Three-dimensional reconstruction of human diaphragm with the use of spiral computed tomography

Pettiaux, Nicolas, Marie Cassart, Manuel Paiva, and MarcEstenne. Three-dimensional reconstruction of human diaphragm withthe use of spiral computed tomography. J. Appl.Physiol. 82(3): 998-1002, 1997.We developed atechnique of diaphragm imaging by using spiral computed tomography, andwe studied four normal subjects who had been previously investigatedwith magnetic resonance imaging (A. P. Gauthier, S. Verbanck,M. Estenne, C. Segebarth, P. T. Macklem, and M. Paiva.J. Appl. Physiol. 76: 495-506,1994). One acquisition of 15- to 25-s duration was performed atresidual volume, functional residual capacity, functional residualcapacity plus one-half inspiratory capacity, and total lung capacitywith the subject holding his breath and relaxing. From theseacquisitions, 20 coronal and 30 sagittal images were reconstructed ateach lung volume; on each image, diaphragm contour in the zone ofapposition and in the dome was digitized with the software Osiris, andthe digitized silhouettes were used for three-dimensionalreconstruction with Matlab. Values of length and surface area for thediaphragm, the dome, and the zone of apposition were very similar tothose obtained with magnetic resonance imaging. We conclude thatsatisfactory three-dimensional reconstruction of the in vivo diaphragmmay be obtained with spiral computed tomography, allowing accurate measurements of muscle length, surface area, and shape.

     

Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects

McKenzie, D. K., G. M. Allen, J. E. Butler, and S. C. Gandevia. Task failure with lack of diaphragm fatigue during inspiratory resistive loading in human subjects. J. Appl. Physiol. 82(6): 2011-2019, 1997.Taskfailure during inspiratory resistive loading is thought to beaccompanied by substantial peripheral fatigue of the inspiratorymuscles. Six healthy subjects performed eight resistive breathingtrials with loads of 35, 50, 75 and 90% of maximal inspiratorypressure (MIP) with and without supplemental oxygen. MIP measuredbefore, after, and at every minute during the trial increased slightlyduring the trials, even when corrected for lung volume (e.g., for 24 trials breathing air, 12.5% increase, P < 0.05). In some trials, taskfailure occurred before 20 min (end point of trial), and in thesetrials there was an increase in end-tidalPCO₂(P < 0.01), despite the absence of peripheral muscle fatigue. In four subjects (6 trials with task failure), there was no decline in twitch amplitude with bilateral phrenic stimulation or in voluntary activation of the diaphragm, eventhough end-tidal PCO₂ rose by 1.6 ± 0.9%. These results suggest that hypoventilation,CO₂ retention, and ultimate taskfailure during resistive breathing are not simply dependent on impairedforce-generating capacity of the diaphragm or impaired voluntaryactivation of the diaphragm.

     

Long-term facilitation of upper airway muscle activities in vagotomized and vagally intact cats

Mateika, J. H., and R. F. Fregosi. Long-termfacilitation of upper airway muscle activities in vagotomized andvagally intact cats. J. Appl. Physiol.82(2): 419-425, 1997.The primary purpose of the presentinvestigation was to determine whether long-term facilitation (LTF) ofupper airway muscle activities occurs in vagotomized and vagally intactcats. Tidal volume and diaphragm, genioglossus, and nasal dilatormuscle activities were recorded before, during, and after one carotidsinus nerve was stimulated five times with 2-min trains of constantcurrent. Sixty minutes after stimulation, nasal dilator andgenioglossus muscle activities were significantly greater than controlin the vagotomized cats but not in the vagally intact cats. Tidalvolume recorded from the vagotomized and vagally intact cats wassignificantly greater than control during the poststimulation period.In contrast, diaphragm activities were not significantly elevated inthe poststimulation period in either group of animals. We conclude that1) LTF of genioglossus and nasaldilator muscle activities can be evoked in vagotomized cats;2) vagal mechanisms inhibit LTF inupper airway muscles; and 3) LTF canbe evoked in accessory inspiratory muscles because LTF of inspiredtidal volume was greater than LTF of diaphragm activity.

