Action of the diaphragm on the rib cage inferred from a force-balance analysis

Displacements of the rib cage are determined by the intrinsic passive properties of the rib cage, rib cage musculature, pleural and abdominal pressures, and the diaphragm. The diaphragm's mechanical actions on the rib cage are inferred from a force-balance analysis in which the diaphragm is seen to cause expansion of the rib cage by pulling cephalad at its insertions on the lower ribs (insertional component) and by raising intra-abdominal pressure, which pushes outward on the diaphragm's zone of apposition to the rib cage (appositional component). Goldman and Mead suggested that the diaphragm, acting alone, could drive both the rib cage and abdomen on their passive characteristics. The force-balance analysis shows that the diaphragm's inspiratory action on the rib cage is less than predicted by Goldman and Mead, but that in the special circumstances of their experiment (low lung volumes), the appositional component is large and the rib cage can be driven close to its passive characteristics. The force-balance analysis is consistent with recent observations by other investigations and is incompatible with the model proposed by Macklem and colleagues and with the Goldman-Mead hypothesis. Experiments on three subjects produced data consistent with the force-balance analysis, showing that the inspiratory action of the diaphragm on the rib cage is greatest at low lung volumes.     

Role of rib cage elastance in the coupling between the abdominal muscles and the lung.

The abdominal muscles expand the rib cage when they contract alone. This expansion opposes the deflation of the lung and may be viewed as pressure dissipation. The hypothesis was raised, therefore, that alterations in rib cage elastance should affect the lung deflating action of these muscles. To test this hypothesis and evaluate the quantitative importance of this effect, we measured the changes in airway opening pressure (Pao), abdominal pressure (Pab), and rib cage transverse diameter during isolated stimulation of the transversus abdominis muscle in anesthetized dogs, first with the rib cage intact and then after rib cage elastance was increased by clamping the ribs and the sternum. Stimulation produced increases in Pao, Pab, and rib cage diameter in both conditions. With the ribs and sternum clamped, however, the change in Pab was unchanged but the change in Pao was increased by 77% (P < 0.001). In a second experiment, the transversus abdominis was stimulated before and after rib cage elastance was reduced by removing the bony ribs 3-8. Although the change in Pab after removal of the the ribs was still unchanged, the change in Pao was reduced by 62% (P < 0.001). These observations, supported by a model analysis, indicate that rib cage elastance is a major determinant of the mechanical coupling between the abdominal muscles and the lung. In fact, in the dog, the effects of rib cage elastance and Pab on the lung-deflating action of the abdominal muscles are of the same order of magnitude.     

Respiratory effect of the lower rib displacement produced by the diaphragm

The diaphragm acting alone causes a cranial displacement of the lower ribs and a caudal displacement of the upper ribs. The respiratory effect of the lower rib displacement, however, is uncertain. In the present study, two sets of experiments were performed in dogs to assess this effect. In the first, all the inspiratory intercostal muscles were severed, so that the diaphragm was the only muscle active during inspiration, and the normal inspiratory cranial displacement of the lower ribs was suppressed at regular intervals. In the second experiment, the animals were given a muscle relaxant to abolish respiratory muscle activity, and external, cranially oriented forces were applied to the lower rib pairs to simulate the action of the diaphragm on these ribs. The data showed that 1) holding the lower ribs stationary during spontaneous, isolated diaphragm contraction had no effect on the change in lung volume during unimpeded inspiration and no effect on the fall in pleural pressure (Ppl) during occluded breaths; 2) the procedure, however, caused an increase in the caudal displacement of the upper ribs; and 3) pulling the lower rib pairs cranially induced a cranial displacement of the upper ribs and a small fall in Ppl. These observations indicate that the force applied on the lower ribs by the diaphragm during spontaneous contraction, acting through the interdependence of the ribs, is transmitted to the upper ribs and has an inspiratory effect on the lung. However, this effect is very small compared to that of the descent of the dome.     

