Effects of acute hyperinflation on chest wall mechanics in dogs

We studied chest wall mechanics at functional residual capacity (FRC) and near total lung capacity (TLC) in 14 supine anesthetized and vagotomized dogs. During breathing near TLC compared with FRC, tidal volume decreased (674 +/- 542 vs. 68 +/- 83 ml; P less than 0.025). Both inspiratory changes in gastric pressure (4.5 +/- 2.5 vs. -0.2 +/- 2.0 cmH2O; P less than 0.005) and changes in abdominal cross-sectional area (25 +/- 17 vs. -1.0 +/- 4.2%; P less than 0.001) markedly decreased; they were both often negative during inspiration near TLC. Parasternal intercostal shortening decreased (-3.0 +/- 3.7 vs. -2.0 +/- 2.7%), whereas diaphragmatic shortening decreased slightly more in both costal and crural parts (costal -8.4 +/- 2.9 vs. -4.3 +/- 4.1%, crural -22.8 +/- 13.2 vs. -10.0 +/- 7.5%; P less than 0.05). As a result, the ratio of parasternal to diaphragm shortening increased near TLC (0.176 +/- 0.135 vs. 0.396 +/- 0.340; P less than 0.05). Electromyographic (EMG) activity in the parasternals slightly decreased near TLC, whereas the EMG activity in the costal and crural parts of the diaphragm slightly increased. We conclude that 1) the mechanical outcome of diaphragmatic contraction near TLC is markedly reduced, and 2) the mechanical outcome of parasternal intercostal contraction near TLC is clearly less affected.     

Relationship between diaphragm length and abdominal dimensions

We examined the relationship between changes in abdominal cross-sectional area, measured by respiratory inductive plethysmography, and changes in length in the costal and crural parts of the diaphragm, measured by sonomicrometry, in nine supine, anesthetized dogs. During passive inflation, both parts of the diaphragm shortened and abdominal cross-sectional area increased. During passive deflation, both parts of the diaphragm lengthened and abdominal cross-sectional area decreased. We subsequently used the relationship between costal and crural diaphragmatic length, respectively, and abdominal cross-sectional area during passive inflation-deflation to predict the length changes in the costal and crural diaphragm during quiet breathing before and after bilateral phrenicotomy. In the intact animal the inspiratory shortening in the crural diaphragm was almost invariably greater than predicted from the relationship during passive inflation. During inspiration after phrenicotomy the crural diaphragm invariably lengthened, whereas the costal diaphragm often shortened. In general there was a good correlation between the measured and predicted length change for the crural diaphragm (r = 0.72 before and 0.79 after phrenicotomy) and a poor one for the costal diaphragm (r = 0.05 before and 0.19 after phrenicotomy).     

Shape and tension distribution of the active canine diaphragm

Both diaphragm shape and tension contribute to transdiaphragmatic pressure, but of the three variables, tension is most difficult to measure. We measured transdiaphragmatic pressure and the global shape of the in vivo canine diaphragm and used principles of mechanics to compute the tension distribution. Our hypotheses were that 1) tension in the active diaphragm is nonuniform with greater tension in the central tendon than in the muscular regions; 2) maximum tension is essentially oriented in the muscle fiber direction, whereas minimum tension is orthogonal to the fiber direction; and 3) during submaximal activation change in the in vivo global shape is small. Metallic markers, each 2 mm in length, were implanted surgically on the peritoneal surface of the diaphragm at 1.5- to 2.0-cm intervals along the muscle bundles at the midline, ventral, middle, and dorsal regions of the left costal diaphragm and along a muscle bundle of the crural diaphragm. Postsurgery, a biplane videofluoroscopic system was used to determine the in vivo three-dimensional coordinates of the markers at end expiration and end inspiration during quiet breathing as well as at end-inspiratory efforts against an occluded airway at lung volumes of functional residual capacity and at one-third maximum inspiratory capacity increments in volume to total lung capacity. A surface was fit to the marker locations using a two-dimensional spline algorithm. Diaphragm surface was modeled as a pressurized membrane, and tension distribution in the active diaphragm was computed using the ANSYS finite element program. We showed that the peak of the diaphragm dome was closer to the ventral surface than to the dorsal surface and that there was a depression or valley in the crural region. In the supine position, during inspiratory efforts, the caudal displacement of the dorsal region of the diaphragm was greater than that of the dome, and the valley along the crural diaphragm was accentuated. In contrast, at lower lung volumes in the prone posture, the caudal displacement of the dome was greater than that of the crural region. At end of inspiration, transdiaphragmatic pressure was approximately 6.5 cmH2O, and tensions were nonuniform in the diaphragm. Maximum principal stress sigma(1) of central tendon was found to be greater than sigma(1) of the costal region, and that was greater than sigma(1) of the crural region, with values of 14-34, 14-29, and 4-14 g/cm, respectively. The corresponding data of the minimum principal stress sigma(2) were 9-18, 3-9, and 0-1.5 g/cm, respectively. Maximum principal tension was approximately parallel to the muscle fibers, whereas minimum tension was essentially orthogonal to the longitudinal direction of the muscle fibers. In the muscular region, sigma(1) was approximately 3-fold sigma(2), whereas in the central tendon, sigma(1) was only approximately 1.5-fold sigma(2.).     

