decerebration reveals a unique effect of CO2-chemoreceptors on t I, an effect found in anesthetized dogs only after carotid denervation.  相似文献   

7.
Mechanical lung function is frequently assessed in terms of lung resistance (R L), lung elastance (E L), and airway resistance (R aw). These quantities are determined by measuring input impedance at various oscillation frequencies, and allow lung tissue resistance (R t) to be estimated as the difference between R L and R aw. These various parameters change in characteristic ways in the presence of lung pathology. In particular, the ratio R t/E L (known as hysteresivity, (η) has been shown both experimentally and in numerical simulations to increase when regional heterogeneities in mechanical function develop throughout the lung. In this study, we performed an analytical investigation of a two-compartment lung model and showed that while heterogeneity always leads to an increase in E L, η will increase only initially. When heterogeneity becomes extreme, η stops increasing and starts to decrease. However, there are no experimental reports of η decreasing under conditions in which heterogeneity would be expected to exist. We speculate that this is because liquid bridges invariably form across airway lumen that narrow to a certain point, thereby preventing them from achieving arbitrarily small non-zero radii. We also show that recruitment of closed lung units during lung inflation may lead to variables responses in both η and E L.  相似文献   

8.
It is unknown how central neural activity produces the repetitive termination and restart of periodic breathing (PB). We hypothesized that inspiratory and expiratory neural activities would be greatest during the waxing phase and least during the waning phase. We analyzed diaphragmatic and medullary respiratory neural activities during PB in intact unanesthetized adult cats. Diaphragmatic activity was increased and phasic during the waxing phase and was decreased and tonic during the waning phase. Activity of expiratory (n=21) and inspiratory (n=40) neurons was generally increased and phasic during the waxing phase and was decreased and more tonic during the waning phase. During apneas associated with PB, diaphragmatic activity was silent and most, but not all, inspiratory cells were inactive whereas most expiratory cells decreased activity but remained tonically active. We suggest that reduced strength of reciprocal inhibition, secondary to reduced respiratory drive, allows for simultaneous tonic activity of inspiratory and expiratory neurons of the central pattern generator, ultimately resulting in central apnea.  相似文献   

9.
The development of fatigue was investigated in the diaphragm of anaesthetized, tracheostomized, spontaneously breathing cats during restricted air flow. Ventilation, transdiaphragmatic pressure (Pdi), integrated electrical activity of diaphragm (Edi) and phrenic nerve (Eph) were measured simultaneously and expressed as a percentage of values at unloaded breathing. Inspiratory loads were 60, 70 and 80% of Pdi max. The Pdi max was measured by airway occlusion at functional residual capacity. The duration of loads was 40–60 min. The diaphragmatic fatigue developed only during heavy inspiratory loading (80% Pdi max). During the first 10 min of heavy load Pdi, Edi and Eph increased to 905 ± 60%, 248 ± 20% and 229 ± 24%, respectively (P < 0.01), and then began to fall gradually. Ventilation declined to 39 ± 3% after 60 min of heavy load (P < 0.01), resulting in acute hypercapnia and hypoxia. Initial fatigue appeared as a decrease in Pdi (to 781 ± 63%) and parallel decline in Edi (to 233 ± 21%) after 30 min of load (P < 0.05). Phrenic nerve activity did not change during this stage. These data suggest a peripheral basis of diaphragmatic fatigue, related to disorders in neuromuscular transmission. After 60 min of heavy load, Pdi fell to 675 ± 49%, Edi declined to 209 ± 28% and Eph decreased to 189 ± 25%. We interpret the decrease in phrenic nerve activity as a weakening of central inspiratory drive and development of the central component of diaphragmatic fatigue in the last stage.  相似文献   

