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J D Road

Publications and source records attributed to J D Road.

At least 19 recordsLinked to original sources

Some effects of vagal blockade on abdominal muscle activation and shortening in awake dogs.

1. The mechanisms of abdominal muscle activation are thought to be different during expiratory threshold loading (ETL) compared with hypercapnia. Our objectives in the present study were to determine the effects of removing excitatory vagal feedback on abdominal muscle activation, shortening and pattern of recruitment during ETL and hypercapnia. Six tracheotomized dogs were chronically implanted with sonomicrometer transducers and fine wire EMG electrodes in each of the four abdominal muscles. Muscle length changes and EMG activity were studied in the awake dog during ETL (6 dogs) and CO2 rebreathing (3 dogs), before and after vagal blockade. 2. Following vagal blockade, the change in volume (increase in functional residual capacity, FRC) during ETL was greater and active phasic shortening of all the abdominal muscles was reduced, when shortening was compared with a similar change in lung volume. Similarly, at comparable minute ventilation, abdominal muscle active shortening was also reduced during hypercapnia. The internal muscle layer was recruited preferentially in both control and vagally blocked dogs during both ETL and hypercapnia. 3. The degree of recruitment of the abdominal muscles during ETL and hypercapnia in awake dogs is influenced by vagal feedback, but less so than in anaesthetized dogs. These results illustrate the importance of the vagi and abdominal muscle activation in load compensation. However, vagal reflexes are apparently not contributing to the preferential recruitment of the internal muscle layer. In awake dogs during vagal blockade abdominal muscle recruitment still occurs by extravagal mechanisms.

Abdominal Muscles

The effect of anesthesia on abdominal muscle resting length and shortening in awake dogs.

The objectives of this study were to examine the effects of anesthesia and implantation of sonomicrometer transducers on tonic and phasic expiratory activity of the abdominal muscles. Eight tracheotomized dogs were chronically instrumented with sonomicrometer transducers placed in each of the four abdominal muscles. The dogs were studied in the lateral decubitus position immediately after transducer implantation, while under halothane anesthesia, and then in the awake dogs 2 to 3 days postimplantation, and repeatedly over a 2- to 8-week period. The resting length (LRL) of the rectus abdominis (RA) was reduced in the first awake study compared to during anesthesia, but there was no change in LRL of the other abdominal muscles. The abdominal muscles phasically, actively, shortened during expiration more in the awake state than in the anesthetized state. The internal abdominal muscle layer (transversus abdominis and internal oblique) shortened phasically more than the external layer (RA and external oblique). Neither the LRL nor the amount of phasic shortening of the abdominal muscles changed significantly over the period in which transducers were in situ (2-8 weeks). Muscle sections excised at the end of each study exhibited small capsules of fibrosis immediately surrounding the transducers with normal muscle tissue between pairs of transducers. In conclusion, both tonic and phasic respiratory activity of the abdominal muscles, reflected by changes in resting length and the amount of active shortening, respectively, were absent during halothane anaesthesia and chronic implantation of sonomicrometer transducers per se had no effect.

Abdominal Muscles

Diaphragm and phrenic nerve activities during inspiratory loading in anesthetized rabbits.

To determine whether decreases in neural activation and/or neuromuscular transmission to the diaphragm contribute to ventilatory failure observed during inspiratory resistive loaded breathing, peak integrated activity of the intact phrenic nerve (ENGdi) and costal diaphragm (EMGdi), transdiaphragmatic pressure swings (Pdi) and evoked diaphragm compound action potentials (M-wave) were measured in anesthetized rabbits subjected to inspiratory resistive loads of varying intensities and duration breathing supplemental oxygen. Sustainable loads were studied for 4 h. Severe loads were applied in increments and studied for 50 min each. Loading resulted in parallel increases in ENGdi, EMGdi and Pdi that stabilized within 20 min. With severe loading, peak inspiratory pressure (Pao = -55 +/- 4 cm H2O) was maintained for 30 min after which there was a significant drop in inspiratory pressure (task failure). Despite hypoventilation and profound changes in blood gases, both activation (ENGdi) and neuromuscular transmission (ENGdi/EMGdi ratio or M-wave) were maintained throughout all loads even at task failure when a critical level of PaO2 (27 +/- 1 mm Hg) was reached. We conclude that neural activation and neuromuscular transmission to the diaphragm do not fail during inspiratory resistive breathing and discuss our findings in terms of current concepts of diaphragm fatigue and control of breathing in this model.

