Normal Diaphragm Research Articles

Use of ion channel blockers in the exploration of possible mechanisms involved in the myopathy of diabetic mice.

Changes in the muscle contractions of the phrenic nerve-diaphragm preparation from the diabetic mouse were investigated by means of K(+)- and Cl(-)-channel blockers and the Ca(2+)-mobilizing agent, selenite. The K(+)-channel blockers (UO2(2+) and 4-aminopyridine) cooperated synergistically with the Cl(-)-channel blockers (Cd2+ and 9-anthracenecarboxylic acid) in increasing normal muscle contraction as described previously, but failed to induce this effect in the diaphragm of the diabetic mouse. Treatment with a Cl(-)-channel blocker alone in 0.25 mmol/l Ca2+ Krebs solution induced a myotonic activity accompanied by stimulus-bound repetitive action potential firings. This effect was also diminished in the diaphragm from diabetic mice. The membrane potential of the muscle cells in the diaphragm of the diabetic mouse was slightly but significantly decreased. The membrane input resistance was also increased and was refractory to being further increased by either a Cl(-)-channel blocker or a low Cl(-)-medium. Furthermore, the membrane chloride conductance was found to be decreased, but the membrane K+ conductance remained unchanged in the muscle from diabetic mice. These changes of membrane properties in the muscles from diabetic mice were shown to be similar to those induced by either Cl(-)-channel blockers or a low Cl(-)-medium. In addition, the combined treatment of the diaphragm from diabetic mice with Cd2+ plus UO2(2+) in 0.25 mmol/l Ca2+ Krebs solution and then stepwise replenishment of Ca2+ led to a greater restoration of muscle contractions at a lower cumulative Ca2+ concentration than that was found with the normal diaphragm.(ABSTRACT TRUNCATED AT 250 WORDS)

Diaphragm reinnervation by laryngeal motoneurons.

Inspiratory activity of the paralyzed diaphragm was restored by reinnervation with brain stem laryngeal motoneurons. In 10 anesthetized cats, the right recurrent laryngeal nerve (RLN) was cut and anastomosed to the distal stump of either one or both roots (C5-C6) of the ipsilateral phrenic nerve. Three to four months later, reinnervation was assessed under deep anesthesia by the reappearance in the paralyzed diaphragm of 1) direct electromyographic (EMG) responses after electrical stimulation of the RLN and 2) spontaneous inspiratory bursts. Serial radiography, performed on five animals, revealed diaphragmatic excursions of comparable amplitude on the normal and reinnervated sides. Six to twelve months after anastomosis, laparotomy (performed under Nembutal anesthesia) allowed inspection and EMG recording of the spontaneous inspiratory contractions of the reinnervated areas and their sustained responses to tetanic RLN stimulation. Inspiratory discharges showed a ramplike recruitment similar to that of the normal diaphragm. Although the RLN contains a number of expiratory axons, multiple-site recordings disclosed expiratory EMG discharges only once. Histological analysis confirmed the substitution of phrenic axons by regenerating RLN fibers.

Incidence and Natural History of Phrenic Neuropathy Occurring During Open Heart Surgery

To study the incidence of phrenic neuropathy following coronary artery bypass grafting and determine long-term outcome. Prospective observational. Surgical ICU in a university hospital, out-patient follow-up. Ninety-two consecutive patients undergoing open heart surgery. None. Chest radiographs (CXR) 48 to 72 h post-operatively, ultrasonography of diaphragm, phrenic nerve conduction studies, diaphragmatic electromyogram, each repeated every 1 to 3 months until normal. Seventy-eight of 92 (78 percent) patients had abnormal radiographs, 42 of 78 (54 percent) with abnormal CXRs had abnormal diaphragm motion, 24 of 42 (57 percent) with abnormal motion had phrenic neuropathy. Patients with normal diaphragm motion improved faster than those without; patients with normal nerve conduction (and abnormal motion) improved faster than those with abnormal nerve conduction. Phrenic neuropathy is relatively common if sensitive tests are utilized for diagnosis. Nerve conduction studies can predict duration of morbidity. Most patients have low morbidity and recover fully. Abnormal diaphragm motion alone is not diagnostic of phrenic nerve injury.