Dissociation between diaphragmatic and rib cage muscle fatigue

To assess rib cage muscle fatigue and its relationship to diaphragmatic fatigue, we recorded the electromyogram (EMG) of the parasternal intercostals (PS), sternocleidomastoid (SM), and platysma with fine wire electrodes and the EMG of the diaphragm (DI) with an esophageal electrode. Six normal subjects were studied during inspiratory resistive breathing. Two different breathing patterns were imposed: mainly diaphragmatic or mainly rib cage breathing. The development of fatigue was assessed by analysis of the high-to-low (H/L) ratio of the EMG. To determine the appropriate frequency bands for the PS and SM, we established their EMG power spectrum by Fourier analysis. The mean and SD for the centroid frequency was 312 +/- 16 Hz for PS and 244 +/- 48 Hz for SM. When breathing with the diaphragmatic patterns, all subjects showed a fall in H/L of the DI and none had a fall in H/L of the PS or SM. During rib cage emphasis, four out of five subjects showed a fall in H/L of the PS and five out of six showed a fall in H/L of the SM. Four subjects showed no fall in H/L of the DI; the other two subjects were unable to inhibit diaphragm activity to a substantial degree and did show a fall in H/L of the DI. Activity of the platysma was minimal or absent during diaphragmatic emphasis but was usually strong during rib cage breathing. We conclude that fatigue of either the diaphragm or the parasternal and sternocleidomastoid can occur independently according to the recruitment pattern of inspiratory muscles.(ABSTRACT TRUNCATED AT 250 WORDS)     

Triangularis sterni: a primary muscle of breathing in the dog

The isolated action, pattern of neural activation, and mechanical contribution to eupnea of the triangularis sterni (transversus thoracis) muscle were studied in supine anesthetized dogs. Linear displacement transducers were used to measure the axial displacements of the ribs and sternum. Tetanic stimulation of the triangularis sterni in the apneic animal caused a marked caudal displacement of the ribs, a moderate cranial displacement of the sternum, and a decrease in lung volume. During quiet breathing, there was invariably a rhythmic activation of the muscle in phase with expiration that was independent of the presence or absence of activity in the abdominal and internal interosseous intercostal muscles. This phasic expiratory activity in the triangularis sterni was of large amplitude and caused the ribs to be more caudal and the sternum to be more cranial during the spontaneous expiratory pause than during relaxation. Additional studies on awake animals showed that rhythmic activation of the triangularis sterni occurs in all body positions and is not caused by anesthesia. These findings indicate that expiration in the dog is not a passive process and that the end-expiratory volume of the rib cage is not determined by an equilibrium of static forces alone. Rather, it is actively determined and maintained below its relaxation volume by contraction of the triangularis sterni throughout expiration. The use of this muscle is likely to facilitate inspiration by increasing the length of the parasternal intercostals and taking on a portion of their work.     

Effect of diaphragmatic contraction on the action of the canine parasternal intercostals.

The inspiratory intercostal muscles enhance the force generated by the diaphragm during lung expansion. However, whether the diaphragm also alters the force developed by the inspiratory intercostals is unknown. Two experiments were performed in dogs to answer the question. In the first experiment, external, cranially oriented forces were applied to the different rib pairs to assess the effect of diaphragmatic contraction on the coupling between the ribs and the lung. The fall in airway opening pressure (deltaPa(O)) produced by a given force on the ribs was invariably greater during phrenic nerve stimulation than with the diaphragm relaxed. The cranial rib displacement (Xr), however, was 40-50% smaller, thus indicating that the increase in deltaPa(O) was exclusively the result of the increase in diaphragmatic elastance. In the second experiment, the parasternal intercostal muscle in the fourth interspace was selectively activated, and the effects of diaphragmatic contraction on the deltaPa(O) and Xr caused by parasternal activation were compared with those observed during the application of external loads on the ribs. Stimulating the phrenic nerves increased the deltaPa(O) and reduced the Xr produced by the parasternal intercostal, and the magnitudes of the changes were identical to those observed during external rib loading. It is concluded, therefore, that the diaphragm has no significant synergistic or antagonistic effect on the force developed by the parasternal intercostals during breathing. This lack of effect is probably related to the constraint imposed on intercostal muscle length by the ribs and sternum.     