     

Functional role and structure of the scalene: an accessory inspiratory muscle in hamster

Fournier, Mario, and Michael I. Lewis. Functional roleand structure of the scalene: an accessory inspiratory muscle inhamster. J. Appl. Physiol. 81(6):2436-2444, 1996.Although the scalene muscle (Sca) is a primaryinspiratory muscle in humans, its respiratory function in other speciesis less clear. The electromyographic (EMG) activity of the Sca wasstudied during resting ventilation (eupnea) in both the awake andanesthetized hamster and after a variety of respiratory challenges inthe anesthetized animal. The EMG activities of the medial Sca and thecostal diaphragm were compared. The medial Sca, the major component ofthe Sca, originates from cervical transverse processes 2 to 5 andinserts primarily onto rib 4, with a small segment onto rib 3. In both the anesthetized and awake animal, the Sca was always silent during quiet breathing. WithCO₂-stimulated hyperpnea, the Scawas always recruited during inspiration in phase with the diaphragm.Active recruitment of the Sca was also observed after resistive loading and total airway occlusion. After ipsilateral phrenicotomy, the Sca waspersistently recruited during eupnea. The specificity of the EMGsignals was tested both by excluding cross contamination from other ribcage muscles and by selective denervation studies. Muscle spindles wereidentified in the medial Sca histochemically, suggesting that therespiratory activity of the Sca can also be modulated by changes inmuscle length and/or load. These results indicate that the Scafunctions as an accessory inspiratory muscle in the hamster and mayplay an important role in conditions of chronic load.

     

Effects of transverse fiber stiffness and central tendon on displacement and shape of a simple diaphragm model

Boriek, Aladin M., and Joseph R. Rodarte. Effects oftransverse fiber stiffness and central tendon on displacement and shapeof a simple diaphragm model. J. Appl. Physiol. 82(5): 1626-1636, 1997.Our previous experimental results (A. M. Boriek, S. Lui, and J. R. Rodarte. J. Appl. Physiol. 75:527-533, 1993 and A. M. Boriek, T. A. Wilson, and J. R. Rodarte.J. Appl. Physiol. 76: 223-229, 1994) showed that1) costal diaphragm shape is similar at functional residualcapacity and end inspiration regardless of whether the diaphragm muscleshortens actively (increased tension) or passively (decreased tension);2) diaphragmatic muscle length changes minimally in thedirection transverse to the muscle fibers, suggesting the diaphragm maybe inextensible in that direction; and 3) the central tendon isnot stretched by physiological stresses. A two-dimensional orthotropicmaterial has two different stiffnesses in orthogonal directions. In theplane tangent to the muscle surface, these directions are along thefibers and transverse to the fibers. We wondered whether orthotropicmaterial properties in the muscular region of the diaphragm andinextensibility of the central tendon might contribute to the constancyof diaphragm shape. Therefore, in the present study, we examined theeffects of stiffness transverse to muscle fibers and inextensibility ofthe central tendon on diaphragmatic displacement and shape. Finiteelement hemispherical models of the diaphragm were developed by usingpressurized isotropic and orthotropic membranes with a wide range ofstiffness ratios. We also tested heterogeneous models, in which themuscle sheet was an orthotropic material, having transverse fiberstiffness greater than that along the fibers, with the central tendonbeing an inextensible isotropic cap. These models revealed thatincreased transverse stiffness limits the shape change of thediaphragm. Furthermore, an inextensible cap simulating the centraltendon dramatically limits the change in shape as well as the membrane displacement in response to pressure. These findings provide a plausible mechanism by which the diaphragm maintains similar shapes despite different physiological loads. This study suggests that changesof diaphragm shape are restricted because the central tendon isessentially inextensible and stiffness in the direction transverse tothe muscle fibers is greater than stiffness along the fibers.