Anesthesia

Stability of evoked parasternal intercostal muscle electromyogram at increased end-expiratory lung volume.

The diaphragmatic electromyogram has been measured as an index of the level of diaphragmatic activation. The diaphragmatic electromyogram, however, even when measured by intramuscular electrodes, can be artifactually altered by a change in lung volume (A. Brancatisano, S. M. Kelly, A. Tully, S. H. Loring, and L. A. Engel. J. Appl. Physiol. 66: 1699-1705, 1989) or by a change in body position. The parasternal intercostal muscle may be less subject to the mechanisms that are believed to produce this artifactual change. We asked whether the parasternal intercostal electromyographic activity could be reliable when lung volume changes. Six supine rabbits were anesthetized with ketamine and xylazine. Fine bipolar copper wires, with their tips exposed, were inserted into the left parasternal intercostal muscle in the third interspace. A stimulus that was three times maximal was applied to the corresponding intercostal nerve, and the resulting action potential (AP) was photographed. Parasternal intercostal muscle length was measured by sonomicrometry over the vital capacity range. There were small nonsignificant changes in the AP from functional residual capacity (FRC) to total lung capacity. From FRC to residual volume there was variation in the AP. The AP was also quite stable when regional conductivity was altered but showed variation when the parasternal intercostal muscle length change was accentuated by traction on the rib cage. We conclude that the parasternal intercostal electromyographic activity can be reliably used to measure inspiratory motoneuron output to it over the range of lung volumes from FRC to total lung capacity.

Animals

Ventilatory muscle strength and endurance in myasthenia gravis.

Patients with generalized myasthenia gravis (MG) often have associated ventilatory muscle involvement. It is not known whether patients with isolated ocular muscle involvement have identifiable involvement of their ventilatory muscles. Most studies have assessed muscle involvement by measuring muscle strength; however, we hypothesized that measures of ventilatory muscle endurance may be more sensitive tests of ventilatory muscle involvement in myasthenia gravis. We studied 17 patients with myasthenia gravis (four with ocular involvement alone and 13 with varying degrees of generalized myasthenia gravis). Spirometry, ventilatory muscle strength (maximum inspiratory and expiratory pressures (MIP and MEP)) and endurance (2 min incremental threshold loading test) were measured before and 20 min after i.m. neostigmine. We compared the results with those of 10 normal controls. We found no difference between patients with isolated ocular involvement and controls. Ocular myasthenia gravis patients did not improve after neostigmine. The patients with generalized myasthenia gravis had reduced baseline ventilatory muscle strength (MIP 67 cmH2O (70% of predicted), MEP 86 cmH2O (50% of pred) and endurance (mean maximal load achieved = 246 g, mean pressure at highest load (P) = 19.4 cmH2O) compared with controls. After neostigmine, there was a significant increase in MIP in patients with generalized myasthenia gravis and a trend towards an increased MEP. As a group, the patients with generalized myasthenia gravis did not demonstrate a change in their ventilatory muscle endurance after neostigmine; however, there was considerable interpatient variability in response. We conclude that patients with isolated ocular MG have normal ventilatory muscle strength when tested conventionally.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Decrease in left ventricular contractility after tumor necrosis factor-alpha infusion in dogs.