Mechanism of the lung-deflating action of the canine diaphragm at extreme lung inflation

When lung volume in animals is passively increased beyond total lung capacity (TLC; transrespiratory pressure = +30 cmH(2)O), stimulation of the phrenic nerves causes a rise, rather than a fall, in pleural pressure. It has been suggested that this was the result of inward displacement of the lower ribs, but the mechanism is uncertain. In the present study, radiopaque markers were attached to muscle bundles in the midcostal region of the diaphragm and to the tenth rib pair in five dogs, and computed tomography was used to measure the displacement, length, and configuration of the muscle and the displacement of the lower ribs during relaxation at seven different lung volumes up to +60 cmH(2)O transrespiratory pressure and during phrenic nerve stimulation at the same lung volumes. The data showed that 1) during phrenic nerve stimulation at 60 cmH(2)O, airway opening pressure increased by 1.5 ± 0.7 cmH(2)O; 2) the dome of the diaphragm and the lower ribs were essentially stationary during such stimulation, but the muscle fibers still shortened significantly; 3) with passive inflation beyond TLC, an area with a cranial concavity appeared at the periphery of the costal portion of the diaphragm, forming a groove along the ventral third of the rib cage; and 4) this area decreased markedly in size or disappeared during phrenic stimulation. It is concluded that the lung-deflating action of the isolated diaphragm beyond TLC is primarily related to the invaginations in the muscle caused by the acute margins of the lower lung lobes. These findings also suggest that the inspiratory inward displacement of the lower ribs commonly observed in patients with emphysema (Hoover's sign) requires not only a marked hyperinflation but also a large fall in pleural pressure.     

Intercostal muscle action inferred from finite-element analysis

The external and internal intercostal muscles are important respiratory muscles in humans, but their mechanical actions have been controversial. We used finite-element analysis based on anatomic and mechanical measurements in dogs to assess the action of the intercostal and other rib cage muscles in a model of an isolated canine rib cage. When intercostal muscle forces of either the internal or the external layer were applied in a single interspace, they pulled the adjacent ribs together, consistent with published observations in dogs. However, when the forces were applied in all interspaces, the external layer caused an inspiratory motion and the internal layer caused an expiratory motion, consistent with conventional understanding of intercostal muscle actions. Parasternal intercostal, levator costae, and transversus thoracis (triangularis sterni) muscle actions were also simulated. These muscles caused expected movements of the ribs and sternum. We conclude that the actions of intercostal muscles depend on the spatial extent of their activation. Their actions in a single interspace and in multiple interspaces can be observed and explained with three-dimensional finite-element models.     

Relative contributions of rib cage and abdomen to breathing in normal subjects.

By use of the method of Konno and Mead and the respiratory magnetometer, the partition of respired gas volumes into rib cage and diaphragm-abdomen components was accomplished in 81 normal subjects including 32 young and middle-aged men, 29 young and middle-aged women, and 20 elderly men. Studied were isovolume maneuvers and the relaxation configuration over the inspiratory capacity range, quiet tidal breathing, increased amplitudes of slow breathing, rapid inspirations and expirations, and both quiet and forceful phonation. No major differences were noted between men and women or between the young and the elderly during any respiratory acts. During quiet breathing most normal subjects are abdominal breathers when supine and thoracic breathers when upright. Rapid respiratory maneuvers were accomplished mostly through rib cage displacement suggesting that rib cage muscles are capable of more rapid action than diaphragm and abdominal muscles. Data from deep breathing and rapid maneuvers supported the view that abdominal and rib cage muscles often act to optimize the mechanical (length-tension) advantage of the diaphragm.     