10.
In anaesthetized rabbits the influence of differential vagal cold blockade on the ventilatory response to inhaled CO2 during hyperoxia was investigated.Following total inactivation, the relationship between ventilation ( ) and arterialPCO2 (P aCO2) was shifted to the left and steepened slightly over a range of modest hypercapnia, but was progressively flattened as hypercapnia intensified. The latter effect, suggestive of a vagally mediated facilitation of ventilatory CO2 responsiveness, was studied further.Differential vagal cold blockade to a temperature (5–11°C) which abolished the Breuer-Hering inflation reflex (end-inspiratory tracheal occlusion no longer eliciting a prolongation of expiratory duration,T E) had no effect on either during normocapnia or at a substantial level of hypercapnia. Only with further vagal cooling to 0°C did the ventilatory depression during hypercapnia emerge, largely becauseT E failed to shorten in response to the hypercapnic stimulus.It is concluded that the integrity of expiratory-terminating mechanisms is crucial for the manifestation of the vagally mediated facilitation of and its CO2 responsiveness which is evident during hyperoxic hypercapnia. A possible role is suggested for lung epithelial irritant receptors or for the tonic late-expiratory activity from pulmonary stretch receptors.Supported by the Deutsche Forschungsgemeinschaft, SFB 114Preliminary reports of this work have been presented in Pflügers Arch 355: (Suppl) R47 (1975); 377: (Suppl) R54 (1978) and in Proc. XXVIII. Int. Congr. of Physiol. Sciences, Budapest, Vol VIV, 515 (1980)  相似文献   

11.
Breath-hold divers train and compete in maximal apnea performance. Glossopharyngeal inhalation (GI) is commonly used to increase lung volume above vital capacity (VC) prior to apnea. We investigated the hypothesis that this practice would increase apnea performance and relaxed airway pressure. Seven well-trained breath-hold divers performed maximal bouts of apnea at three different lung volumes (85% VC, VC and VC + GI) both at rest (dry static apnea) and during underwater swimming (dynamic apnea). Heart rate, apnea time and end tidal PCO2 and PO2 (P ET CO2 and P ET O2) were recorded. In addition, relaxed airway pressure was measured after GI. Maximal GI increased lung volume by 1.59±0.57 l above VC and increased relaxed airway pressure to from 3.5±0.5 to 8.7±1.7 kPa. Dry static apnea time was higher at VC + GI (346±46 s) than at VC (309±38 s, P<0.05) and 85% VC (297±48 s, P<0.01). Likewise, dynamic apnea time was higher at VC + GI (97±27 s) than at VC (78±14 s, P<0.05) and 85% VC (71±17 s, P<0.05). P ET O2 values reached 3.5±0.6 kPa at the end of dry static apnea bouts and this was not different from dynamic apnea when taking hydrostatic pressure at swimming depth into account (3.7±0.6 kPa, P=0.48). In conclusion, GI increases lung volume, relaxed airway pressure and apnea performance in well-trained breath-hold divers.  相似文献   

12.
The fetal respiratory response to acute hypoxia is characterized by depression, often to apnea. This study examined the effect of hypoxia on the electromyogram (EMG) of the thyroarytenoid (TA) muscle. Under anesthesia catheters were placed in the fetal sheep carotid artery, fourth cerebral ventricle, trachea and amniotic fluid and wires sewn into the diaphragm and TA muscle. During normoxic episodes of slow fetal breathing (<40 breaths per min) TA EMG activity was phasic beginning immediately after diaphragmatic EMG bursts and ending well before the next burst. This timing is consistent with the post-inspiratory (post-I) phase of the respiratory cycle. Lowering fetal arterial Pa O2 from ∼20 mmHg to ∼13 mmHg resulted in arrest of diaphragm EMG and tonic TA activity. Instillation of the (R,S)- -amino-3- hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) ionotrophic glutamate receptor antagonist 2,3-dihydro-6-nitro-7-sulphamoyl-benzo(f) quinoxaline (NBQX) into the cerebrospinal fluid (CSF) of the fourth ventricle abolished tracheal pressure deflections and diaphragmatic EMG activity. Tonic TA activity, however, could still be evoked by hypoxia. These results indicate that fetal post-I motoneurons are not inhibited by moderate hypoxia and that their tonic activity may be due to a loss of inhibitory input.  相似文献   