     

N-acetylcysteine administration alters the response to inspiratory loading in oxygen-supplemented rats

Supinski, G. S., D. Stofan, R. Ciufo, and A. DiMarco.N-acetylcysteine administrationalters the response to inspiratory loading in oxygen-supplemented rats.J. Appl. Physiol. 82(4): 1119-1125, 1997.Based on recent studies, it has been suggested that free radicals are elaborated in the respiratory muscles during strenuous contractions and contribute to the development of muscle fatigue. If this theory is correct, then it should be possible toattenuate the development of diaphragm fatigue and/or delay theonset of respiratory failure during loaded breathing by administering afree radical scavenger. The purpose of the present experiment was,therefore, to examine the effect ofN-acetylcysteine (NAC), a free radicalscavenger and glutathione precursor, on the evolution of respiratoryfailure in decerebrate unanesthetized rats breathing against a largeinspiratory resistive load. We compared the inspiratory volume andpressure generation over time in animals pretreated with either salineor NAC (150 mg/kg) and then loaded until respiratory arrest. Afterarrest, the diaphragm was excised, and samples were assayed for reduced(GSH) and oxidized glutathione. As a control, we also assessedrespiratory function and glutathione concentrations in groups ofnonloaded saline- and NAC-treated animals. We found that NAC-treatedanimals were able to tolerate loading better than the saline-treatedgroup, maintaining higher inspiratory pressures and sustaining higherinspired volumes. Administration of NAC also increased the time thatanimals could tolerate loading before the development of respiratoryarrest. In addition, although saline-treated loaded animals hadsignificant reductions in diaphragmatic GSH levels compared withunloaded controls, the magnitude of this reduction was blunted by NACadministration (i.e., GSH averaged 965 ± 113, 568 ± 83, 907 ± 39, and 784 ± 61 nmol/g for unloaded-saline, loaded-saline,unloaded-NAC, and loaded-NAC groups, P < 0.05, with the value for the loaded-saline group lower than thevalues for the two unloaded groups; GSH for the loaded-NAC group was not different, however, from unloaded controls). These data demonstrate that administration of NAC, a free radical scavenger, slows the rate ofdevelopment of respiratory failure during inspiratory resistiveloading.

     

Muscle fiber architecture of the dog diaphragm

Boriek, Aladin M., Charles C. Miller III, and Joseph R. Rodarte. Muscle fiber architecture of the dog diaphragm.J. Appl. Physiol. 84(1): 318-326, 1998.Previous measurements of muscle thickness and length ratio ofcostal diaphragm insertions in the dog (A. M. Boriek and J. R. Rodarte.J. Appl. Physiol. 77: 2065-2070,1994) suggested, but did not prove, discontinuous muscle fiberarchitecture. We examined diaphragmatic muscle fiber architecture usingmorphological and histochemical methods. In 15 mongrel dogs, transversesections along the length of the muscle fibers were analyzedmorphometrically at ×20, by using the BioQuant System IVsoftware. We measured fiber diameters, cross-sectional fiber shapes,and cross-sectional area distributions of fibers. We also determinednumbers of muscle fibers per cross-sectional area and ratio ofconnective tissue to muscle fibers along a course of the muscle fromnear the chest wall (CW) to near the central tendon (CT) for midcostalleft and right hemidiaphragms, as well as ventral, middle, and dorsalregions of the left costal hemidiaphragm. In six other mongrel dogs,the macroscopic distribution of neuromuscular junctions (NMJ) onthoracic and abdominal diaphragm surfaces was determined by stainingthe intact diaphragmatic muscle for acetylcholinesterase activity. Theaverage major diameter of muscle fibers was significantly smaller, andthe number of fibers was significantly larger midspan between CT and CWthan near the insertions. The ratio of connective tissues to musclefibers was largest at CW compared with other regions along the lengthof the muscle. The diaphragm is transversely crossed by multiplescattered NMJ bands with fairly regular intervals offset in adjacentstrips. Muscle fascicles traverse two to five NMJ, consistent withfibers that do not span the entire fascicle from CT to CW. Theseresults suggest that the diaphragm has a discontinuous fiberarchitecture in which contractile forces may be transmitted among themuscle fibers through the connective tissue adjacent to the fibers.