Shape of the chest wall in the prone and supine anesthetized dog

The shape of the passive chest wall of six anesthetized dogs was determined at total lung capacity (TLC) and functional residual capacity (FRC) in the prone and supine body positions by use of volumetric-computed tomographic images. The transverse cross-sectional areas of the rib cage, mediastinum, and diaphragm were calculated every 1.6 mm along the length of the thorax. The changes in the volume and the axial distribution of transverse area of the three chest wall components with lung volume and body position were evaluated. The decrease of the transverse area within the rib cage between TLC and FRC, as a fraction of the area at TLC, was uniform from the apex of the thorax to the base. The volume of the mediastinum increased slightly between TLC and FRC (14% of its TLC volume supine and 20% prone), squeezing the lung between it and the rib cage. In the transverse plane, the heart was positioned in the midthorax and moved little between TLC and FRC. The shape, position, and displacement of the diaphragm were described by contour plots. In both postures, the diaphragm was flatter at FRC than at TLC, because of larger displacements in the dorsal than in the ventral region of the diaphragm. Rotation from the prone to supine body position produced a lever motion of the diaphragm, displacing the dorsal portion of the diaphragm cephalad and the ventral portion caudad. In five of the six dogs, bilateral isovolume pneumothorax was induced in the supine body position while intrathoracic gas volume was held constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Action of abdominal muscles on rib cage in humans

To assess the actions of the rectus abdominis and external oblique muscles on the rib cage in humans, these two muscles were stimulated with surface electrodes in four normal supine subjects at functional residual capacity. Changes in anteroposterior and transverse rib cage diameters and changes in xiphipubic distance were measured with pairs of magnetometers. Stimulation of rectus abdominis produced a marked decrease in the xiphipubic distance and in the anteroposterior diameter, thus making the rib cage more elliptic. In contrast, stimulation of the external oblique caused a decrease in the transverse diameter, making the rib cage more cylindrical. When both muscles were stimulated simultaneously, the resultant rib cage distortion depended on the relative voltage at which each muscle was stimulated. Electromyogram recordings showed that there was no cross contamination or activity of the diaphragm during the muscle stimulations. Transdiaphragmatic pressure increased with the voltage of stimulation, suggesting passive lengthening of the diaphragm. X-ray studies were performed in two subjects and confirmed the main magnetometer findings. These studies thus confirm that the rib cage in humans is more easily distortable than conventionally thought. The abdominal muscles can distort it in either direction depending on which muscles are contracting.     

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.     

Passive mechanics of upright human chest wall during immersion from hips to neck

We have determined the mechanical effects of immersion to the neck on the passive chest wall of seated upright humans. Repeated measurements were made at relaxed end expiration on four subjects. Changes in relaxed chest wall configuration were measured using magnetometers. Gastric and esophageal pressures were measured with balloon-tipped catheters in three subjects; from these, transdiaphragmatic pressure was calculated. Transabdominal pressure was estimated using a fluid-filled, open-tipped catheter referenced to the abdomen's exterior vertical surface. We found that immersion progressively reduced mean transabdominal pressure to near zero and that the relaxed abdominal wall was moved inward 3-4 cm. The viscera were displaced upward into the thorax, gastric pressure increased by 20 cmH2O, and transdiaphragmatic pressure decreased by 10-15 cmH2O. This lengthened the diaphragm, elevating the diaphragmatic dome 3-4 cm. Esophageal pressure became progressively more positive throughout immersion, increasing by 8 cmH2O. The relaxed rib cage was elevated and expanded by raising water from hips to lower sternum; this passively shortened the inspiratory intercostals and the accessory muscles of inspiration. Deeper immersion distorted the thorax markedly: the upper rib cage was forced inward while lower rib cage shape was not systematically altered and the rib cage remained elevated. Such distortion may have passively lengthened or shortened the inspiratory muscles of the rib cage, depending on their location. We conclude that the nonuniform forcing produced by immersion provides unique insights into the mechanical characteristics of the abdomen and rib cage, that immersion-induced length changes differ among the inspiratory muscles according to their locations and the depth of immersion, and that such length changes may have implications for patients with inspiratory muscle deficits.     

On the respiratory function of the ribs.

To assess the respiratory function of the ribs, we measured the changes in airway opening pressure (Pao) induced by stimulation of the parasternal and external intercostal muscles in anesthetized dogs, first before and then after the bony ribs were removed from both sides of the chest. Stimulating either set of muscles with the rib cage intact elicited a fall in Pao in all animals. After removal of the ribs, however, the fall in Pao produced by the parasternal intercostals was reduced by 60% and the fall produced by the external intercostals was eliminated. The normal outward curvature of the rib cage was also abolished in this condition, and when the curvature was restored by a small inflation, external intercostal stimulation consistently elicited a rise rather than a fall in Pao. These findings thus confirm that the ribs play a critical role in the act of breathing by converting intercostal muscle shortening into lung volume expansion. In addition, they carry the compression that is required to balance the pressure difference across the chest wall.     