13.
The use of non-invasive resistive breathing to task failure to assess inspiratory muscle performance remains a matter of debate. CO2 retention rather than diaphragmatic fatigue was suggested to limit endurance during inspiratory resistive breathing. Cervical magnetic stimulation (CMS) allows discrimination between diaphragmatic and rib cage muscle fatigue. We tested a new protocol with respect to the extent and the partitioning of inspiratory muscle fatigue at task failure. Nine healthy subjects performed two runs of inspiratory resistive breathing at 67 (12)% of their maximal inspiratory mouth pressure, respiratory rate ( fR), paced at 18 min–1, with a 15-min pause between runs. Diaphragm and rib cage muscle contractility were assessed from CMS-induced esophageal (Pes,tw), gastric (Pga,tw), and transdiaphragmatic (Pdi,tw) twitch pressures. Average endurance times of the first and second runs were similar [9.1 (6.7) and 8.4 (3.5) min]. Pdi,tw significantly decreased from 33.1 to 25.9 cmH2O in the first run, partially recovered (27.6 cmH2O), and decreased further in the second run (23.4 cmH2O). Pes,tw also decreased significantly (–5.1 and –2.4 cmH2O), while Pga,tw did not change significantly (–2.0 and –1.9 cmH2O), indicating more pronounced rib cage rather than diaphragmatic fatigue. End-tidal partial pressure of CO2 (PETCO2) rose from 37.2 to 44.0 and 45.3 mmHg, and arterial oxygen saturation (SaO2) decreased in both runs from 98% to 94%. Thus, task failure in mouth-pressure-targeted, inspiratory resistive breathing is associated with both diaphragmatic and rib cage muscle fatigue. Similar endurance times despite different degrees of muscle fatigue at the start of the runs indicate that other factors, e.g. increases in PETCO2, and/or decreases in SaO2, probably contributed to task-failure.  相似文献   

14.
In eight mechanically ventilated, anaesthetized pigs weighing 10.3 ± 0.8 kg (mean ± SD) we studied the effect of the inflation time of the lung on the estimation of the mean systemic filling pressure (P sf) from the changes in venous return and central venous pressure during inflation of the lung. For this purpose we applied slow inflation procedures (SIP) to the lung with inflation times of 2.4, 4.8, 7.2, 9.6 and 12 s at tidal volumes (V T) of 15 and 30 ml/kg. The data were compared with the values of P sf obtained from inspiratory pause procedures (IPPs). A linear regression between venous return and central venous pressure applied during a SIP underestimated P sf compared with the value obtained with IPPs. An exponential fit through the values of P sf obtained from the different SIPs predicted an inflation time of about 15 s for an estimation of P sf that is not different from the P sf (IPP). The advantage of the SIP method is that the P sf can be determined much faster than with the method based on IPPs. However, due to the rather long inflation time needed, the method may be only applicable under circumstances where neurohumoral control mechanisms are suppressed as during intensive care and anaesthesia. Received: 18 July 1995/Received after revision: 22 November 1995 /Accepted: 15 December 1995  相似文献   

15.
The correlation between pulmonary stretch receptor activity and inspiration-expiration duration quotient as well as respiratory frequency (Hering-Breuer reflexes) has been established before and during an asthma attack in the guinea-pig. The Hering-Breuer reflexes subserving the self-regulation of breathing during uninfluenced spontaneous breathing no longer prevail after induction of a bronchial asthma attack. Increased stretch receptor activity following increased lung volume does not lead to inhibition of inspiratory activity (lung inflation reflex), but to an enhancement of the asthmatic tachypnoea. The latter is assumed to result from the expiratory self-compression of the lungs (lung deflation reflex). The enhancement of the deflation reflex by increasing lung volume during the asthma attack is discussed with regard to the uneven ventilation and the conditions in lung mechanics underlying the excitation of the lung deflation or collapse endings.  相似文献   

16.
Summary Twelve subjects with chronic obstructive lung disease and a partially reversible obstruction received increasing single doses of bopindolol (1, 2, 4, and 8 mg), pindolol (7.5, 15, and 30 mg), and atenolol (50 and 100 mg). Resting heart rate and blood pressure were reduced in a dose-dependent fashion. The actions of the drugs on lung function were assessed by whole body plethysmography. Pindolol did not influence mean airway resistance (R aw). Bopindolol (1, 2 and 4 mg) and atenolol (50 mg) exhibited a neutral effect on meanR aw. Atenolol (100 mg) and to a lesser extent bopindolol (8 mg) induced a long-lasting increase in mean Raw.Abbreviations Raw airway resistance - HR heart rate  相似文献   