In vivo length-force relationship of canine diaphragm

Diaphragmatic length was measured by sonomicrometry and transdiaphragmatic pressure (Pdi) by conventional latex balloons in eight dogs anesthetized with pentobarbital sodium under passive conditions and during supramaximal phrenic stimulation. The passive length-pressure relationship indicates that the crural part of the diaphragm is more compliant than the costal part. With supramaximal stimulation the costal diaphragm showed a length-pressure relationship similar in shape to in vitro length-tension curves previously described for the canine diaphragm. The crural part has a smaller pressure-length slope than the costal part in the length range from 80% of optimum muscle length (Lo) to Lo. At supine functional residual capacity (FRC) the resting length (LFRC) of the costal and crural diaphragms are not at Lo. The costal part is distended to 105% of Lo, and crural is shortened to 92% of Lo. Tidal shortening will increase the force output of costal while decreasing that of the crural diaphragm. The major forces setting the passive supine LFRC are the abdominal weight (pressure) and the elastic recoil of the lungs. The equilibrium length (resting length of excised diaphragmatic strips) was 79 +/- 3.6% LFRC for the costal diaphragm and 87 +/- 3.9% LFRC for the crural diaphragm. Similar shortening was obtained in the upright position, indicating passive diaphragmatic stretch at supine LFRC.     

Effect of lung inflation on diaphragmatic shortening

The effect of lung inflation on chest wall mechanics was studied in 11 vagotomized pentobarbital sodium-anesthetized dogs. Diaphragmatic shortening (percent change from initial length at functional residual capacity, %LFRC) and transdiaphragmatic pressure swings (delta Pdi) were compared with control values over a range of positive-pressure breathing that produced a maximum increase in lung volume to 40% of inspiratory capacity. There was no change in the electromyogram of the diaphragm or parasternal intercostals during positive-pressure breathing. delta Pdi and tidal volume (VT) fell to 52 +/- 3.3 and 42.5 +/- 5% (SE) of control. This was associated with a reduction in the initial resting length of 13 +/- 1.9 and 21 +/- 2.2%LFRC (SE) in the costal and crural diaphragms, respectively. Tidal diaphragmatic shortening, however, decreased to 66 +/- 7 and 57 +/- 7 and the mean velocity decreased to 78 +/- 10 and 63 +/- 8% (SE) of control for the costal and crural diaphragms, respectively. We conclude that the reduction in diaphragmatic shortening is the main determinant of the reduced delta Pdi and VT during lung inflation and relate this to what is currently known about diaphragmatic contractile properties.     