Pulmonary vascular abnormalities in experimentally induced congenital diaphragmatic hernia in rats

In infants with congenital diaphragmatic hernia (CDH), abnormalities of the pulmonary arteries are present consisting of increased medial wall thickness and decreased external diameter. This forms the morphological substrate for persistent pulmonary hypertension, one of the leading causes of the high mortality in these patients. To elucidate the significance of these abnormalities, experimental models are required that mimic as close as possible the human situation. In our rat model we are able to study the hypoplastic CDH lungs extensively. In this study we performed a histological evaluation of the pulmonary arterial bed in the control group and the nitrofen-treated group in which the latter was divided into two subgroups, CDH and normal diaphragm. We examined the newborn rats after perfusion of the pulmonary arteries with barium gelatine and subsequent fixation. At the level of the respiratory bronchioles significant differences in the vessels were found consisting of decreased external diameter and increased wall thickness as percentage of the external thickness in CDH lungs compared with controls. Abnormal muscularization of the peripheral branches of the CDH pulmonary arteries was also found. We concluded that the rat model strongly resembles the human situation concerning the arterial bed in the lungs.

Coordinated development of myofibrils, sarcoplasmic reticulum and transverse tubules in normal and dysgenic mouse skeletal muscle, in vivo and in vitro

We studied the development of transverse (T)-tubules and sarcoplasmic reticulum (SR) in relationship to myofibrillogenesis in normal and dysgenic ( mdg mdg ) mouse skeletal muscle by immunofluorescent labeling of specific membrane and myofibrillar proteins. At E16 the development of the myofibrils and membranes in dysgenic and normal diaphragm was indistinguishable, including well developed myofibrils, a delicate network of T-tubules, and a prominent SR which was not yet cross-striated. In diaphragms of E18 dysgenic mice, both the number and size of muscle fibers and myofibrillar organization were deficient in comparison to normal diaphragms, as previously reported. T-tubule labeling was abnormal, showing only scattered tubules and fragments. However, many muscle fibers displayed cross striation of sarcomeric proteins and SR comparable to normal muscle. In cultured myotubes, cross-striated organization of sarcomeric proteins proceeded essentially in two stages: first around the Z-line and later in the A-band. Sarcomeric organization of the SR coincided with the first stage, while the appearance of T-tubules in the mature transverse orientation occurred infrequently, only after A-band maturation. In culture, myofibrillar and membrane organization was equivalent in normal and dysgenic muscle at the earlier stage of development, but half as many dysgenic myotubes reached the later stage as compared to normal. We conclude that the mdg mutation has little effect on the initial stage of membrane and myofibril development and that the deficiencies often seen at later stages result indirectly from the previously described absence of dihydropyridine receptor function in the mutant.

Effects of neuroleptic agents on rat skeletal muscle contracture in vitro.

The purpose of this investigation was to examine and compare the effects of both in vivo pretreatment and in vitro treatment with the neuroleptic agents droperidol, haloperidol, and trifluoperazine on skeletal muscle contracture using an in vitro model. Strips of normal rat diaphragm were challenged with succinylcholine and halothane (halothane: 1% and 3%) subsequent to either in vitro administration (10-100 microM) or in vivo pretreatment (0.35-2.80 mg/kg) with droperidol, haloperidol, or trifluoperazine. After equilibration, maximum increases in tension were recorded and mean data analyzed by analysis of variance (P less than 0.05). When either droperidol or trifluoperazine was administered in vivo, contracture values after exposure to succinylcholine and halothane were significantly decreased. After in vivo pretreatment with haloperidol or in vitro administration of droperidol, succinylcholine-induced contractures were significantly reduced; contractures subsequently induced by halothane did not significantly differ from that of controls. In vitro treatment with haloperidol and trifluoperazine, however, produced significant increases in tension in muscles exposed to succinylcholine and halothane. This study provides evidence that droperidol may be considered a safe anesthetic adjunct in malignant hyperthermia-susceptible patients, and, additionally, that caution should be exercised when interpreting results from studies in which contracture testing is performed on muscle from patients treated with neuroleptic agents.

