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PubMed1985

Effects of succinylcholine on respiratory and nonrespiratory muscle strength in humans.

Succinylcholine was administered to 10 healthy unanesthetized volunteers to assess its effect on respiratory and nonrespiratory muscle strength and the ventilatory response to CO2. Iso hypercapnia with PETCO2 8-10 mmHg above control was maintained throughout the study, succinylcholine infusion rates were increased from 20 micrograms X kg-1 X min-1 until grip strength (GS) was 20% of control. CO2-stimulated ventilation was 16.1 +/- 1.8 l/min (mean +/- SD), approximately three times control, and remained at that level throughout the study because of nonsignificant decreases in tidal volume and increases in respiratory frequency. Respiratory strength, as measured by maximum inspiratory pressure (IP), maximum expiratory pressure (EP), and forced vital capacity (FVC), was spared relative to GS. When GS = 50% of control, IP = 86 +/- 8% of control, EP = 78 +/- 15%, and FVC = 86 +/- 9%. Wide variation occurred from subject to subject in the succinylcholine versus GS dose-response curve position. However, in all subjects the slope of the dose-response curve was very steep.

Adult↗
PubMed1982

Improvement in ventilatory muscle function with running.

We studied the effects of running on ventilatory muscle strength and endurance in 11 adults enrolled in a physical fitness program. Twelve healthy volunteers were used as a control group. Maximum expiratory pressure (Paomax), maximum voluntary ventilation (MVV), peak inspiratory flow, forced expiratory volume in 1 s, forced vital capacity, and maximum sustainable ventilatory capacity for 15 min (MSVC) were measured at 0, 10, and 20 wk. At the end of the 10-wk program, the subject group demonstrated a significant increase in both MSVC and MVV. At the end of the 20-wk period, the subject group demonstrated a significant increase in expiratory Paomax (14.4%), MVV (13.6%), and MSVC (15.8%). There was no significant change at the end of the 20-wk period in any of the tests in the control group. These data indicate that running can improve ventilatory muscle strength and endurance in healthy, previously sedentary individuals.

Adult↗
PubMed1987

Effects of lung volume on maximal methacholine-induced bronchoconstriction in normal humans.

We examined the effects of lung volume on the bronchoconstriction induced by inhaled aerosolized methacholine (MCh) in seven normal subjects. We constructed dose-response curves to MCh, using measurements of inspiratory pulmonary resistance (RL) during tidal breathing at functional residual capacity (FRC) and after a change in end-expiratory lung volume (EEV) to either FRC -0.5 liter (n = 5) or FRC +0.5 liter (n = 2). Aerosols of MCh were generated using a nebulizer with an output of 0.12 ml/min and administered for 2 min in progressively doubling concentrations from 1 to 256 mg/ml. After MCh, RL rose from a base-line value of 2.1 +/- 0.3 cmH2O. 1-1 X s (mean +/- SE; n = 7) to a maximum of 13.9 +/- 1.8. In five of the seven subjects a plateau response to MCh was obtained at FRC. There was no correlation between the concentration of MCh required to double RL and the maximum value of RL. The dose-response relationship to MCh was markedly altered by changing lung volume. The bronchoconstrictor response was enhanced at FRC - 0.5 liter; RL reached a maximum of 39.0 +/- 4.0 cmH2O X 1-1 X s. Conversely, at FRC + 0.5 liter the maximum value of RL was reduced in both subjects from 8.2 and 16.6 to 6.0 and 7.7 cmH2O X 1-1 X s, respectively. We conclude that lung volume is a major determinant of the bronchoconstrictor response to MCh in normal subjects. We suggest that changes in lung volume act to alter the forces of interdependence between airways and parenchyma that oppose airway smooth muscle contraction.

Adult↗
PubMed2001

Respiratory abdominal muscle recruitment and chest wall motion in myotonic muscular dystrophy.