     

Respiratory-related neurons of the fastigial nucleus in response to chemical and mechanical challenges

Xu, Fadi, and Donald T. Frazier. Respiratory-relatedneurons of the fastigial nucleus in response to chemical and mechanical challenges. J. Appl. Physiol. 82(4):1177-1184, 1997.Responses of cerebellar respiratory-relatedneurons (CRRNs) within the rostral fastigial nucleus and the phrenicneurogram to activation of respiratory mechano- and chemoreceptors wererecorded in anesthetized, paralyzed, and ventilated cats. Respiratorychallenges included the following: 1) cessation of the ventilator for asingle breath at the end of inspiration (lung inflation) or atfunctional residual capacity, 2)cessation of the ventilator for multiple breaths, and3) exposure to hypercapnia. NineteenCRRNs having spontaneous activity during control conditions werecharacterized as either independent (basic, n = 14) or dependent (pump,n = 5) on the ventilator movement. Thirteen recruited CRRNs showed no respiratory-related activity untilbreathing was stressed. Burst durations of expiratory CRRNs wereprolonged by sustained lung inflation but were inhibited when thevolume was sustained at functional residual capacity; it was vice versafor inspiratory CRRNs. Multiple-breath cessation of the ventilator andhypercapnia significantly increased the firing rate and/orburst duration concomitant with changes noted in the phrenic neurogram.We conclude that CRRNs respond to respiratory inputs fromCO₂ chemo- and pulmonarymechanoreceptors in the absence of skeletal muscle contraction.

     

Ultrasound evaluation of piglet diaphragm function before and after fatigue

Kocis, Keith C., Peter J. Radell, Wayne I. Sternberger, JaneE. Benson, Richard J. Traystman, and David G. Nichols. Ultrasound evaluation of piglet diaphragm function before and after fatigue. J. Appl. Physiol. 83(5):1654-1659, 1997.Clinically, a noninvasive measure of diaphragmfunction is needed. The purpose of this study is to determine whetherultrasonography can be used to 1)quantify diaphragm function and 2)identify fatigue in a piglet model. Five piglets were anesthetized withpentobarbital sodium and halothane and studied during the followingconditions: 1) baseline (spontaneous breathing); 2) baseline + CO₂ [inhaledCO₂ to increase arterial PCO₂ to 50-60 Torr (6.6-8kPa)]; 3) fatigue + CO₂ (fatigue induced with 30 minof phrenic nerve pacing); and 4)recovery + CO₂ (recovery after 1 hof mechanical ventilation). Ultrasound measurements of the posteriordiaphragm were made (inspiratory mean velocity) in the transverseplane. Images were obtained from the midline, just inferior to thexiphoid process, and perpendicular to the abdomen. M-mode measures weremade of the right posterior hemidiaphragm in the plane just lateral tothe inferior vena cava. Abdominal and esophageal pressures weremeasured and transdiaphragmatic pressure (Pdi) was calculated duringspontaneous (Sp) and paced (Pace) breaths. Arterial blood gases werealso measured. Pdi(Sp) and Pdi(Pace)during baseline + CO₂ were 8 ± 0.7 and 49 ± 11 cmH₂O, respectively, anddecreased to 6 ± 1.0 and 27 ± 7 cmH₂O,respectively, during fatigue + CO₂. Mean inspiratory velocityalso decreased from 13 ± 2 to 8 ± 1 cm/s during theseconditions. All variables returned to baseline during recovery + CO₂. Ultrasonography can beused to quantify diaphragm function and identify piglet diaphragm fatigue.

     

Ratio of active to passive muscle shortening in the canine diaphragm.

Active and passive shortening of muscle bundles in the canine diaphragm were measured with the objective of testing a consequence of the minimal-work hypothesis: namely, that the ratio of active to passive shortening is the same for all active muscles. Lengths of six muscle bundles in the costal diaphragm and two muscle bundles in the crural diaphragm of each of four bred-for-research beagle dogs were measured by the radiopaque marker technique during the following maneuvers: a passive deflation maneuver from total lung capacity to functional residual capacity, quiet breathing, and forceful inspiratory efforts against an occluded airway at different lung volumes. Shortening per liter increase in lung volume was, on average, 70% greater during quiet breathing than during passive inflation in the prone posture and 40% greater in the supine posture. For the prone posture, the ratio of active to passive shortening was larger in the ventral and midcostal diaphragm than at the dorsal end of the costal diaphragm. For both postures, active shortening during quiet breathing was poorly correlated with passive shortening. However, shortening during forceful inspiratory efforts was highly correlated with passive shortening. The average ratios of active to passive shortening were 1.23 +/- 0.02 and 1.32 +/- 0.03 for the prone and supine postures, respectively. These data, taken together with the data reported in the companion paper (T. A. Wilson, M. Angelillo, A. Legrand, and A. De Troyer, J. Appl. Physiol. 87: 554-560, 1999), support the hypothesis that, during forceful inspiratory efforts, the inspiratory muscles drive the chest wall along the minimal-work trajectory.     