Aminophylline and human diaphragm strength in vivo

The transdiaphragmatic pressure (Pdi) twitch response to single shocks from supramaximal bilateral phrenic nerve stimulation was studied before and after acute intravenous infusions of aminophylline [14.9 +/- 3.1 (SD) micrograms/ml] in nine normal subjects. Stimulation was performed with subjects in the sitting position against an occluded airway from end expiration. Baseline gastric pressure and abdominal and rib cage configuration were kept constant. There was no significant difference in peak twitch Pdi from the relaxed diaphragm between control (38.8 +/- 3.3 cmH2O) and aminophylline (40.2 +/- 5.2 cmH2O) experiments. Other twitch characteristics including contraction time, half-relaxation time, and maximum relaxation rate were also unchanged. The Pdi-twitch amplitude at different levels of voluntary Pdi was measured with the twitch occlusion technique, and this relationship was found to be similar under control conditions and after aminophylline. With this technique, maximum Pdi (Pdimax) was calculated as the Pdi at which stimulation would result in no Pdi twitch because all motor units are already maximally activated. No significant change was found in mean calculated Pdimax between control (146.9 +/- 27.0 cmH2O) and aminophylline (149.2 +/- 26.0 cmH2O) experiments. We conclude from this study that the acute administration of aminophylline at therapeutic concentrations does not significantly affect contractility or maximum strength of the normal human diaphragm in vivo.

Three myosin heavy chain isoforms in type 2 skeletal muscle fibres

Mammalian skeletal muscles consist of three main fibre types, type 1,2A and 2B fibres, with different myosin heavy chain (MHC) composition. We have now identified another fibre type, called type 2X fibre, characterized by a specific MHC isoform. Type 2X fibres, which are widely distributed in rat skeletal muscles, can be distinguished from 2A and 2B fibres by histochemical ATPase activity and by their unique staining pattern with seven anti-MHC monoclonal antibodies. The existence of the 2X-MHC isoform was confirmed by immunoblotting analysis using muscles containing 2X fibres as a major component, such as the normal and hyperthyroid diaphragm, and the soleus muscle after high frequency chronic stimulation. 2X-MHC contains one determinant common to 2B-MHC and another common to all type 2-MHCs, but lacks epitopes specific for 2A- and 2B-MHCs, as well as an epitope present on all other MHCs. By SDS-polyacrylamide gel electrophoresis 2X-MHC shows a lower mobility compared to 2B-MHC and appears to comigrate with 2A-MHC. Muscles containing predominantly 2X-MHC display a velocity of shortening intermediate between that of slow muscles and that of fast muscles composed predominantly of 2B fibres.

Oesophageal Pressures during Maximal Sniff in Subjects with Normal Diaphragm Strength

Oesophageal Pressures during Maximal Sniff in Subjects with Normal Diaphragm Strength

Acetylcholine-sensitivity in fast and slow twitch muscle of normal and dystrophic (C57 BL/6J dy2J/dy2J) mice.

Small bundles of muscle fibres were isolated from diaphragm, extensor digitorum longus (EDL) and soleus (SOL) muscles of normal and dystrophic (C57 BL/6J dy2J/dy2J) mice, and their isometric tension developed in response to acetylcholine (ACh) was recorded. For each type of muscle the relationship between the maximum amplitude of the ACh-contracture and log [ACh] was similar in normal and dystrophic animals. However, this relationship was steeper for normal and dystrophic SOL than for EDL and diaphragm muscles. Dystrophy did not induce changes in the time course of the ACh-contractures, except a significant 'speeding' of dystrophic SOL that appeared in the time to peak of the contractile response. The amplitude of ACh-contractures of both normal and dystrophic diaphragm preparations increased by about 50% after perfusion for 80-90 min in physiological solution containing phospholipase C 5 mU/ml. ACh-sensitivity was measured in normal and dystrophic diaphragm preparations by iontophoretic application of ACh from high resistance pipettes. ACh-potentials were similar in time course in the two types of muscle fibres, and there was also no significant difference in the length of sensitive fibre segments and maximum sensitivity values. Extrajunctional ACh-sensitivity was absent in normal as well as in dystrophic fibres. It is concluded that the absence in dystrophic muscles of stronger ACh-contractures and of extrajunctional sensitivity can be considered as evidence against a primary neuronal involvement in murine dystrophy of the dy2J strain.

Effect of aminophylline on the human diaphragm.

The effect of intravenous aminophylline on the contractile function of the diaphragm was studied in four normal subjects. The contractility of the diaphragm was assessed by the measurement of transdiaphragmatic pressure (Pdi) after right phrenic nerve stimulation at 1 Hz. Pdi was measured before and during aminophylline infusion (6 mg/kg over 30 minutes), during which therapeutic concentrations of theophylline were attained (mean 13.8 mg/l, range 8.5-20.2). The Pdi achieved was not affected by aminophylline. This result suggests that theophylline at therapeutic concentrations has little effect on the contractility of the normal human diaphragm.