Role of pleural pressure in the coupling between the intercostal muscles and the ribs.

The inspiratory intercostal muscles elevate the ribs and thereby elicit a fall in pleural pressure (DeltaPpl) when they contract. In the present study, we initially tested the hypothesis that this DeltaPpl does, in turn, oppose the rib elevation. The cranial rib displacement (Xr) produced by selective activation of the parasternal intercostal muscle in the fourth interspace was measured in dogs, first with the rib cage intact and then after DeltaPpl was eliminated by bilateral pneumothorax. For a given parasternal contraction, Xr was greater after pneumothorax; the increase in Xr per unit decrease in DeltaPpl was 0.98+/-0.11 mm/cmH2O. Because this relation was similar to that obtained during isolated diaphragmatic contraction, we subsequently tested the hypothesis that the increase in Xr observed during breathing after diaphragmatic paralysis was, in part, the result of the decrease in DeltaPpl, and the contribution of the difference in DeltaPpl to the difference in Xr was determined by using the relation between Xr and DeltaPpl during passive inflation. With diaphragmatic paralysis, Xr during inspiration increased approximately threefold, and 47+/-8% of this increase was accounted for by the decrease in DeltaPpl. These observations indicate that 1) DeltaPpl is a primary determinant of rib motion during intercostal muscle contraction and 2) the decrease in DeltaPpl and the increase in intercostal muscle activity contribute equally to the increase in inspiratory cranial displacement of the ribs after diaphragm paralysis.     

Relationship between parasternal intercostal length and rib cage displacement in dogs

The relationship between parasternal intercostal length and rib cage cross-sectional area was examined in nine supine dogs during passive inflation and during quiet breathing before and after phrenicotomy. Parasternal intercostal length (PSL) was measured with a sonomicrometry technique, and rib cage cross-sectional area (Arc) was measured with a Respitrace coil placed around the middle rib cage. During active inspiration as well as during passive inflation, PSL decreased as Arc increased. However, the relationship between PSL and Arc during active inspiration, whether in the intact or phrenicotomized animal, was almost invariably different from that during passive inflation, so that the same increase in Arc was associated with a greater decrease in PSL in the former than in the latter instance. This difference between passive inflation and active inspiration is probably due to the active contraction of the parasternals during inspiration and the consequent caudal displacement of the sternum. In upright humans, the sternum moves cephalad and not caudad during inspiration, so the relationship between PSL and Arc during active breathing might be similar to that during passive inflation.     

Hox patterning of the vertebrate rib cage

Unlike the rest of the axial skeleton, which develops solely from somitic mesoderm, patterning of the rib cage is complicated by its derivation from two distinct tissues. The thoracic skeleton is derived from both somitic mesoderm, which forms the vertebral bodies and ribs, and from lateral plate mesoderm, which forms the sternum. By generating mouse mutants in Hox5, Hox6 and Hox9 paralogous group genes, along with a dissection of the Hox10 and Hox11 group mutants, several important conclusions regarding the nature of the ;Hox code' in rib cage and axial skeleton development are revealed. First, axial patterning is consistently coded by the unique and redundant functions of Hox paralogous groups throughout the axial skeleton. Loss of paralogous function leads to anterior homeotic transformations of colinear regions throughout the somite-derived axial skeleton. In the thoracic region, Hox genes pattern the lateral plate-derived sternum in a non-colinear manner, independent from the patterning of the somite-derived vertebrae and vertebral ribs. Finally, between adjacent sets of paralogous mutants, the regions of vertebral phenotypes overlap considerably; however, each paralogous group imparts unique morphologies within these regions. In all cases examined, the next-most posterior Hox paralogous group does not prevent the function of the more-anterior Hox group in axial patterning. Thus, the ;Hox code' in somitic mesoderm is the result of the distinct, graded effects of two or more Hox paralogous groups functioning in any anteroposterior location.     