Length and curvature of the dog diaphragm.

Transdiaphragmatic pressure is a result of both tension in the muscles of the diaphragm and curvature of the muscles. As lung volume increases, the pressure-generating capability of the diaphragm decreases. Whether decrease in curvature contributes to the loss in transdiaphragmatic pressure and, if so, under what conditions it contributes are unknown. Here we report data on muscle length and curvature in the supine dog. Radiopaque markers were attached along muscle bundles in the midcostal region of the diaphragm in six beagle dogs of approximately 8 kg, and marker locations were obtained from biplanar images at functional residual capacity (FRC), during spontaneous inspiratory efforts against a closed airway at lung volumes from FRC to total lung capacity, and during bilateral maximal phrenic nerve stimulation at the same lung volumes. Muscle length and curvature were obtained from these data. During spontaneous inspiratory efforts, muscle shortened by 15-40% of length at FRC, but curvature remained unchanged. During phrenic nerve stimulation, muscle shortened by 30 to nearly 50%, and, for shortening exceeding 52%, curvature appeared to decrease sharply. We conclude that diaphragm curvature is nearly constant during spontaneous breathing maneuvers in normal animals. However, we speculate that it is possible, if lung compliance were increased and the chest wall and the diameter of the diaphragm ring of insertion were enlarged, as in the case of chronic obstructive pulmonary disease, that decrease in diaphragm curvature could contribute to loss of diaphragm function.     

Expression of the inducible nitric oxide synthase gene in diaphragm and skeletal muscle

Thompson, Marita, Lisa Becker, Debbie Bryant, Gary Williams,Daniel Levin, Linda Margraf, and Brett P. Giroir. Expression ofthe inducible nitric oxide synthase gene in diaphragm and skeletal muscle. J. Appl. Physiol. 81(6):2415-2420, 1996.Nitric oxide (NO) is a pluripotent molecule thatcan be secreted by skeletal muscle through the activity of the neuronalconstitutive isoform of NO synthase. To determine whether skeletalmuscle and diaphragm might also express the macrophage-inducible formof NO synthase (iNOS) during provocative states, we examined tissuefrom mice at serial times after intravenous administration ofEscherichia coli endotoxin. In thesestudies, iNOS mRNA was strongly expressed in the diaphragm and skeletalmuscle of mice 4 h after intravenous endotoxin and was significantlydiminished by 8 h after challenge. Induction of iNOS mRNA was followedby expression of iNOS immunoreactive protein on Western immunoblots.Increased iNOS activity was demonstrated by conversion of arginine tocitrulline. Immunochemical analysis of diaphragmatic explants exposedto endotoxin in vitro revealed specific iNOS staining in myocytes, inaddition to macrophages and endothelium. These results may be importantin understanding the pathogenesis of respiratory pump failure duringseptic shock, as well as skeletal muscle injury during inflammation ormetabolic stress.

     

Chest wall muscle cross talk in canine costal diaphragm electromyogram

Sinderby, C., S. Friberg, N. Comtois, and A. Grassino.Chest wall muscle cross talk in the canine costal diaphragm electromyogram. J. Appl. Physiol.81(5): 2312-2327, 1996.The present paper describes the influenceof cross talk from the abdominal and intercostal muscles on the caninediaphragm electromyogram (EMG). The diaphragm EMG was recorded withbipolar surface electrodes placed on the costal portion of thediaphragm (abdominal side), aligned in the fiber direction, andpositioned in a region with a relatively low density of motor endplates. The results indicated that cross talk may occur in thediaphragm EMG, especially during conditions of loaded breathing andlight general anesthesia. The cross-talk signals showed characteristicsthat were entirely different from the diaphragm EMG. Although thediaphragm EMG was typical for signals recorded with electrodes alignedin the fiber direction, the cross-talk signals were characteristic ofthose obtained with electrode pairs not aligned in the direction of themuscle fibers. Alterations in electrode positioning, interelectrodedistance, and/or electrode surface area cannot guarantee theelimination of cross-talk signals, whereas spinal anesthesia at a highthoracic level will paralyze the sources of the cross talk and henceeliminate the cross-talk signals. By taking advantage of thedifferences in EMG signal characteristics for the diaphragm EMG andcross-talk signals, an index that has the capability to detect crosstalk was developed.

