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PubMed1999

Activation of respiratory afferents by resistive loaded breathing modifies somatosensory evoked potentials to median nerve stimulation in humans.

The cortical projections of respiratory afferents (vagus and respiratory muscle nerves) are well documented in humans. It is also shown that their activation during loaded breathing modifies the perception of tactile sensation as well as the motor drive to skeletal muscles. The effects of expiratory or inspiratory loaded breathing on somatosensory evoked potentials (SEPs) elicited by median nerve stimulation were studied in eight healthy subjects. No significant changes occurred in latencies of N20, N30 and P40 throughout the expiratory loading period, except for a significant lengthening in P1 latency compared with unloaded breathing. However, inspiratory loading induced a significant increase in peak latency of N20, N30 and P40 components. We suggest that projections of inspiratory afferents from the diaphragm and the intercostal muscles, activated by inspiratory loading, could be responsible for the lengthened latency of median nerve SEP components. Thus, respiratory afferents very likely interact with pathways of the somatosensory system.

Adult↗
PubMed1992

Effect of respiratory muscle tension on lung volume.

The chest wall is modeled as a linear system for which the displacements of points on the chest wall are proportional to the forces that act on the chest wall, namely, airway opening pressure and active tension in the respiratory muscles. A standard theorem of mechanics, the Maxwell reciprocity theorem, is invoked to show that the effect of active muscle tension on lung volume, or airway pressure if the airway is closed, is proportional to the change of muscle length in the relaxation maneuver. This relation was tested experimentally. The shortening of the cranial-caudal distance between a rib pair and the sternum was measured during a relaxation maneuver. These data were used to predict the respiratory effect of forces applied to the ribs and sternum. To test this prediction, a cranial force was applied to the rib pair and a caudal force was applied to the sternum, simulating the forces applied by active tension in the parasternal intercostal muscles. The change in airway pressure, with lung volume held constant, was measured. The measured change in airway pressure agreed well with the prediction. In some dogs, nonlinear deviations from the linear prediction occurred at higher loads. The model and the theorem offer the promise that existing data on the configuration of the chest wall during the relaxation maneuver can be used to compute the mechanical advantage of the respiratory muscles.

Body Weight↗
PubMed1998

Mechanical advantage of the canine diaphragm.

The mechanical advantage (mu) of a respiratory muscle is defined as the respiratory pressure generated per unit muscle mass and per unit active stress. The value of mu can be obtained by measuring the change in the length of the muscle during inflation of the passive lung and chest wall. We report values of mu for the muscles of the canine diaphragm that were obtained by measuring the lengths of the muscles during a passive quasistatic vital capacity maneuver. Radiopaque markers were attached along six muscle bundles of the costal and two muscle bundles of the crural left hemidiaphragms of four bred-for-research beagle dogs. The three-dimensional locations of the markers were obtained from biplane video-fluoroscopic images taken at four volumes during a passive relaxation maneuver from total lung capacity to functional residual capacity in the prone and supine postures. Muscle lengths were determined as a function of lung volume, and from these data, values of mu were obtained. Values of mu are fairly uniform around the ventral midcostal and crural diaphragm but significantly lower at the dorsal end of the costal diaphragm. The average values of mu are -0.35 +/- 0.18 and -0.27 +/- 0.16 cmH2O. g-1. kg-1. cm-2 in the prone and supine dog, respectively. These values are 1. 5-2 times larger than the largest values of mu of the intercostal muscles in the supine dog. From these data we estimate that during spontaneous breathing the diaphragm contributes approximately 40% of inspiratory pressure in the prone posture and approximately 30% in the supine posture. Passive shortening, and hence mu, in the upper one-third of inspiratory capacity is less than one-half of that at lower lung volume. The lower mu is attributed primarily to a lower abdominal compliance at high lung volume.

Animals↗
PubMed1979

Thoracic dorsal rhizotomy in the anesthetized cat: maintenance of eupnic breathing.

In order to assess the level of participation of thoracic afferents in the determination of the eupnic breathing pattern, thoracic dorsal rhizotomies from T1 through T13 were performed in cats anesthetized with alpha-chloralose or sodium pentobarbital, with or without intact vagi. While recording several respiratory parameters, no consistent changes in the spontaneous breathing pattern could be demonstrated either 10--20 min or 90--100 min following disruption of thoracic afferent input. Thus, respiratory frequency, tidal volume and total ventilation were unaffected by rhizotomy. Inspiratory (TI) and expiratory (TE) durations and TI/TE ratios remained constant. Tracheal air flows during inspiration and expiration and intrapleural pressure were not altered. Finally, end-expiratory %CO2 and %O2 did not change after section of the thoracic dorsal roots. Only arterial blood pressure was found to fall as a function of time into the experiment. Since the results were identical in vagotomized and in vagi intact preparations, thoracic reflexes were not being masked by vagal dominance in eupnea. Rather, thoracic afferents, including intercostal muscle spindle afferents, appear to be ineffective in shaping the pattern of quiet breathing in anesthetized cats. This is unlike situations of loaded or stressed breathing where these afferents assume a more active role in the modulation of rate and depth mechanisms.