Abdominal muscles are selectively active in normal subjects during stress and may increase the potential energy for inspiration by reducing the end-expiratory lung volume (EELV). We hypothesized that a similar process would occur in subjects with myotonic muscular dystrophy (MMD), but would be less effective, because of to their weakness and altered chest wall mechanics. Fine-wire electromyography (EMG) of the transversus abdominis (TA), internal oblique (IO), external oblique, and rectus abdominis was recorded in 10 MMD and 10 control subjects. EMG activity, respiratory inductive plethysmography, and gastric pressure were recorded during static pressure measurement and at increasing levels of inspiratory resistance breathing. EELV was reduced and chest wall motion was synchronous only in controls. Although the TA and IO were selectively recruited in both groups, EMG activity of the MMD group was twice that of controls at the same inspiratory pressure. In MMD subjects with mildly reduced forced vital capacity, significant differences can be seen in abdominal muscle recruitment, wall motion, work of breathing, and ventilatory parameters.

Abdomen↗
PubMedDate not supplied

Comparison of pulsatile and nonpulsatile perfusion of the lung in an extracorporeal large animal model.

OBJECTIVE: Extracorporeal lung-perfusion models are widely used to evaluate pulmonary preservation techniques and reperfusion injury. However, these models mainly depend on nonpulsatile flow, which is not physiological and can subsequently lead to pulmonary edema. Observation in a standardized setting and reliability of functional and structural data assessment are therefore limited. To overcome these limitations we developed a new extracorporeal large animal lung perfusion model utilizing pulsatile flow to perfuse the pulmonary vasculature. METHODS: Lungs of juvenile domestic pigs were in situ preserved with 2 liters Perfadex and stored for 3 h at 10 degrees C. Thereafter, reperfusion of the lung was performed in an extracorporeal blood perfusion circuit employing either a modified roller pump with pulsatile module (300 ml/min; pulsation rate 90/min) or a standardized roller pump with continuous flow (30 ml/min). Ventilation was performed with physiologic room air (350 ml; 16/min) for 1 h. Pulsatile and nonpulsatile perfusion was performed in 2 groups (group NP: nonpulsatile; group P: pulsatile flow, n = 7) during reperfusion. Peak inspiratory pressure (PIP), mean pulmonary artery pressure (PAP), and oxygenation capacity (DeltaPO(2)) were continuously measured. For control of the effectiveness of the pulsatile perfusion pressure waveforms were obtained directly from the native pulmonary artery of both groups. Malondialdehyde (MDA) as a parameter for lipid peroxidation and endothelial cell damage was assessed at 10, 30 and 50 min reperfusion. At the end of the study, pulmonary water content was assessed by means of wet-to-dry ratio (W/D ratio). The tissue was further processed for microscopic analysis. RESULTS: PIP increased significantly in both groups during reperfusion. Mean PAP in both groups increased to 60 mm Hg after 20 min followed by a decrease after 60 min to 40 mm Hg. Pressure waveforms of the pulmonary artery showed sufficient pulsatility in the pulmonary vasculature with a systolic/diastolic pressure difference of 15 mm Hg whereas the pressure difference was 3-5 mm Hg in the nonpulsatile group. DeltaPO(2) was stable in groups NP and P during reperfusion (30 min: NP: 66.4 (62.2-88) mm Hg; P: 74.8 (65-81.7) mm Hg) without any statistically significant differences between the groups. MDA in group NP decreased over the reperfusion period from 6.2 (3.3-6.3) microM at 10 min to 5.2 (3.2-6.1) microM at 50 min, whereas in group P the level increased and was significantly higher after 50 min reperfusion compared to group NP [6.6 (6.1-9.2) microM at 50 min; p = 0.016]. W/D ratio was 6.7 (6.3-7.0) in group NP and 6.8 (6.3-7.6) in group P. Light microscopy evaluation showed no differences between both groups regarding severity of intra-alveolar and interstitial edema and numbers of intra-alveolar, intracapillary and interstitial granulocytes. CONCLUSION: Although effective pulsatile perfusion of the pulmonary vasculature was achieved by means of a modified roller pump, this measure obviously did not improve functional parameters nor did it significantly reduce the edema formation after 3 h ischemia in this extracorporeal lung perfusion model. The use of pulsatile perfusion is therefore not mandatory in the extracorporeal setting of a large animal lung perfusion model.

Animals↗
PubMed2006

Angiotensin II blockers in obstructive pulmonary disease: a randomised controlled trial.