Whether systolic contractility or diastolic compliance changes soon after tumor necrosis factor-alpha (TNF-alpha) exposure is not known. Accordingly, we measured hemodynamics, left ventricular contractility using the slope of the end-systolic pressure-volume relationship, and diastolic pressure-volume relationships in six control dogs and in six dogs receiving 60 micrograms.kg-1.h-1 i.v. of TNF-alpha. Mean aortic pressure decreased by 22% 1 h after TNF-alpha infusion and remained decreased (P < 0.05). Cardiac output increased by 19% 1 h after TNF-alpha infusion and remained significantly greater than control values (P < 0.05). Left ventricular contractility decreased by 23% (P < 0.05) 1 h after TNF-alpha infusion and decreased by 52% (P < 0.01) 5 h after TNF-alpha infusion. The diastolic pressure-volume relationship did not change in the TNF-alpha group or the control group. Ejection fraction did not change after TNF-alpha infusion despite the decrease in contractility because afterload decreased. We conclude that TNF-alpha is important in causing the hypotensive, hyperdynamic circulation of sepsis. The new finding that left ventricular contractility is decreased shortly after TNF-alpha infusion suggests that TNF-alpha, or another mediator released very soon after TNF-alpha, is an important myocardial depressant factor.

Animals

Abdominal muscle activity during hypercapnia in awake dogs.

We previously found the internal abdominal muscle layer to be preferentially recruited during expiratory threshold loading in anesthetized and awake dogs. Expiratory threshold loading increases end-expiratory lung volume and hence can activate reflex pathways such as tonic vagal reflexes, which could influence abdominal muscle recruitment. Our objectives in the present study were to determine the effects of hypercapnia on abdominal muscle activation and the pattern of recruitment in awake dogs. Five tracheotomized dogs were chronically implanted with sonomicrometer transducers and fine-wire electromyogram (EMG) electrodes in each of the four abdominal muscles: transversus abdominis, internal oblique, external oblique, and rectus abdominis. Muscle length changes and EMG activity were studied in the awake dog at rest and during CO2 rebreathing. CO2 rebreathing produced a tripling of tidal volume and activation of the abdominal muscles. Despite the increase in tidal volume, there was no significant change in abdominal muscle end-inspiratory length. Both tonic and phasic expiratory shortening were greater in the internal muscle layer (transversus abdominis and internal oblique) than in the external muscle layer (external oblique and rectus abdominis). We conclude that the internal abdominal muscles are preferentially recruited by hypercapnia and vagal reflexes probably do not contribute to this differential recruitment but that segmental reflexes may be involved. The mechanical consequences of this recruitment are discussed.

Abdominal Muscles

Regional diaphragm shortening measured by sonomicrometry.

Diaphragmatic shortening measured by sonomicrometry has been compared in the two major anatomic segments, costal and crural. Data obtained by videofluoroscopy found a variation in subsegmental shortening within segments (Sprung et al. J. Appl. Physiol. 67: 655-662, 1989). No reproducible pattern of subsegmental shortening has emerged, and the mechanisms leading to this subsegmental variation in shortening are unknown. Therefore, we compared subsegmental shortening in both segments of the diaphragm in seven supine pentobarbital-anesthetized dogs. Seven pairs of sonomicrometer transducers were implanted in the two segments, and subsegmental shortening during spontaneous breathing was measured. To determine potential mechanisms contributing to the variation in shortening, measurements were made during stimulated breathing, after epiphrenic stimulation, and during occluded breaths. We found electrical stimulation at physiological frequencies of 10 and 20 Hz reduced the variation in subsegmental shortening, whereas stimulated breathing did not. Occluded breaths showed a consistent decrease in the amount of shortening, particularly in the dome of the costal diaphragm, compared with shortening in the area of apposition. Comparison of shortening between segments revealed greater crural than costal shortening. We conclude that subsegmental variation in activation can contribute to variation in subsegmental shortening and that the afterload can effect shortening during occluded breaths.

Animals

Abdominal muscle activation by expiratory threshold loading in awake dogs.