Costal vs. crural diaphragmatic blood flow during submaximal and near-maximal exercise in ponies

The present study was carried out 1) to compare blood flow in the costal and crural regions of the equine diaphragm during quiet breathing at rest and during graded exercise and 2) to determine the fraction of cardiac output needed to perfuse the diaphragm during near-maximal exercise. By the use of radionuclide-labeled 15-micron-diam microspheres injected into the left atrium, diaphragmatic and intercostal muscle blood flow was studied in 10 healthy ponies at rest and during three levels of exercise (moderate: 12 mph, heavy: 15 mph, and near-maximal: 19-20 mph) performed on a treadmill. At rest, in eucapnic ponies, costal (13 +/- 3 ml.min-1.100 g-1) and crural (13 +/- 2 ml.min-1.100 g-1) phrenic blood flows were similar, but the costal diaphragm received a much larger percentage of cardiac output (0.51 +/- 0.12% vs. 0.15 +/- 0.03% for crural diaphragm). Intercostal muscle perfusion at rest was significantly less than in either phrenic region. Graded exercise resulted in significant progressive increments in perfusion to these tissues. Although during exercise, crural diaphragmatic blood flow was not different from intercostal muscle blood flow, these values remained significantly less (P less than 0.01) than in the costal diaphragm. At moderate, heavy, and near-maximal exercise, costal diaphragmatic blood flow (123 +/- 12, 190 +/- 12, and 245 +/- 18 ml.min-1.100 g-1) was 143%, 162%, and 162%, respectively, of that for the crural diaphragm (86 +/- 10, 117 +/- 8, and 151 +/- 14 ml.min-1.100 g-1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Inspiratory and expiratory muscle function during continuous positive airway pressure in dogs

Continuous positive airway pressure (CPAP) is known to produce activation of the expiratory muscles. Several factors may determine whether this activation can assist inspiration. In this study we asked how and to what extent expiratory muscle contraction can assist inspiration during CPAP. Respiratory muscle response to CPAP was studied in eight supine anesthetized dogs. Lung volume and diaphragmatic initial length were defended by recruitment of the expiratory muscles. At the maximum CPAP of 18 cmH2O, diaphragmatic initial lengths were longer than predicted by the passive relationship by 52 and 46% in the costal and crural diaphragmatic segments, respectively. During tidal breathing after cessation of expiratory muscle activity, a component of passive inspiration occurred before the onset of inspiratory diaphragmatic electromyogram (EMG). At CPAP of 18 cmH2O, passive inspiration represented 24% of the tidal volume (VT) and tidal breathing was within the relaxation characteristic. Diaphragmatic EMG decreased at CPAP of 18 cmH2O; however, VT and tidal shortening were unchanged. We identified passive and active components of inspiration. Passive inspiration was limited by the time between the cessation of expiratory activity and the onset of inspiratory activity. We conclude that increased expiratory activity during CPAP defends diaphragmatic initial length, assists inspiration, and preserves VT. Even though breathing appeared to be an expiratory act, there remained a significant component of active inspiratory diaphragmatic shortening, and the major portion of VT was produced during active inspiration.     

Restriction of regional blood flow and diaphragmatic contractility

We have tested the hypothesis that the diaphragmatic head-to-head arterial anastomosis system should maintain adequate diaphragmatic function even during occlusion of some of its arteries. In six anesthetized open-chest dogs, left phrenic vein blood flow (Qphv) was measured by pulsed Doppler flowmetry. Contractility was measured by sonomicrometry in the left costal and crural diaphragm. The diaphragm was paced for 15 min by continuous bilateral supramaximal phrenic nerve stimulation. In five separate runs the following arteries were occluded at minute 5: 1) left phrenic artery, 2) internal mammary artery (IMA), 3) left phrenic artery and IMA, 4) descending aorta, and 5) descending aorta and IMA. Occlusion was then released at minute 10 of the run. In runs 1-3 there were no changes in contractility in costal or crural diaphragm and no changes in Qphv. However, in runs 4 and 5, Qphv decreased to 55.2 +/- 7.4 and 24.0 +/- 6.5% of control values, respectively. In run 4, percent maximum shortening from functional residual capacity (%LFRC) of the crural diaphragm decreased by 39.1%, while %LFRC of the costal diaphragm increased by 41.4% and abdominal pressure decreased by 47.0%. In run 5, abdominal pressure decreased by 53.5% and %LFRC of the crural and costal diaphragm decreased by 45.5 and 5.8%, respectively. Also relative postocclusion hyperemia was greater in run 5 (64.8%) than in run 4 (40.2%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Regional distribution of blood flow within the diaphragm