The Diaphragmatic Echo Complex: An In Vitro Study

The brightly echogenic appearance of the diaphragm on routine clinical scans is not easily reconciled with the well-documented echo-poor appearance of muscle elsewhere in the body. A series of specimens of normal human diaphragm freshly excised at autopsy were suspended in a water bath. Articulated arm scans were done varying the angle of the incident beam to the specimen by 5-degree increments and recording the maximum attenuation which allowed visualization (ie, an extinction point). This was accomplished for intact diaphragm, peritoneal membrane alone, and diaphragmatic muscle alone with both membranes stripped. The bright specular echoes seen are due almost exclusively to the membranes (parietal pleura and peritoneum) and the diaphragmatic muscle itself produces only low-level scattered echoes as elsewhere. However, these scattered echoes account for persistent visualization of the diaphragm at steep angles of the incident beam. A considerable portion of the in vivo thickness of the diaphragmatic echo complex is, therefore, produced by diaphragm-lung interface.

FETAL AUDITORY RESPONSES

The eyelids, midface, and mouth are monitored ultrasonically during transuterine vibroacoustic stimulation. The test sequence is an orienting, .5 second noise burst (150-1600 Hz, 100 dB), followed after 30 seconds with 10 bursts spaced one second apart. We have shown previously that motor responses begun abruptly at 24½ weeks gestational and are elicited invariably by 28 weeks in normal fetuses. Head aversion, eyelid, and mouth movements are dissociated initially. By 28 weeks these startle components are linked. We now report decremental response after 32 weeks for head aversion (but not eyeblink), which is exponential with gestational age. The effect may represent discriminatory response threshold, progressive cerebral modification of a midbrain response mechanism, or a type of prestimulus inhibition. Deafness is diagnosed by absence of any response in the presence of normal eye and diaphragm movements (or other indicator of wellbeing). Declining fetal condition is associated with irritability, reversal of startle decrement, and finally, loss of responsiveness. Delayed response patterns were seen in individual cases of fetal alcohol and marijuana sydromes, triplody, trisomy 18, and 3 cases of hydrocephalus, but not in one case of Down's syndrome.

A comparative study of contractile responses in diaphragm muscles of normal and dystrophic ( [formula omitted]) mice

Potassium and caffeine contractures of isolated small bundles (100 to 200 μm diameter) of muscle fibers isolated from the diaphragm of normal and dystrophic ( C57BL 6J dy 2J dy 2J ) mice were compared. In diaphragms of pathologic mice (3 to 5 months old) the resting potential, the characteristics of the twitch, and some histological examinations were typical of dystrophic muscles. The slopes of the relationships between the steady membrane potential and log [K] 0 were similar for the two types of cells. In 110 m M and 146 m M K there were no significant differences in the time course of the contractures and reduction in [Ca] 0 decreased the time to peak and the time constant of relaxation to the same extent; the relative efficiency of [Mg] 0 compared with [Ca] 0 was equivalent. Repriming of K contractures at different external calcium concentrations indicated that the normal diaphragm did not have any special advantage. The exposure of isolated strips to a solution containing caffeine resulted in a similar increase of the strength of the regularly evoked twitch responses. However, the contractures elicited by 1.25 to 20 m M caffeine showed a subsensitivity of the dystrophic diaphragm ( K mDys = 9.3 K mN) and the rate of relaxation was significantly slower than in normal muscle (in 20 m M caffeine, 50% decay time for normal muscle was 25.2 ± 7.6 s and for dystrophic muscle 54.8 ± 11.2 s. THese results suggest an absence of major alterations in the mechanism of excitation-contraction coupling associated with dystrophy, except for a change in the specific element of the sarcoplasmic reticulum where caffeine acts.

Distribution and quantification of ACh receptors and innervation in diaphragm muscle of normal and mdg mouse embryos