In chronic obstructive pulmonary disease (COPD), the sympathetic nervous system, as well as the renin-angiotensin system, is activated with possible negative systemic effects on skeletal muscles. Angiotensin II type-1 receptor blockers inhibit the sympathetic and renin-angiotensin systems and might improve skeletal and respiratory muscle strength in patients in whom these systems are activated. The effects of the angiotensin receptor blocker irbesartan given over 4 months was evaluated in 60 patients with COPD and a forced expiratory volume in one second of <50% of the predicted value and without obvious cardiovascular disease that would necessitate the administration of an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Irbesartan was well tolerated, but did not exert a significant effect on the primary end-point maximum inspiratory pressure. Spirometric results were not affected, but total lung capacity was reduced. Irbesartan led to a significant decrease in haematocrit (46.4+/-3.6 to 43.9+/-4.3% versus 47.5+/-2.4 to 48.7+/-3.0% with placebo). In conclusion, respiratory muscle strength in chronic obstructive pulmonary disease patients was not influenced by angiotensin II receptor blockade. However, the changes in haematocrit and total lung capacity following irbesartan raise the possibility that well-known cardiovascular drugs can produce unanticipated beneficial effects in chronic obstructive pulmonary disease patients.

Angiotensin II Type 1 Receptor Blockers↗
PubMed1976

[Functional diagnosis of laryngeal and tracheal stenoses].

In 20 patients with upper airway obstruction in the region of the larynx and the extrathoracic and intrathoracic trachea, inspiratory and expiratory resistance, FIV1, FEV1 and total and vital capacity were determined. In patients with obstruction in the larynx and the extrathoracic trachea FIV1 is generally below FEV1. So-called "dynamic" obstruction, depending on flow and direction of flow, leads to a considerable descrepancy between FIV1 and FEV1. Impairment of respiration can be assummed if, in the adult, airway resistance during spontaneous breathing is higher than 6 cm H2O/l/sec during inspiration and/or expiration. After successful surgical correction airway resistance and FIV1 and FEV1 are restored to normal values.

Adolescent↗
PubMed1992

Respiratory function during wakefulness and sleep among survivors of respiratory and non-respiratory poliomyelitis.

The purpose of this study was to determine whether there is a difference in respiratory mechanics and gas exchange between polio survivors and healthy, age-matched controls during wakefulness and sleep. Polio survivors were divided into four groups. The first group included those who had evidence of respiratory muscle involvement originally (PRM) and the second group included those who had bulbar muscle involvement originally (PBM). The third and fourth groups had only limb involvement originally but were separated by absence (PSL) or presence of a scoliosis (PSS) at the time of their evaluation. Each subject completed baseline and one year follow-up measurements of lung volumes, diffusion, flow rates, respiratory muscle strength, central and peripheral chemoreflexes and arterial blood gases. Sleep measurements included a full respiratory polysomnographic study. Fifty polio survivors and 13 controls completed the study. The PRM and PSS groups had an elevated arterial carbon dioxide tension (PaCO2) (mean +/- SE 6.0 +/- 0.4 and 6.0 +/- 0.3 kPa, respectively), reduced vital capacity (2.8 +/- 0.3 and 2.9 +/- 0.3 l, respectively), reduced maximal inspiratory pressure (-5.9 +/- 0.7 and -5.4 +/- 0.8 kPa, respectively) and reduced maximal expiratory pressure (9.8 +/- 1.1 and 9.1 +/- 1.2 kPa, respectively), when compared with non-polio controls. During sleep PRM and PSS groups experienced a higher PaCO2 (6.5 +/- 0.5 and 6.7 +/- 0.4 kPa, respectively) and a lower arterial oxygen saturation (SaO2) (89 +/- 4 and 86 +/- 3%, respectively). There were no differences among groups for diffusion, flow rates and chemoreflexes. All other polio survivors showed essentially normal respiratory function.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1978

The effects of cardiopulmonary bypass upon pulmonary gas exchange.