We investigated the regional distribution of blood flow (Q) within the costal and crural portions of the diaphragm in a total of eight anesthetized supine mongrel dogs. Q was measured with 15-microns microspheres, radiolabeled with three different isotopes, injected into the left ventricle during spontaneous breathing (SB), inspiratory resistive loading (IR), and mechanical ventilation after paralysis (P). At necropsy, the costal and crural portions of each hemidiaphragm were arbitrarily subdivided along a sagittal plane into five to seven and three sections, respectively. During P, there was a dorsoventral Q gradient within the costal part of the diaphragm. During SB there was a fourfold increase in the gradient of Q. Furthermore, during IR, in which mouth pressures of -16 +/- 4 cmH2O were generated, there was a further increase in the gradient of Q. During both SB and IR, Q to the most ventral portion of the costal diaphragm was 26 +/- 6% less than the peak value. In two dogs, studied prone and supine, there was no difference in the Q gradients between the two postures. Over the dorsal 80% of the costal diaphragm there was also a dorsoventral gradient of muscle thickness, such that the most dorsal part was 54 +/- 2% (n = 5) that of the ventral portion. In contrast, there was no consistent gradient of Q or muscle thickness within the crural diaphragm. Our results demonstrate a topographical gravity-independent distribution of Q in the costal, but not the crural, diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)     

Functional characteristics of canine costal and crural diaphragm

We estimated the in situ force-generating capacity of the costal and crural portions of the canine diaphragm by relating in vitro contractile properties and diaphragmatic dimensions to in situ lengths. Piezoelectric crystals were implanted on right costal and left crural diaphragms of anesthetized dogs, via midline laparatomy. With the abdomen reclosed, diaphragm lengths were recorded at five lung volumes. Contractile properties of excised muscle bundles were then measured. In vitro force-frequency and length-tension characteristics of the costal and crural diaphragms were virtually identical; their optimal force values were 2.15 and 2.22 kg/cm2, respectively. In situ, at residual volume, functional residual capacity (FRC), and total lung capacity the costal diaphragm lay at 102, 95, and 60% of optimal length (Lo), whereas the crural diaphragm lay at 88, 84, and 66% of Lo. Muscle cross-sectional area was 40% greater in costal than in crural diaphragms. Considering in situ lengths, cross-sectional areas, and in vitro length-tension characteristics at FRC, the costal diaphragm could exert 60% more force than the crural diaphragm.     

Costal and crural diaphragm in early inspiration: free breathing and occlusion

Changes in length of costal and crural segments of the canine diaphragm were measured by sonomicrometry within the first 100-300 ms of inspiration during CO2 rebreathing in anesthetized animals. Both segments showed small but significant decreases in end-expiratory length during progressive hypercapnia. Although both costal and crural segments showed electromyographic activity within the first 100 ms of inspiration, in early inspiration crural shortening predominated with minimal costal shortening. Neither segment contracted isometrically early in inspiration in the presence of airway occlusion. The amount of crural shortening during airway occlusion exceeded costal shortening; both segments showed increased shortening with prolonged occlusion and increasing CO2. Costal and crural shortening at 100 ms was not different for unoccluded and occluded states. These observations suggest that neural control patterns evoke discrete and unequal contributions from the diaphragmatic segments at the beginning of an inspiration; the crural segment may be predominately recruited in early inspiration. Despite traditional assumptions about occlusion pressure measurement (P0.1), diaphragm segments do not contract isometrically during early inspiratory effort against an occluded airway.     