17.
In an attempt to define the role of SARs on the breathing pattern and respiratory mechanics, we have studied adult rabbits anaesthetised, supine and tracheostomised during air breathing (A), after SO2 breathing (200 ppm for a period long enough to abolish the apnea following lung inflation, 10–30 min) (S), and after bilateral vagotomy (V). Tidal volume and inspiratory time increased, while breathing frequency decreased from A to V. The effects of S depended upon the type of anaesthesia used, with a definite increase in volume and a drop in frequency in the urethane anaesthetized animals and a trend toward opposite changes with barbiturate anaesthesia. Total and lung compliance increased and total pulmonary resistance decreased from A to S; no further changes were observed with V. The combined changes in breathing pattern and mechanics decreased the respiratory work per minute from A to V, suggesting that the primary concern of the vagal afferent information is to regulation even with SO2 concentration up to 330 ppm for 30 min. From A to V the changes in breathing pattern and compliance were similar to those observed in the adult.  相似文献   

18.
Summary Since elastic and flow-resistive respiratory work are volume dependent, changes in lung volume during immersion affect respiratory effort. This investigation examined changes in lung volume with air delivery pressure modifications during upright immersion. Static pressure-volume relaxation relationships and lung volumes were obtained from ten immersed subjects breathing air at four delivery pressures: mouth pressure, lung centroid pressure (P LC), and 0.98 kPa above and belowP LC. TheP LC is the static lung pressure which returns the respiratory relaxation volume (V R) to normal and was previously determined to be + 1.33 kPa relative to pressure at the sternal notch. Lung volume changes observed when breathing air at mouth pressure were reversed when air was supplied atP LC. The expiratory reserve volume (ERV) and VR were reduced by 58% and 87%, respectively, during uncompensated immersion. These differences indicated an active defence of ERV and implied that additional static respiratory work was required to overcome transrespiratory pressure gradients.  相似文献   

19.
Background: Diaphragm movement is well correlated with inspired volume of the lung. Dexmedetomidine (DEX) has less effect on respiratory functions than other sedatives. The objective of this study was to investigate diaphragmatic movement using ultrasound (US) during DEX infusion for sedation in spontaneously breathing patients undergoing unilateral upper limb surgery.Methods: A total of 33 consecutive patients were enrolled in this study. Patients were sedated using DEX with ipsilateral axillary brachial nerve plexus block. Diaphragmatic activity was evaluated using diaphragmatic thickening at end-inspiration (TEI), diaphragmatic thickening at end-expiration (TEE), and diaphragmatic thickening fraction (DTF) measured by diaphragmatic US at three time-points; T0, baseline; T1, after DEX sedation; and T2, after DEX recovery. Supplementary oxygen was applied with a simple mask at 5 L/min. Peripheral oxygen saturation (SpO2), end tidal CO2 (EtCO2), and respiratory rate (RR) were recorded.Results: TEI and TEE showed no significant changes during the study period (P = 0.394 and P = 0.205, respectively). DTF was maintained at both T0 and T1 (P = 1.000). At recovery after DEX infusion discontinued, DTF was increased by 3.85%, although such increase was not statistically significant (T0 vs. T2, P = 0.525). SpO2 remained above 99% and EtCO2 remained below 36 mmHg. Desaturation episodes were not observed during the study period.Conclusions: Results of this study showed that DEX sedation did not affect the diaphragmatic movement in situation of decreased RR induced by DEX. This finding implies that DEX-induced sedation does not result in clinically significant respiratory depression.  相似文献   

20.
1. The effects of bilateral cervical vagotomy, of bilateral vagal cooling and of efferent vagal stimulation were studied on rabbits anaesthetized with pentobarbitone sodium. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The changes in lung conductance were consistent with the presence of a tonic efferent vagal discharge in bronchoconstrictor fibres, reflexly damped down by a tonic afferent vagal discharge dilator to the airways, probably the Hering-Breuer inflation reflex.3. Neither vagotomy nor efferent vagal stimulation significantly influenced lung compliance, right atrial pressure or end-tidal CO(2)%; vagal cooling lowered end-tidal CO(2)% in spontaneously breathing rabbits, but did not affect the other variables.4. Efferent vagal stimulation in the rabbit decreased lung conductance with no significant change in lung compliance.5. In the rabbit, vagal efferent activity affects primarily the larger (resistance) air passages with little action on the distal (compliance-influencing) airways.  相似文献   

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