Cardiac output, venous admixture, physiological dead space, blood gas tensions, inspired gas distribution, and other respiratory variables were measured in 10 patients breathing both air and oxygen before and on five occasions up to 10 days after coronary artery vein-graft operations under cardiopulmonary bypass with moderate hypothermia. Cardiac output was unchanged at 8 hours but fell 8 percent by 22 hours. Thereafter it progressively increased and at 10 days was higher than before the operation. Venous admixture rose to a maximum at 28 to 48 hours, postoperatively, but the increase was inversely related to the magnitude of preoperative admixture. The part played by airway and alveolar closure in determining venous admixture is discussed. While admixture increased, the nitrogen-clearance curve improved, presumably due to progressive "dropout" of the worst-ventilated regions. Physiological dead space fell to a minimum at 28 hours after operation; this was attributed to a fall in the end-inspiratory position consequent upon a reduction in both functional residual capacity and tidal volume. There was an increase in ventilation after operation, and this persisted at 10 days; it appeared to be due to reflex stimulation from the lungs and chest wall.

Adolescent↗
PubMed2001

[Functional respiratory evaluation in patients with high traumatic spinal injury].

The restrictive defect was quantified (Forced vital capacity, FVC) and their postural dependence and the respiratory muscle weakness (Maximal inspiratory and expiratory pressures, MIP and MEP) in 29 patients (12 to 46 years) with spinal injury from cervical (C) 4 to thoracic (T) 7 (30 days to 48 months post injury period). The FVC in C (seated) was 2200 +/- 560 ml (47.2%), and in T was 2940 +/- 750 ml (66.6%), p < 0.008. The postural dependence of the FVC was higher in C with an increase of 25% and only of 10% in the T (p < 0.03). This postural dependence was a function of the FVC according to the regression equation: FVC % (supine) = 24.73+ 0.7341* FVC % seated (r 0.8771, p < 0.001). The MIP in C was 61.59 (53.82%) +/- 17.26 cm H2O and in T was 87.25 (77.85%) +/- 24.27 cmH2O (p < 0.05). The MEP in C was 48.53 (24.97%) +/- 18.09 cm H2O, and in T was 58.75 (30.74%) +/- 27.67 cmH2O (p NS). No correlation was found between FVC and maximal statics respiratory pressures. In conclusion, the C showed more significant restrictive defect and a great postural dependence of the FVC. In both, the expiratory muscle weakness was more severe than the inspiratory group. Inspiratory muscle weakness was higher in C.

Adolescent↗
PubMed1976

Respiratory volume-time relationships during resistive loading in the cat.

The first-breath (neural) effects of graded resistive loads added separately during inspiration and expiration was studied in seven anesthetized cats before and after bilateral vagotomy. Additions of airflow resistance during inspiration reduced the volume inspired (VI) and increased inspiratory duration (TI). The duration of the ensuing unloaded expiration (TE) was unchanged. Vagotomy eliminated the TI modulation with inspiratory loads. Tracheal occlusion at the onset of inspiration yielded TI values similar to the fixed values observed following vagotomy. Resistive loads added during expiration produced similar results. Expired volume (VE) decreased and (TE) increased approaching the values obtained after vagotomy. Unlike the inspiratory resistive loads, loading during expiration results in an upward shift in the functional residual capacity (FRC). The FRC shift produces a time lag between the onset of diaphragmatic (EMG) activity and the initiation of airflow of the next (unloaded) inspiration. These studies suggest separate volume-time relationships for the inspiratory and expiratory phases of the breathing cycle. Both relationships are dependent upon vagally mediated volume feedback.

Airway Resistance↗
PubMed1996

Respiratory muscle testing.

When addressing the question of whether or not the respiratory muscles are weak, and quantifying exactly how severe any weakness might be, it is sensible to regard the tests available as complimentary, and to proceed by using simple tests first and invasive tests only when appropriate. This sequential and complimentary approach is illustrated in table 1. Thus, if the supine vital capacity is normal, it is very unlikely that there is clinically significant respiratory muscle weakness. However, if the vital capacity is low, it may then be appropriate to measure the maximal inspiratory and maximal expiratory pressures. If the mouth pressures are normal, weakness has been excluded, but if the pressures are low it will then be necessary to proceed to the next tests on the list. Thus, the process continues and, when all of the tests have been performed, a comprehensive description can be achieved of any respiratory muscle weakness that is present. We now have the capacity, if we so wish, to measure respiratory muscle weakness accurately. The challenge is to use these techniques to demonstrate the undoubted importance of respiratory muscle weakness in a wide variety of clinical circumstances.