Effect of abdominal compression on maximum transdiaphragmatic pressure

Transdiaphragmatic pressure (Pdi) is lower during maximum inspiratory effort with the diaphragm alone than when maximum inspiratory and expulsive efforts are combined. The increase in Pdi with expulsive effort has been attributed to increased neural activation of the diaphragm. Alternatively, the increase could be due to stretching of the contracted diaphragm. If this were so, Pdi measured during a combined maximum effort would overestimate the capacity of the diaphragm to generate inspiratory force. This study determined the likely contribution of stretching of the contracted diaphragm to estimates of maximum Pdi (Pdimax) obtained during combined inspiratory and expulsive effort. Three healthy trained subjects were studied standing. Diaphragmatic Mueller maneuvers were performed at functional residual capacity and sustained during subsequent abdominal compression by either abdominal muscle expulsive effort or externally applied pressure. Measurements were made of changes in abdominal (Pab) and pleural (Ppl) pressure, Pdi, rib cage and abdominal dimensions and respiratory electromyograms. Three reproducible performances of each maneuver from each subject were analyzed. When expulsive effort was added to maximum diaphragmatic inspiratory effort, Pdimax increased from 86 +/- 12 to 148 +/- 14 (SD) cmH2O within the 1st s and was 128 +/- 14 cmH2O 2 s later. When external compression was added to maximum diaphragmatic inspiratory effort, Pdimax increased from 87 +/- 16 to 171 +/- 19 cmH2O within the 1st s and was 152 +/- 16 cmH2O 2 s later.(ABSTRACT TRUNCATED AT 250 WORDS)     

Respiratory muscle blood flows during physiological and chemical hyperpnea in the rat.

Whether the diaphragm retains a vasodilator reserve at maximal exercise is controversial. To address this issue, we measured respiratory and hindlimb muscle blood flows and vascular conductances using radiolabeled microspheres in rats running at their maximal attainable treadmill speed (96 +/- 5 m/min; range 71-116 m/min) and at rest while breathing either room air or 10% O(2)-8% CO(2) (balance N(2)). All hindlimb and respiratory muscle blood flows measured increased during exercise (P < 0.001), whereas increases in blood flow while breathing 10% O(2)-8% CO(2) were restricted to the diaphragm only. During exercise, muscle blood flow increased up to 18-fold above rest values, with the greatest mass specific flows (in ml. min(-1). 100 g(-1)) found in the vastus intermedius (680 +/- 44), red vastus lateralis (536 +/- 18), red gastrocnemius (565 +/- 47), and red tibialis anterior (602 +/- 44). During exercise, blood flow was higher (P < 0.05) in the costal diaphragm (395 +/- 31 ml. min(-1). 100 g(-1)) than in the crural diaphragm (286 +/- 17 ml. min(-1). 100 g(-1)). During hypoxia+hypercapnia, blood flows in both the costal and crural diaphragms (550 +/- 70 and 423 +/- 53 ml. min(-1). 100 g(-1), respectively) were elevated (P < 0.05) above those found during maximal exercise. These data demonstrate that there is a substantial functional vasodilator reserve in the rat diaphragm at maximal exercise and that hypoxia + hypercapnia-induced hyperpnea is necessary to elevate diaphragm blood flow to a level commensurate with its high oxidative capacity.     

Effect of intestinal afferent stimulation on pattern of respiratory muscle activation

The purpose of the present study was to examine the reflex effects of mechanical stimulation of intestinal visceral afferents on the pattern of respiratory muscle activation. In 14 dogs anesthetized with pentobarbital sodium, electromyographic activity of the costal and crural diaphragm, parasternal intercostal, and upper airway respiratory muscles was measured during distension of the small intestine. Rib cage and abdominal motion and tidal volume were also recorded. Distension produced an immediate apnea (11.16 +/- 0.80 s). During the first postapneic breath, costal (43 +/- 7% control) and crural (64 +/- 6% control) activity were reduced (P less than 0.001). In contrast, intercostal (137 +/- 11%) and upper airway muscle activity, including alae nasi (157 +/- 16%), genioglossus (170 +/- 15%), and posterior cricoarytenoid muscles (142 +/- 7%) all increased (P less than 0.005). There was greater outward rib cage motion although the abdomen moved paradoxically inward during inspiration, resulting in a reduction in tidal volume (82 +/- 6% control) (P less than 0.005). Postvagotomy distension produced a similar apnea and subsequent reduction in costal and crural activity. However, enhancement of intercostal and upper airway muscle activation was abolished and there was a greater fall in tidal volume (65 +/- 14%). In conclusion, mechanical stimulation of intestinal afferents affects the various inspiratory muscles differently; nonvagal afferents produce an initial apnea and subsequent depression of diaphragm activity whereas vagal pathways mediate selective enhancement of intercostal and upper airway muscle activation.     