Afferent Pathways↗
PubMed2004

The novel mouse connexin39 gene is expressed in developing striated muscle fibers.

The recently identified mouse connexin39 (mCx39) gene encodes a peptide of 364 amino acids that shows only 61% sequence similarity to its putative human orthologue connexin40.1 (hCx40.1). The coding regions of mCx39 and hCx40.1 are located on two different exons as described for murine and human connexin36. Northern blot and RT-PCR analyses revealed that mCx39 is expressed after embryonic day (ED) 13.5 up to birth and is absent from the adult stage. Polyclonal antibodies raised to a peptide corresponding to the 16 C-terminal amino acid residues detected a protein band of about 40 kDa apparent molecular mass in lysates of several embryonic tissues. In sections of ED14.5, ED16.5 and neonatal (P0) tissues, immunofluorescent signals were prominent between myotubes in the developing diaphragm, within the intercostal muscle, in the region around the occipital bone, as well as in muscles of the limb, tongue and connective tissue around the eye. These antibodies yielded punctate signals on apposed plasma membranes of HeLa cells transfected with Cx39 cDNA but did not react with wild-type cells. Furthermore, no intercellular permeation of microinjected neurobiotin and other tracers could be detected in Cx39 transfected HeLa cells. However, after microinjection of Alexa488 into myotubes of dissected neonatal diaphragm, we found spreading of this dye into neighbouring cells. As expression of no other known connexin could be verified in these cells, intercellular dye transfer might result from functional expression of Cx39 in developing striated muscle fibers.

Amino Acid Sequence↗
PubMed2004

Electrophysiological and morphological characterization of a case of autosomal recessive congenital myasthenic syndrome with acetylcholine receptor deficiency due to a N88K rapsyn homozygous mutation.

Congenital myasthenic syndromes are rare heterogeneous hereditary disorders, which lead to defective neuromuscular transmission resulting in fatigable muscle weakness. Post-synaptic congenital myasthenic syndromes are caused by acetylcholine receptor kinetic abnormalities or by acetylcholine receptor deficiency. Most of the congenital myasthenic syndromes with acetylcholine receptor deficiency are due to mutations in acetylcholine receptor subunit genes. Some have recently been attributed to mutations in the rapsyn gene. Here, we report the case of a 28-year-old French congenital myasthenic syndrome patient who had mild diplopia and fatigability from the age of 5 years. His muscle biopsy revealed a marked reduction in rapsyn and acetylcholine receptor at neuromuscular junctions together with a simplification of the subneural apparatus structure. In this patient, we excluded mutations in the acetylcholine receptor subunit genes and identified the homozygous N88K rapsyn mutation, which has already been shown by cell expression to impair rapsyn and acetylcholine receptor aggregation at the neuromuscular junction. The detection of the N88K mutation at the heterozygous state in five of 300 unrelated control subjects shows that this mutation is not infrequent in the healthy population. Electrophysiological measurements on biopsied intercostal muscle from this patient showed that his rapsyn mutation-induced fatigable weakness is expressed not only in a diminution in acetylcholine receptor membrane density but also in a decline of endplate potentials evoked at low frequency.

Adult↗
PubMed1977

Neonatal chest wall afferents and regulation of respiration.

We have studied two groups of eight preterm infants, relating chest wall afferent information to respiratory timing. Rib cage and abdominal motion were monitored by magnetometers and flow and tidal volume via a face mask. In the first group, studies were done in REM sleep when spontaneously occurring distortion of the rib cage occurred and a significant linear relationship between the rate of distortion of the chest wall and shortening of the inspiratory time (Ti) was found in all infants. Reduction in this distortion by the use of continuous positive airway pressure (CPAP) or continuous negative pressure at the body surface (CNeg) was associated with a significant (P less than 0.01) lengthening of Ti. Absence of changes in Ti when pressure was applied in quiet sleep suggested that lung volume or chemical changes were not involved. In the second group of infants we artificially generated the afferent inflow by using vibratory stimuli applied in one intercostal interspace and produced a significant (P less than 0.05) shortening in Ti. We suggest that the distortion of the rib cage in REM sleep generates afferent information from intercostal muscle spindles that is related to the rate of distortion and this, via a supraspinal reflex, inhibits phrenic motoneuron discharge. It may then be of importance in the etiology of apneic episodes in these infants. Applied pressure may be of benefit because it reduces an inhibitory afferent inflow.