Humans↗
PubMed1994

Prospective evaluation of epidural versus intrapleural catheters for analgesia in chest wall trauma.

Severe blunt chest trauma can produce multiple rib fractures, flail segments, and pulmonary contusions. All of these injuries produce pain and diminished pulmonary function. The effectiveness of intrapleural and epidural administration of bupivacaine was prospectively evaluated in 19 patients with severe chest trauma. Pain relief and pulmonary function were evaluated for 72 hours after catheter placement. Epidural administration of bupivacaine significantly reduced pain at rest and with motion compared with the intrapleural route (p < 0.05). Parenteral narcotic use was also significantly less in the epidural group (p < 0.05). Negative inspiratory pressure and tidal volume were significantly increased with epidural anesthesia (p < 0.05). Vital capacity, FIO2, minute ventilation, and respiratory rate were not affected. Mild hypotension was a common complication with epidural catheters. We conclude that continuous epidural analgesia is superior to intrapleural block and significantly improves tidal volume and negative inspiratory pressure.

Adult↗
PubMed2000

Specific inspiratory muscle training in well-trained endurance athletes.

PURPOSE: It has been reported that arterial O2 desaturation occurs during maximal aerobic exercise in elite endurance athletes and that it might be associated with respiratory muscle fatigue and relative hypoventilation. We hypothesized that specific inspiratory muscle training (SIMT) will result in improvement in respiratory muscle function and thereupon in aerobic capacity in well-trained endurance athletes. METHODS: Twenty well-trained endurance athletes volunteered to the study and were randomized into two groups: 10 athletes comprised the training group and received SIMT, and 10 athletes were assigned to a control group and received sham training. Inspiratory training was performed using a threshold inspiratory muscle trainer, for 0.5 h x d(-1) six times a week for 10 wk. Subjects in the control group received sham training with the same device, but with no resistance. RESULTS: Inspiratory muscle strength (PImax) increased significantly from 142.2 +/- 24.8 to 177.2 +/- 32.9 cm H2O (P < 0.005) in the training but remained unchanged in the control group. Inspiratory muscle endurance (PmPeak) also increased significantly, from 121.6 +/- 13.7 to 154.4 +/- 22.1 cm H2O (P < 0.005), in the training group, but not in the control group. The improvement in the inspiratory muscle performance in the training group was not associated with improvement in peak VEmax, VO2max breathing reserve (BR). or arterial O2 saturation (%SaO2), measured during or at the peak of the exercise test. CONCLUSIONS: It may be concluded that 10 wk of SIMT can increase the inspiratory muscle performance in well-trained athletes. However, this increase was not associated with improvement in aerobic capacity, as determined by VO2max, or in arterial O2 desaturation during maximal graded exercise challenge. The significance of such results is uncertain and further studies are needed to elucidate the role of respiratory muscle training in the improvement of aerobic-type exercise capacity.

Adolescent↗
PubMed1983

Effect of analgesia on respiratory muscle function after upper abdominal surgery.

The effects of three methods of analgesia (intravenous morphine, epidural lidocaine and epidural morphine) on vital capacity (VC), forced expiratory volume in 1 s (FEV1) and maximal expiratory and inspiratory pressures (MEP and MIP) at the mouth were studied in 12 high respiratory risk patients following upper abdominal surgery. VC, FEV1, MEP and MIP markedly decreased following laparotomy. VC and FEV1, were partially restored by epidural analgesia and remained unchanged following intravenous morphine. MEP and MIP remained unchanged after each of the three methods of analgesia. This suggests the existence of a non-analgesic dependent dysfunction of inspiratory and expiratory muscles following upper abdominal surgery.

Aged↗
PubMed1995

Efficacy of tracheal and bronchial stent placement on respiratory functional tests.