The effect of lung inflation on the inspiratory action of the canine parasternal intercostals.

Inflation induces a marked decrease in the lung-expanding ability of the diaphragm, but its effect on the parasternal intercostal muscles is uncertain. To assess this effect, the phrenic nerves and the external intercostals were severed in anesthetized, vagotomized dogs, such that the parasternal intercostals were the only muscles active during inspiration, and the endotracheal tube was occluded at different lung volumes. Although the inspiratory electromyographic activity recorded from the muscles was constant, the change in airway opening pressure decreased with inflation from -7.2+/-0.6 cmH2O at functional residual capacity to -2.2+/-0.2 cmH2O at 20-cmH2O transrespiratory pressure (P<0.001). The inspiratory cranial displacement of the ribs remained virtually unchanged, and the inspiratory caudal displacement of the sternum decreased moderately. However, the inspiratory outward rib displacement decreased markedly and continuously; at 20 cmH2O, this displacement was only 23+/-2% of the value at functional residual capacity. Calculations based on this alteration yielded substantial decreases in the change in airway opening pressure. It is concluded that, in the dog, 1) inflation affects adversely the lung-expanding actions of both the parasternal intercostals and the diaphragm; and 2) the adverse effect of inflation on the parasternal intercostals is primarily related to the alteration in the kinematics of the ribs. As a corollary, it is likely that hyperinflation also has a negative impact on the parasternal intercostals in patients with chronic obstructive pulmonary disease.     

Effect of body position on regional diaphragm function in dogs

The in situ lengths of muscle bundles of the crural and three regions of the costal diaphragm between origin and insertion were determined with a video roentgenographic technique in dogs. At total lung capacity (TLC) in both the prone and supine positions, the length of the diaphragm is not significantly different from the unstressed excised length, suggesting that the diaphragm is not under tension at TLC and that there is a hydrostatic gradient of pleural pressure on the diaphragmatic surface. Except for the ventral region of the costal diaphragm, which does not change length at lung volumes greater than 70% TLC, all other regions are stretched during passive deflations from TLC. Therefore below TLC the diaphragm is under passive tension and supports a transdiaphragmatic pressure (Pdi). The length of the diaphragm relative to its unstressed length is not uniform at functional residual capacity (FRC) and does not follow a strict vertical gradient that reverses when the animal is changed from the supine to the prone position. By inference, the length of muscle bundles is determined by factors other than the vertical gradient of Pdi. During mechanical ventilation, regional shortening is identical to the passive deflation length-volume relationship near FRC. Prone and supine FRC is the same, but the diaphragm is slightly shorter in the prone position. In both positions, during spontaneous ventilation there are no consistent differences in regional fractional shortening, despite regional differences in initial length relative to unstressed length.     

Regional deformation of the canine diaphragm.

To follow regional deformation of the diaphragm in dogs, radiopaque markers were implanted under surgical anesthesia into different anatomic regions of the muscle in triangular arrays (approximately 1 cm to a side). After recovery from surgery, changes in area and shape of the triangles were followed with biplane cinefluorography during quiet breathing and during inspiratory efforts against an occluded airway (Mueller maneuvers). From changes in shape of the triangles during contraction, area changes were decomposed into a major direction and magnitude of shortening (Eg1) and a minor length change (Eg2) perpendicular to Eg1, both expressed as a fraction of initial length at end expiration. With the use of these techniques, systematic differences in regional area change were observed in different parts of the diaphragm during inspiratory efforts at different lung volumes. Regional area always decreased during contraction in the crural and midcostal zones of apposition to the rib cage. Area decreased less and often increased during inspiratory efforts in the costal dome near the central tendon and in the costal region near its rib cage insertion. Differences in regional area change were not due to differences in the Eg1 in different parts of the diaphragm but were a consequence of differences in widening of the muscle along Eg2 perpendicular to the direction of Eg1. As lung volume was passively increased above functional residual capacity, regional area decreased in all parts of the diaphragm except in the costal regions near rib cage insertion, where area increased.     