     

Superior laryngeal nerve section alters responses to upper airway distortion in sleeping dogs

Curran, Aidan K., Peter R. Eastwood, Craig A. Harms, CurtisA. Smith, and Jerome A. Dempsey. Superior laryngeal nerve sectionalters responses to upper airway distortion in sleeping dogs.J. Appl. Physiol. 83(3): 768-775, 1997.We investigated the effect of superior laryngeal nerve (SLN)section on expiratory time(TE) and genioglossuselectromyogram (EMGgg) responses to upper airway (UA) negative pressure(UANP) in sleeping dogs. The same dogs used in a similar intact study(C. A. Harms, C. A., Y.-J. Zeng, C. A. Smith, E. H. Vidruk, and J. A. Dempsey. J. Appl. Physiol. 80:1528-1539, 1996) were bilaterally SLN sectioned. After recovery,the UA was isolated while the animal breathed through a tracheostomy.Square waves of negative pressure were applied to the UA from below thelarynx or from the mask (nares) at end expiration and held until thenext inspiratory effort. Section of the SLN increased eupneicrespiratory frequency and minute ventilation. Relative to the same dogsbefore SLN section, sublaryngeal UANP caused lessTE prolongation while activation of the genioglossus required less negative pressures. Mask UANP had noeffect on TE or EMGgg activity.We conclude that the SLN 1) is notobligatory for the reflex prolongation ofTE and activation of EMGggactivity produced by UANP and 2)plays an important role in the maintenance of UA stability and thepattern of breathing in sleeping dogs.

     

Zone of apposition in the passive diaphragm of the dog

Boriek, Aladin M., Joseph R. Rodarte, and Susan S. Margulies. Zone of apposition in the passive diaphragm of thedog. J. Appl. Physiol. 81(5): 1929-1940, 1996.Wedetermined the regional area of the diaphragmatic zone of apposition(ZAP) as well as the regional craniocaudal extent of the ZAP(ZAP_ht) of the passive diaphragm in six paralyzedanesthetized beagle dogs (8-12 kg) at residual lung volume (RV),functional residual capacity (FRC), FRC + 0.25 and FRC + 0.5 inspiratory capacity, and total lung capacity (TLC) in prone and supinepostures. To identify the caudal boundary of the ZAP, 17 lead markers(1 mm) were sutured to the abdominal side of the costal and cruraldiaphragms around the diaphragm insertion on the chest wall. Two weekslater, the dogs' caudal thoraces were scanned by the use of thedynamic spatial reconstructor (DSR), a prototype fast volumetric X-raycomputer tomographic scanner, developed at the Mayo Clinic. Thethree-dimensional spatial coordinates of the markers were identified(±1.4 mm), and the cranial boundary of the ZAP was determined from30-40 1.4-mm-thick sagittal and coronal slices in each DSR image.We interpolated the DSR data to find the position of the cranial andcaudal boundaries of the ZAP every 5° around the thorax and computedthe distribution of regional variation of area of the ZAP andZAP_ht as well as the total area of ZAP. TheZAP_ht and area of ZAP increased as lung volume decreasedand were largest near the lateral extremes of the rib cage. We measuredthe surface area of the rib cage cephaled to the ZAP(A_L) in both postures in another six beagle dogs(12-16 kg) of similar stature, scanned previously in the DSR. Weestimated the entire rib cage surface area(A_rc = A_ZAP +A_L). The A_ZAP as a percentageof A_rc increased more than threefold as lung volumedecreased from TLC to RV, from ~9 to 29% of A_rc.