Muscular dysgenesis ( mdg) in the mouse is an autosomal recessive mutation, expressed in the homozygous state ( in vivo and in vitro) as an absence of skeletal muscle contraction. The distribution of acetylcholine receptors (ACh R) in the diaphragms of phenotypically normal and dysgenic ( mdg mdg ) embryos was studied from the 14th to 19th day of gestation by binding of 125I-α-bungarotoxin to the muscle, followed by autoradiography of longitudinally sectioned hemidiaphragms and/or of isolated muscle fibers. Localization of ACh R at putative motor end-plate regions begins 14 to 15 days in utero in both normal and dysgenic diaphragms. The distribution of high ACh R density patches is aberrantly scattered beyond the normal innervation pattern in dysgenic diaphragms. Isolated mutant fibers possess (1) multiple ACh R clusters, up to five per single fiber, (2) larger clusters of more variable morphology and variable receptor density than normal clusters, and (3) higher levels of extrajunctional receptors than normal fibers. These autoradiographic results correlate well with higher total level of toxin binding sites per diaphragm and per milligram protein in dysgenic vs normal muscle, as quantified from γ counting of sucrose density gradient isolation of 125I-toxin-ACh R complexes. The dispersed distribution of ACh R patches on dysgenic muscle may be correlated with extensive phrenic nerve branching as demonstrated by silver impregnation technique. We suggest that the aberrant ACh R cluster distribution is a result of multiple innervation of single fibers from the branched nerve terminals. Possible causes of the excessive nerve branching in the mutant are discussed in light of generalized nerve sprouting found in paralyzed muscle.

<b>EFFECTS OF RYANODINE AND IODOACETAMIDE ON NORMAL AND DYSTROPHIC C57 BL MOUSE DIAPHRAGM </b><b>MUSCLES </b>

The effects of ryanodine and iodoacetamide were examined on bundles isolated from diaphragm muscles of normal and dystrophic mice (C57 BL 6J strains). At 22°C, the addition of ryanodine or iodoacetamide for external concentrations higher than 10-7 M and 5 × 10-4 M respectively produced an irreversible increase in the resting tension after a period of 20-40 min. For both drugs the latent period was reduced if K-contractures were generated simultaneously. However, in the presence of ryanodine the phasic K-contracture was followed by a slow and transient increase in tension. The peak value of this second phase related to the amplitude of the 110 mM K-contracture was always smaller in dystrophic than in normal diaphragm muscle. Using lower concentrations, the effects of the two drugs were examined on the repriming of 110 mM [K]0-contractures. Following application of iodoacetamide (5-10-6 M to 10-4 M) the recovery time was increased to the same extent in both types of muscle. By contrast, for a given amount of ryanodine, the rate of repriming was more affected in normal than in dystrophic muscles. It is proposed that ryanodine acts at a specific site of the terminal cisternae from the sarcoplasmic reticulum (SR) where dystrophy induces pathological modifications.

Decrease of the spontaneous non-quantal release of acetylcholine from the phrenic nerve in botulinum-poisoned rat diaphragm

Botulinum type A toxin (BoTx) has been found to diminish by 40% the spontaneous release of acetylcholine (ACh) from normal (acutely denervated) rat diaphragms incubated in the presence of 5 mM K+, while the release of ACh from chronically (4 days) denervated diaphragms was not affected during 2 h incubations. The toxin has been found to rapidly remove (within 10 min) the local depolarization of about 8 mV which developed in the end-plate zones of the diaphragms after the inhibition of cholinesterases; after the administration of BoTx, tubocurarine lost its ability to increase the resting membrane potential (H-response, Katz and Miledi 1977) in the end-plate area of anticholinesterase-treated muscles. It is concluded that BoTx inhibits the non-quantal release of ACh from the motor nerve fibres and that it probably acts directly on the nerve terminal surface membrane (without internalization). The H-response in the rat diaphragm reflects the non-quantal release of ACh from the nerve terminals and not from the muscle fibres.

Denervation increases the degradation rate of acetylcholine receptors at end‐plates in vivo and in vitro.

We have studied the effect of denervation on the degradation of the existing junctional acetylcholine (ACh) receptors at end-plates in rat muscles. ACh receptors were labelled by injecting animals with iodinated alpha-bungarotoxin (I-alpha BT); 1 day later the left hemidiaphragm was denervated. The degradation of bound I-alpha BT in normal and denervated muscles was examined in organ culture, beginning at various times after denervation in vivo. The original, pre-labelled end-plate ACh receptors are degraded more rapidly after denervation. The rate of degradation begins to increase shortly after the nerve is cut and reaches a maximum value at about 9 days of denervation. Muscles denervated only on transfer to organ culture also show an increase in the degradation rate of bound I-alpha BT with increasing time of denervation (time in culture). In normal diaphragm muscles, the initial rate of degradation of functional ACh receptors, after correcting for non-degradative loss of I-alpha BT, is 0.0018 h-1 (t1/2 = 383 h). The maximal rate at denervated end-plates is 0.0073 h-1 (t1/2 = 94 h). For soleus, sternomastoid, plantaris and intercostal innervated muscles the apparent rate of ACh receptor degradation either in vitro or in vivo ranged from 0.0005 h-1 to 0.002 h-1. The rate of loss of bound I-alpha BT in vivo is more rapid at denervated end-plates than at innervated end-plates. For diaphragm muscles, the rates of I-alpha BT degradation measured in organ culture are able to describe the relative rates of loss of I-alpha BT from innervated and denervated muscles in vivo. At short times after labelling, a fraction (10-20%) of the I-alpha BT bound to innervated muscles is degraded more rapidly than the remaining toxin. The possibility that these I-alpha BT binding sites are degraded at the rate characteristic of extrajunctional receptors on denervated muscle fibres is discussed.