Abdominal muscle activation produced by expiratory threshold loading (ETL) helps prevent an increase in FRC thus, optimizing diaphragm length and defending VT. However, anesthesia may affect abdominal muscle activation, and the pattern of recruitment and level of activation of individual abdominal muscles may well be dependent on body position. Therefore, individual abdominal muscle response to ETL was assessed in awake dogs, lying in the lateral decubitus position. Eight, tracheotomized dogs were chronically instrumented with sonomicrometer transducers and bipolar, fine wire EMG electrodes, in each of the four abdominal muscles. ETL produced increases in active, expiratory shortening of the transversus abdominis (TA), internal oblique (IO) and external oblique (EO). In addition, tonic activity, assessed from a decrease in baseline length, increased in the IO. There was a significant increase in FRC during ETL but it was less than would be expected without tonic and phasic abdominal muscle activation. Although FRC increased, VT and breathing frequency were maintained. As was found previously in supine, anesthetized dogs, the internal abdominal muscle layer (TA and IO) was recruited preferentially; substantiating its greater role in the defence of lung volume.

Abdominal Muscles

Delayed poststimulus decrease of phrenic motoneuron output produced by phrenic nerve afferent stimulation.

The immediate effects of phrenic afferent nerve activation on ventilation have been shown to be both excitatory and inhibitory. Long-lasting inhibitory effects on respiratory motoneuron output have been reported after stimulation of afferent nerves from limb muscles. However, whether respiratory muscle afferent nerves can produce this effect is unknown. We therefore hypothesized that activation of phrenic afferent nerves may produce a prolonged decrease of respiratory motoneuron output. Six alpha-chloralose-anesthetized dogs were studied after vagotomy and bilateral carotid sinus nerve section. The dogs were paralyzed, and end-tidal CO2 was controlled by mechanical ventilation. The proximal end of the cut thoracic phrenic nerve was electrically stimulated for 1 min at intensities that produced activation of thin-fiber afferents. The contralateral efferent phrenic integrated electroneurogram (ENG) was recorded. During stimulation, phrenic ENG activity increased. ENG activity was recorded during recovery and reached a peak decrease compared with control of 19 +/- 11% (SD) 9.0 +/- 6 min after stimulation and returned to control after 30 min. A qualitatively similar response was seen after stimulation of the gastrocnemius nerve. We conclude that activation of thin-fiber afferents in the phrenic nerve can produce a delayed and prolonged decrease of respiratory motoneuron output similar to that of limb muscle afferent nerves.

Anesthesia

Effects of posture on abdominal muscle shortening in awake dogs.

The objective of this study was to examine the effects of posture on tonic and phasic expiratory activity of the abdominal muscles in awake dogs. Six tracheostomized dogs were chronically instrumented with sonomicrometer transducers and bipolar electromyographic electrodes placed in each of the four abdominal muscles. To determine the effects of posture on tonic and phasic activity of individual abdominal muscles, muscle resting length (Lr) and tidal length changes (%Lr), respectively, were measured in awake dogs in the left lateral decubitus (LLD), sitting, and standing (STAND) positions. The transversus abdominis Lr consistently shortened when the dog was moved from LLD to STAND and lengthened when the dog was moved from LLD to the sitting position, and the external oblique Lr consistently lengthened when the dog went from LLD to STAND. The internal oblique and rectus abdominis had no consistent changes in Lr with a change in position. All four abdominal muscles actively shortened (%Lr) more in the upright positions. In addition, the internal layer (transversus abdominis and internal oblique) actively shortened more than the external layer (rectus abdominis and external oblique). In conclusion, both tonic and phasic respiratory activity of the abdominal muscles, reflected by changes in Lr and %Lr, respectively, were affected by changes in posture.

Abdominal Muscles

Energy balance in stable malnourished patients with chronic obstructive pulmonary disease.