Activity of respiratory muscles in upright and recumbent humans

It is established that during tidal breathing the rib cage expands more than the abdomen in the upright posture, whereas the reverse is usually true in the supine posture. To explore the reasons for this, we studied nine normal subjects in the supine, standing, and sitting postures, measuring thoracoabdominal movement with magnetometers and respiratory muscle activity via integrated electromyograms. In eight of the subjects, gastric and esophageal pressures and diaphragmatic electromyograms via esophageal electrodes were also measured. In the upright postures, there was generally more phasic and tonic activity in the scalene, sternocleidomastoid, and parasternal intercostal muscles. The diaphragm showed more phasic (but not more tonic) activity in the upright postures, and the abdominal oblique muscle showed more tonic (but not phasic) activity in the standing posture. Relative to the esophageal pressure change with inspiration, the inspiratory gastric pressure change was greater in the upright than in the supine posture. We conclude that the increased rib cage motion characteristic of the upright posture owes to a combination of increased activation of rib cage inspiratory muscles plus greater activation of the diaphragm that, together with a stiffened abdomen, acts to move the rib cage more effectively.     

Dysfunction of the canine respiratory muscle pump in ascites.

Ascites, a complicating feature of many diseases of the liver and peritoneum, commonly causes dyspnea. The mechanism of this symptom, however, is uncertain. In the present study, progressively increasing ascites was induced in anesthetized dogs, and the hypothesis was initially tested that ascites increases the impedance on the diaphragm and, so, adversely affects the lung-expanding action of the muscle. Ascites produced a gradual increase in abdominal elastance and an expansion of the lower rib cage. Concomitantly, the caudal displacement of the diaphragm and the fall in airway opening pressure during isolated stimulation of the phrenic nerves decreased markedly; transdiaphragmatic pressure during phrenic stimulation also decreased. To assess the adaptation to ascites of the respiratory system overall, we subsequently measured the changes in lung volume, the arterial blood gases, and the electromyogram of the parasternal intercostal muscles during spontaneous breathing. Tidal volume and minute ventilation decreased progressively as ascites increased, leading to an increase in arterial PCO2 and parasternal intercostal inspiratory activity. It is concluded that 1) ascites, acting through an increase in abdominal elastance and an expansion of the lower rib cage, impairs the lung-expanding action of the diaphragm; 2) this impairment elicits a compensatory increase in neural drive to the inspiratory muscles, but the compensation is not sufficient to maintain ventilation; and 3) dyspnea in this setting results in part from the dissociation between increased neural drive and decreased ventilation.     

Pleural pressure increases during inspiration in the zone of apposition of diaphragm to rib cage

The zone of apposition of diaphragm to rib cage provides a theoretical mechanism that may, in part, contribute to rib cage expansion during inspiration. Increases in intra-abdominal pressure (Pab) that are generated by diaphragmatic contraction are indirectly applied to the inner rib cage wall in the zone of apposition. We explored this mechanism, with the expectation that pleural pressure in this zone (Pap) would increase during inspiration and that local transdiaphragmatic pressure in this zone (Pdiap) must be different from conventionally determined transdiaphragmatic pressure (Pdi) during inspiration. Direct measurements of Pap, as well as measurements of pleural pressure (Ppl) cephalad to the zone of apposition, were made during tidal inspiration, during phrenic stimulation, and during inspiratory efforts in anesthetized dogs. Pab and esophageal pressure (Pes) were measured simultaneously. By measuring Ppl's with cannulas placed through ribs, we found that Pap consistently increased during both maneuvers, whereas Ppl and Pes decreased. Whereas changes in Pdi of up to -19 cmH2O were measured, Pdiap never departed from zero by greater than -4.5 cmH2O. We conclude that there can be marked regional differences in Ppl and Pdi between the zone of apposition and regions cephalad to the zone. Our results support the concept of the zone of apposition as an anatomic region where Pab is transmitted to the interior surface of the lower rib cage.