The synthesis and release of acetylcholine in normal and denervated rat diaphragms during incubation in vitro.

1. Normal and denervated rat diaphragms and neural (central) and aneural (peripheral) parts of normal diaphragms were incubated under several different conditions likely to affect the metabolism of acetylcholine (ACh), with the aim of discovering specific features of the control of neural and aneural ACh in the muscle. The concentrations of ACh in the tissue and the medium were measured at the end of the incubations using a radioenzymatic assay, and the amount of ACh synthesized during the incubations was calculated by subtracting the initial amount of ACh present in the tissue from that found in the tissue plus the medium at the end of the incubations.2. Confirming earlier results obtained with bioassays, it was found that, in a medium with 5 mM-K(+) and 2.5 mM-Ca(2+), denervated diaphragms released ACh into the medium at a rate equal to 47% of that observed in normal diaphragms; the amount of ACh released from aneural parts of normal diaphragms was 51% of that released from their neural parts. The release from normal diaphragms was increased (83%) in a Ca(2+)-dependent manner by raising the concentration of K(+) to 30 mM. In the denervated diaphragms, 30 mM-K(+) brought about a Ca(2+)-independent increase (67%) in the rate of ACh release. The elevation of K(+) was without effect on the release of ACh from aneural parts of normal diaphragms.3. The results indicate that a Ca(2+)-dependent mechanism of ACh release, known to function in the nerve terminals, is not likely to participate in the efflux of ACh from the muscle fibres. The K(+)-induced but Ca(2+)-independent enhancement of ACh release from the denervated diaphragms probably occurs by diffusion of ACh along the altered electrochemical gradient. It is suggested that the surface membranes of the muscle fibres become more permeable to ACh after denervation.4. During incubations with 30 mM-K(+) and 10 muM-hemicholinium-3 (HC-3), an inhibitor of the carrier-mediated transport of choline, the rates of ACh release and synthesis in normal diaphragms were diminished to the levels found in the denervated diaphragms, in which the concentration, release and synthesis of ACh were not affected by HC-3. The synthesis of aneural ACh thus appears to be independent of the carrier-mediated supply of choline across cell membranes.5. The release of ACh from normal diaphragms incubated with 5 mM-K(+) was increased in the presence of 100 muM-ouabain, whereas the release from denervated diaphragms was not affected. This finding suggests that the mechanism of ACh release that is activated by ouabain in the nerve cells involves, in addition to the inhibition of Na(+)-K(+)-ATPase, some other steps which are not operative in the muscle fibres.6. The results corroborate earlier evidence indicating that aneural ACh is produced, stored and released in the diaphragms. They fit the view that the aneural ACh is located in the cytoplasm of the muscle fibres and that it leaves the muscle fibres by molecular ;leakage' rather than by a specialized release mechanism. The efflux of ACh from the muscle fibres is likely to constitute about 50% of the total resting efflux (release) of ACh from normal diaphragms.

Normal ventilatory movement of the right hemidiaphragm studied by ultrasonography and pneumotachography.

The ventilatory movement of the right dome of the diaphragm was studied over the range of the inspiratory capacity in 50 healthy adults in the supine position using simultaneous ultrasonography and pneumotachography. Regional differences were found in movement of the hemidiaphragm; there was greater movement of the middle and posterior thirds of the diaphragm than of the anterior third. A significant positive correlation was found between body weight and amount of diaphragm movement. An apparently greater degree of movement of the diaphragm was found in males than females; this may be related to weight. About 64% of diaphragm movement has occurred by the time midinspiratory capacity is reached. These data may help to define normal movement and also to differentiate abnormal from normal diaphragm movement.