Stent placement is the only available treatment in patients presenting either a localized external compression or a malacia of the tracheobronchial tree. To assess the functional benefit of prosthesis insertion in these indications, we compared functional respiratory values before, immediately after (48 h), and at sometime after (mean, 10.1 months) operation in 24 patients presenting with a bronchial lesion (B group, n = 5) or a lesion of the intrathoracic part (ITT group, n = 9) or of the extrathoracic part of the trachea (ETT group, n = 10). Before treatment, airflow was severely impaired in most patients without significant differences among the groups. After prosthesis insertion, airflow parameters increased [change in forced expiratory volume in 1 s (delta FEV1 = 440 mL; delta peak expiratory flow (PEF) = 0.92 L.s-1; delta maximum expiratory flow 25/75 (delta MEF25/75) = 0.47 L.s-1; and delta forced inspiratory volume in 1 s (delta FIV1 = 310 mL)] and airway resistances (Raws) decreased (delta Raw = -0.43 kPa.s-1.s-1) without any significant variation in either forced vital capacity (FVC) or total lung capacity. Airflow improvement was more apparent in ITT and ETT groups than in the B group. Moreover, inspiratory flow increase and decrease of FEV1/PEF ratio were only observed in the ETT group. This airflow improvement was maintained for a long time after and was associated with a good clinical tolerance. This study supports the clinical and functional benefits of prosthesis placement both in benign and malignant airway compressions for palliative treatment.

Adult↗
PubMed1998

Exercise training in chronic hypoxia has no effect on ventilatory muscle function in humans.

At the highest altitude, aerobic work is limited by environmental oxygen availability. We therefore reasoned that the hyperpnea associated with endurance training at altitude should provide a strong stimulus for adaptation of the ventilatory muscles. We measured peak inspiratory muscle pressure-flow characteristics (inspiring through graded resistors) and maximum sustainable ventilation capacity in ten permanent residents of La Paz, Bolivia (3600 m) prior to and immediately following 6 weeks of incremental endurance training. Additionally, eight local residents did no training and functioned as controls for the capacity test. While V(O2)max measured in hypoxia increased by 19% (Favier et al., 1995b. J. Appl Physiol. 78, 2286-2293.), none of the tested ventilatory variables showed significant changes. The values for the group mean slopes of maximum inspiratory pressure-flow pairs (- 10.5 vs. - 9.8 cm H2O x sec x L(-1), P=0.301; before versus after training, respectively), maximum inspiratory pressure (112.1+/-8.9 vs. 106.9+/-8.6 cmH2O, P=0.163), peak inspiratory flow (9.8+/-0.41 vs. 10.2+/-0.55 L x sec(-1) P=0.172) and the maximum volitional volume in 12 sec (43.9+/-2.4 vs. 45.6+/-2.4 L in 12 sec, P=0.133) were unchanged with exercise training. Likewise, maximal sustainable minute volume was not different between post-training and control subjects (177.4+/-7.9 vs. 165.4+/-8.4 L x min(-1), P=0.141). These data support the concept that endurance training fails to elicit functional adaptations in ventilatory muscles in humans, even when exercise is done in hypoxia.

Acclimatization↗
PubMed1991

Thoracic gas volume at functional residual capacity measured with an integrated-flow plethysmograph in infants and young children.

Thoracic gas volume (TGV) was measured with an integrated flow plethysmograph in 15 infants aged 2-34 months. End-expiratory (TGVe) and end-inspiratory (TGVi) airway occlusions were compared, after correction of TGV for the occluded volume above functional residual capacity (FRC). The relationship between pressure at the airway opening (Pao) and volume displaced from the box during airway occlusion (Vg) was studied numerically by: 1) an algorithm including a correction for the drift of Vg and linear regression analysis (LR); and 2) Fourier analysis of the signals (FFT). TGVe was significantly higher than TGVi (256 vs 237 ml, 20.4 (square root of residual variance; p less than 0.002). The correlation coefficient of the Pao-Vg relationship was slightly but significantly higher for TGVi than for TGVe: 0.9968 (0.9937-0.9995) vs 0.9947 (0.9840-0.9990) (means and range). No difference was observed between LR and FFT, although the intra-individual coefficient of variation was lower for LR than FFT: 5.2% (1.6-11.3) vs 7.9% (1.9-21.0) (means and range). Model simulations suggested that the difference between TGVe and TGVi could be mainly attributed to gas compression in the instrumental deadspace and upper airway wall motion and/or to uneven distribution of alveolar and pleural pressure associated with chest wall distortion.

Airway Resistance↗