We have measured caloric intake, energy expenditure, and the thermogenic effect of food in ten patients with stable COPD who had a history of involuntary weight loss over several years and were malnourished (< 85 percent ideal body weight). Each patient completed a 7-day food record. Indirect calorimetry was performed in the resting postabsorptive state. After placement of a nasoenteric tube, patients were randomly assigned to be refed or sham-fed (mean +/- SD, 16 +/- 3 days), following which, metabolic measurements were repeated. Indirect calorimetry was also performed before and after a large meal in each patient. Home caloric intake was 135 +/- 23 percent of resting energy expenditure. Resting energy expenditure was 94 +/- 16 percent of that predicted by the Harris-Benedict equation and did not change significantly during inpatient refeeding. Refeeding resulted in weight gain (2.4 +/- 1.9 kg, p < 0.02). A large meal caused substantial increases in energy expenditure (24 +/- 18 percent), carbon dioxide production (39 +/- 18 percent), and oxygen consumption (23 +/- 16 percent). We conclude that stable malnourished COPD patients consume adequate calories to meet average energy requirements and are not hypermetabolic. Inpatient refeeding by nocturnal nasoenteric infusion is well tolerated and results in weight gain, but the thermogenic effect of a large meal poses a considerable metabolic and ventilatory load that could precipitate acute respiratory failure.

Aged

Expiratory muscle activity in the awake and sleeping human during lung inflation and hypercapnia.

Expiratory muscle activity has been shown to occur in awake humans during lung inflation; however, whether this activity is dependent on consciousness is unclear. Therefore we measured abdominal muscle electromyograms (intramuscular electrodes) in 13 subjects studied in the supine position during wakefulness and non-rapid-eye-movement sleep. Lung inflation was produced by nasal continuous positive airway pressure (CPAP). CPAP at 10-15 cmH2O produced phasic expiratory activity in two subjects during wakefulness but produced no activity in any subject during sleep. During sleep, CPAP to 15 cmH2O increased lung volume by 1,260 +/- 215 (SE) ml, but there was no change in minute ventilation. The ventilatory threshold at which phasic abdominal muscle activity was first recorded during hypercapnia was 10.3 +/- 1.1 l/min while awake and 13.8 +/- 1 l/min while asleep (P less than 0.05). Higher lung volumes reduced the threshold for abdominal muscle recruitment during hypercapnia. We conclude that lung inflation alone over the range that we studied does not alter ventilation or produce recruitment of the abdominal muscles in sleeping humans. The internal oblique and transversus abdominis are activated at a lower ventilatory threshold during hypercapnia, and this activation is influenced by state and lung volume.

Abdominal Muscles

Effect of vagal stimulation and parenteral acetylcholine on canine trachealis muscle shortening.

Canine trachealis smooth muscle shortening (TMS) in response to vagal nerve stimulation is approximately 30%, far less than the 70% predicted from in vitro studies. We hypothesized that in vivo airway smooth muscle activation during vagal stimulation may be submaximal, and in this study we wished to determine TMS during maximal activation. TMS was studied in 12 alpha-chloralose-anesthetized dogs during vagal stimulation, systemic acetylcholine injection, and local acetylcholine injection. Bilateral vagal stimulation produced TMS of 26 +/- 5% (SE) length at functional residual capacity (LFRC). Maximal TMS during systemic injection of acetylcholine was 28 +/- 12% LFRC but may have been limited by delivery of acetylcholine to the muscle because asystole occurred at higher concentrations. TMS was greatest during local injection of acetylcholine (48 +/- 7% LFRC). There was a greater increase in pulmonary resistance and decrease in dynamic compliance during systemic acetylcholine injection than during vagal stimulation. We conclude that bilateral vagal nerve stimulation does not maximally activate trachealis smooth muscle but that the maximal shortening achieved with local injection of acetylcholine is still less than isotonic shortening in vitro. These data suggest that maximal shortening in vivo is limited by the afterload provided by the tracheal cartilaginous rings.

Acetylcholine

Ventilatory dysfunction in severe anorexia nervosa.

A 25-year-old woman suffering from chronic anorexia nervosa lost more than 50 percent of her body weight and presented with generalized muscle weakness. Pulmonary function tests showed a severe restrictive defect, and she had marked impairment of respiratory muscle strength and endurance, peripheral muscle function, and hypercapnic ventilatory responses, all of which improved following refeeding. The interaction and response to treatment of these effects on respiratory function are discussed.

Adult

The effect of salbutamol on performance in elite nonasthmatic athletes.