Characteristics and functional significance of canine abdominal muscles

To assess the characteristics and function of the muscles of the anterolateral abdominal wall, we have examined the isometric contractile properties of bundles of canine rectus abdominis (RA) and external oblique (EO) muscles. In addition, we have related the lengths of these muscles measured sonometrically in vivo at supine functional residual capacity (FRC) to in vitro optimal force-producing length (Lo). We also investigated the action of the abdominal muscles on the displacement of costal and crural diaphragm. We found that 1) contraction time of RA was longer and that the RA developed greater force than the EO at submaximal stimulation frequencies; 2) maximal tetanic force and the active length-tension curves were similar in both abdominal muscles; 3) on passive stretch, the compliance of the RA was one-third that of the EO; 4) at supine FRC, the EO is operating at 83% of Lo, whereas the RA is operating at 105% of Lo; 5) stimulation of either RA or EO (abdominal pressure of 15 cmH2O) lengthened the costal and crural diaphragm toward their Lo values, with greater crural excursion occurring than costal. We conclude that the RA is well suited for restraining the abdominal viscera in prone quadrupeds, whereas the EO is better designed to assist expiration. Stimulation of both muscles improves in situ diaphragmatic operating length.     

Bilateral phrenic stimulation: a simple technique to assess diaphragmatic fatigue in humans

Transdiaphragmatic pressure (Pdi) and the rate of relaxation of the diaphragm (tau) were measured at functional residual capacity (FRC) in six normal seated subjects during single-twitch stimulation of both phrenic nerves. The latter were stimulated supramaximally with needle electrodes with square-wave impulses of 0.1-ms duration at 1 Hz before and after diaphragmatic fatigue produced by resistive loaded breathing. Constancy of chest wall configuration was achieved by monitoring the diameter of the abdomen and the rib cage with a respiratory inductive plethysmograph system. During control the peak Pdi generated during the phrenic stimulation amounted to 34.4 +/- 4.2 (SE) cmH2O and represented in each subject a fixed fraction (17%) of its maximal transdiaphragmatic pressure. After diaphragmatic fatigue the peak Pdi decreased by an average of 45%, amounting to 18.1 +/- 2.7 cmH2O 5 min after the fatigue run, and tau increased from 55.2 +/- 9 ms during control to 77 +/- 8 ms 5 min after the fatigue run. The decrease in peak Pdi and the increase in tau observed after the fatigue run persisted throughout the 30 min of the recovery period studied, the peak Pdi amounting to 18.4 +/- 2.8 and 18.9 +/- 3.3 cmH2O and tau to 81.3 +/- 5.7 and 88.7 +/- 10 ms at 15 and 30 min after the end of the fatigue run, respectively. It is concluded that diaphragmatic fatigue can be detected in man by bilateral phrenic stimulation with needle electrodes without any discomfort for the subject and that the decrease in diaphragmatic strength after fatigue is long lasting.     

Effects of PGF2 alpha on the EMG of costal and crural parts of the diaphragm of the newborn pig

We investigated the effects of PGF2 alpha on the breathing patterns and electric activity of costal and crural parts of the diaphragm in 9 anesthetized newborn pigs. The change in diaphragmatic tension was evaluated as the change in transdiaphragmatic pressure. Because PGF2 alpha induces bronchoconstriction and an increase in respiratory resistances, the changes induced by prostaglandin were evaluated as differences between bronchoconstriction after PGF2 alpha and resistive load obtained by applying gradual occlusion to the inspiratory line of the breathing circuit. Our results show that PGF2 alpha decreased respiratory frequency with lengthening of expiratory time, while the resistive load increased both respiratory phases. The changes in breathing pattern were associated with different electrical activities of the diaphragm. While resistive load did not significantly change the EMG power spectrum, PGF2 alpha recruited new motor units. Furthermore, resistive load induced synchronization of the inspiratory time discharge of the costal and crural parts of the diaphragm, while after PGF2 alpha infusion there was an early inspiratory discharge of the crural part.