     

A model of the spontaneously breathing patient: applications to intrinsic PEEP and work of breathing

Schuessler, Thomas F., Stewart B. Gottfried, and Jason H. T. Bates. A model of the spontaneously breathing patient: applications to intrinsic PEEP and work of breathing.J. Appl. Physiol. 82(5):1694-1703, 1997.Intrinsic positive end-expiratory pressure(PEEP_i) and inspiratory work ofbreathing (WI) are important factors in the management of severe obstructive respiratory disease. Weused a computer model of spontaneously breathing patients with chronicobstructive pulmonary disease to assess the sensitivity of measurementtechniques for dynamic PEEP_i(PEEP_{i dyn}) andWI to expiratory muscle activity(EMA) and cardiogenic oscillations (CGO) on esophageal pressure.Without EMA and CGO, bothPEEP_{i dyn} andWI were accurately estimated(r = 0.999 and 0.95, respectively). Addition of moderate EMA causedPEEP_{i dyn} andWI to be systematically overestimated by 141 and 52%, respectively. Furthermore, CGOintroduced large random errors, obliterating the correlation betweenthe true and estimated values for bothPEEP_{i dyn}(r = 0.29) andWI (r = 0.38). Thus the accurateestimation of PEEP_{i dyn} andWI requires steps to be taken toameliorate the adverse effects of both EMA and CGO. Taking advantage ofour simulations, we also investigated the relationship betweenPEEP_{i dyn} and staticPEEP_i(PEEP_{i stat}). ThePEEP_{i dyn}/PEEP_{i stat}ratio decreased as stress adaptation in the lung was increased,suggesting that heterogeneity of expiratory flow limitation isresponsible for the discrepancies betweenPEEP_{i dyn} andPEEP_{i stat} thathave been reported in patients with severe airwayobstruction.

     

Phrenic motoneuron discharge during sustained inspiratory resistive loading

Iscoe, Steve. Phrenic motoneuron discharge duringsustained inspiratory resistive loading. J. Appl.Physiol. 81(5): 2260-2266, 1996.I determinedwhether prolonged inspiratory resistive loading (IRL) affects phrenicmotoneuron discharge, independent of changes in chemical drive. Inseven decerebrate spontaneously breathing cats, the discharge patternsof eight phrenic motoneurons from filaments of one phrenic nerve weremonitored, along with the global activity of the contralateral phrenicnerve, transdiaphragmatic pressure, and fractional end-tidalCO₂ levels. Discharge patterns during hyperoxic CO₂ rebreathingand breathing against an IRL (2,500-4,000cmH₂O ^· l^{1 ·} s)were compared. During IRL, transdiaphragmatic pressure increased andthen either plateaued or decreased. At the highest fractional end-tidalCO₂ common to both runs,instantaneous discharge frequencies in six motoneurons were greaterduring sustained IRL than during rebreathing, when compared at the sametime after the onset of inspiration. These increased dischargefrequencies suggest the presence of a load-induced nonchemical drive tophrenic motoneurons from unidentified source(s).

     

Laryngeal and abdominal muscle electrical activity during periodic breathing in nonsedated lambs

Kianicka, Irenej, Véronique Diaz, Sylvain Renolleau,Emmanuel Canet, and Jean-Paul Praud. Laryngeal and abdominal muscle electrical activity during periodic breathing in nonsedated lambs. J. Appl. Physiol. 84(2):669-675, 1998.We recently reported that glottic closure waspresent throughout central apneas in awake lambs. The present studytested whether glottic closure was also observed during periodicbreathing (PB). We attempted to induce PB in 21 nonsedated lambs onreturn from hypocapnic hypoxia to room air. Airflow and thyroarytenoid(a laryngeal constrictor, n = 16),cricothyroid (a laryngeal dilator, n = 10), and abdominal (n = 9) muscleelectrical activity (EMG) were monitored continuously. PB was observedin 16 lambs, with apneic phases in 8 lambs. Thyroarytenoid muscle EMGwas observed at the nadir of PB, either throughout apnea or withprolonged expiration during the lowest respiratory efforts. Phasicinspiratory cricothyroid muscle EMG and phasic expiratory abdominal EMGdisappeared at the nadir of PB. Active glottic closure at the nadir ofPB, without abdominal muscle contraction, could be a beneficialmechanism, preserving alveolar gas stores for continuing gas exchangeduring the apneic/hypopneic phase of PB. However, consequences ofactive glottic closure on ventilatory instability, either enhancing orreducing, are unknown.