The effect of salbutamol on performance was studied in seven male nonasthmatic highly trained (VO2max > or = 60 ml.kg-1 x min-1) cyclists. Salbutamol (S = 2 puffs = 200 micrograms) or placebo (P) was administered by metered-dose inhaler, through a spacer device, 20 min prior to testing in a double-blind, randomized cross-over design. Testing sessions on a cycle ergometer included the measurement of maximal oxygen uptake (VO2max), peak power, maximal heart rate, and pulmonary function. A timed sprint to exhaustion was performed after 45 min of exercise at 70% of VO2max, and a Wingate anaerobic test was used to measure total work and peak power. There was a nonsignificant decrease in VO2max (P = 63.5 +/- 3.2; S = 62.6 +/- 3.3 ml.kg-1 x min-1). No difference was found in peak power, maximum heart rate, endurance sprint time, Wingate peak power, or total work. After an anticipated baseline increase was taken into account, the pattern of change in FEV1 over time did not differ between salbutamol and placebo. It was concluded that a therapeutic dose of aerosol salbutamol does not have an ergogenic effect in elite nonasthmatic athletes, and it is therefore recommended that inhaled salbutamol continue to be permitted in international competition for individuals with exercise induced bronchospasm.

Albuterol

Effect of lung inflation and upright posture on diaphragmatic shortening in dogs.

In an earlier study (Road and Leevers (1988), J. Appl. Physiol. 65: 2283-2389), the application of continuous positive airway pressure (CPAP) produced a marked reduction in diaphragm initial length (LFRC) and tidal diaphragmatic shortening (%LFRC), tidal volume (VT) and transdiaphragmatic pressure swings (delta Pdi) in supine dogs after vagotomy. We postulated that the reduced diaphragmatic shortening was mainly a result of the decrease in diaphragm LFRC but an increase in afterload could not be excluded. In this study, we attempted to define the role of these two mechanisms during postural change. Eight, pentobarbital-anaesthetized, vagotomized dogs were studied in the supine position during CPAP and during postural change (tilting towards upright). As before, CPAP produced a prompt reduction in diaphragm LFRC and tidal %LFRC, VT and delta Pdi. Tilting produced similar decreases in crural diaphragm LFRC (23% from control values) as the weight of the abdominal contents was removed, but less decrease in costal LFRC (17% during CPAP compared to 10% during tilting). A given reduction in crural diaphragm initial length (15%) resulted in less tidal shortening during tilting compared to CPAP, whereas costal diaphragm shortening was similar at a given reduction in initial length (10%). Both CPAP and tilting reduced tidal volumes (47.8 +/- 5.1 and 56.5 +/- 3.1% of control), however, delta Pdi decreased less during tilting (20%) than CPAP (47%). There was no significant change in the level of diaphragmatic EMG with either CPAP or tilting.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Respiratory muscle coordination and diaphragm length during expiratory threshold loading.

Active expiration is produced by the abdominal muscles and the rib cage expiratory muscles. We hypothesized that the relative contribution of these two groups to expiration would affect diaphragmatic length and, hence, influence the subsequent inspiration. To address this question we measured the respiratory muscle response to expiratory threshold loading in spontaneously breathing anesthetized dogs. Prevagotomy, the increase in lung volume (functional residual capacity) and decrease in initial resting length of the diaphragm were attenuated by greater than 50% of values predicted by the passive relationships. Diaphragmatic activation (electromyogram) increased and tidal volume (VT) was preserved. Postvagotomy, effective expiratory muscle recruitment was abolished. The triangularis sterni muscle remained active, and the increase in lung volume was attenuated by less than 15% of that predicted by the passive relationship. Diaphragmatic length was shorter than predicted. VT was not restored, even though costal diaphragmatic and parasternal intercostal electromyogram increased. During expiratory threshold loading with abdominal muscles resected and vagus intact, recruitment of the rib cage expiratory muscles produced a reduction in lung volume comparable with prevagotomy; however, diaphragmatic length decreased markedly. Both the rib cage and abdominal expiratory muscles may defend lung volume; however, their combined action is important to restore diaphragmatic initial length and, accordingly, to preserve VT.

Animals