     

Diaphragm thickening during inspiration

Cohn, David, Joshua O. Benditt, Scott Eveloff, and F. DennisMcCool. Diaphragm thickening during inspiration.J. Appl. Physiol. 83(1): 291-296, 1997.Ultrasound has been used to measure diaphragm thickness(T_di) in thearea where the diaphragm abuts the rib cage (zone of apposition).However, the degree of diaphragm thickening during inspiration reportedas obtained by one-dimensional M-mode ultrasound was greater than thatpredicted by using other radiographic techniques. Becausetwo-dimensional (2-D) ultrasound provides greater anatomic definitionof the diaphragm and neighboring structures, we used this technique toreevaluate the relationship between lung volume andT_di. We firstestablished the accuracy and reproducibility of 2-D ultrasound bymeasuring T_diwith a 7.5-MHz transducer in 26 cadavers. We found thatT_di measured byultrasound correlated significantly with that measured by ruler (R² = 0.89), withthe slope of this relationship approximating a line of identity(y = 0.89x + 0.04 mm). The relationship between lung volume andT_di was thenstudied in nine subjects by obtaining diaphragm images at the fivetarget lung volumes [25% increments from residual volume (RV) tototal lung capacity (TLC)]. Plots ofT_di vs. lungvolume demonstrated that the diaphragm thickened as lung volumeincreased, with a more rapid rate of thickening at the higher lungvolumes[T_di = 1.74 vital capacity (VC)² + 0.26 VC + 2.7 mm] (R² = 0.99; P < 0.001) where lung volumeis expressed as a fraction of VC. The mean increase inT_di between RVand TLC for the group was 54% (range 42-78%). We conclude that2-D ultrasound can accurately measureT_di and that theaverage thickening of the diaphragm when a subject is inhaling from RVto TLC using this technique is in the range of what would be predictedfrom a 35% shortening of the diaphragm.

     

Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration

Beck, Jennifer, Christer Sinderby, Lars Lindström, andAlex Grassino. Diaphragm interference pattern EMG and compound muscle action potentials: effects of chest wall configuration. J. Appl. Physiol. 82(2): 520-530, 1997.The effect of chest wall configuration on the diaphragmelectromyogram (EMGdi) was evaluated in five healthy subjects with anesophageal electrode for both interference pattern EMGdi (voluntarycontractions) and electrically evoked diaphragm compound muscle actionpotentials (CMAPs). Diaphragm CMAPs (both unilateral and bilateral)were evaluated for the baseline-to-peak amplitude (Ampl), the time fromthe onset of the CMAP to first peak (T1), root mean square (RMS), andcenter frequency (CF) values of the CMAP power spectrum. CF values fromthe interference pattern EMGdi power spectrum were also calculated. ForCMAPs obtained at an electrode position least influenced by variationsinduced by electrode positioning, Ampl increased with diaphragmshortening from functional residual capacity (FRC) to total lungcapacity (TLC) by 101 and 98% (unilateral and bilateral,respectively). Bilateral CMAP RMS values increased 116% from FRC toTLC. CMAP T1 values decreased with diaphragm shortening from FRC to TLC by 1.1 and 2.1 ms for the unilateral and bilateral stimulations, respectively, and CF increased for the bilateral diaphragm CMAPs withdiaphragm shortening. CF values from the interference pattern EMGdi didnot show any consistent change with chest wall configuration. Thus CFvalues of the interference pattern EMGdi obtained with an esophagealelectrode can be considered reliable for physiological interpretation,at any diaphragm length (if electrode positioning and signalcontamination are controlled for), contrary to the diaphragm CMAPs,which are sensitive to changes in chest wall configuration. It isspeculated that the different results (over the effects of chest wallconfiguration on interference pattern EMGdi and diaphragm CMAPs) may bebecause of summation properties of the signals and how these influencethe EMG power spectrum.