Afferent Pathways↗
PubMed1992

Changes in respiratory muscle activity in conscious cats during experimental dives at 101 ATA.

The rationale for the present study was to test the hypothesis that increased work of breathing during experimental deep diving may lead to respiratory muscle fatigue. For this purpose, electromyograms (EMGs) of respiratory and skeletal muscles, plus electrocardiogram and electroencephalogram (EEG) derivatives, were continuously recorded in conscious cats. In each muscle group, the ratio of power in a high (H) to that in a low (L) band of EMG frequencies was computed. Direct diaphragmatic stimulation in selected animals produced a mass action potential to obtain the muscle fiber conduction velocity (MFCV). The maximal pressure was 101 ATA (1,000 msw) with a maximal duration of 72 h. Four cats breathed an He-O2 mixture and five others a ternary mixture (10% N2 in He-O2). Inspired O2 partial pressure was 350 Torr. With the He-O2 mixture, all the animals died within 2-54 h during the study at maximal depth. EEG signs of high-pressure nervous syndrome (HPNS) were present in all cats, and low-frequency (11-14 Hz) hyperbaric tremor discontinuously contaminated all EMG tracings. The H/L ratio computed from diaphragmatic and intercostal muscle EMGs increased after 12 h at 101 ATA. With the He-N2-O2 mixture, the cats survived until the end of the sojourn at 101 ATA, during which no hyperbaric tremor was detected from EMG tracings, and EEG signs of HPNS were weak or absent. From 31 ATA, the H/L ratio decreased significantly in respiratory but not in skeletal muscles; this was associated with decreased MFCV in the diaphragm after several hours at maximal depth.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Disruption of the mouse MRF4 gene identifies multiple waves of myogenesis in the myotome.

MRF4 (herculin/Myf-6) is one of the four member MyoD family of transcription factors identified by their ability to enforce skeletal muscle differentiation upon a wide variety of nonmuscle cell types. In this study the mouse germline MRF4 gene was disrupted by targeted recombination. Animals homozygous for the MRF4bh1 allele, a deletion of the functionally essential bHLH domain, displayed defective axial myogenesis and rib pattern formation, and they died at birth. Differences in somitogenesis between homozygous MRF4bh1 embryos and their wild-type littermates provided evidence for three distinct myogenic regulatory programs (My1-My3) in the somite, which correlate temporally and spatially with three waves of cellular recruitment to the expanding myotome. The first program (My1), marked initially by Myf-5 expression and followed by myogenin, began on schedule in the MRF4bh1/bh1 embryos at day 8 post coitum (E8). A second program (My2) was highly deficient in homozygous mutant MRF4 embryos, and normal expansion of the myotome failed. Moreover, expression of downstream muscle-specific genes, including FGF-6, which is a candidate regulator of inductive interactions, did not occur normally. The onset of MyoD expression around E10.5 in wild-type embryos marks a third myotomal program (My3), the execution of which was somewhat delayed in MRF4 mutant embryos but ultimately led to extensive myogenesis in the trunk. By E15 it appeared to have largely compensated for the defective My2 program in MRF4 mutants. Homozygous MRF4bh1 animals also showed improper rib pattern formation perhaps due to the absence of signals from cells expressing the My2 program. Finally, a later and relatively mild phenotype was detected in intercostal muscles of newborn animals.

Animals↗
PubMed1985

Respiratory muscle and organ blood flow with inspiratory elastic loading and shock.

Since respiratory muscles fail when blood flow is inadequate, we asked whether their blood flow would be maintained in severe hypotensive states at the expense of other vital organs (brain, heart, kidney, gut, spleen). We measured blood flow (radiolabeled microspheres) to respiratory muscles and vital organs in 11 dogs breathing against an inspiratory elastic load, first with normal blood pressure (BP) and then hypotension produced by cardiac tamponade. With the elastic load alone, there was no change in BP or cardiac output; diaphragmatic blood flow (Qdi) increased from 12.8 +/- 7.0 to 34.1 +/- 15.6 ml/100 g, and total respiratory muscle flow (QTR) increased from 56.5 +/- 19.1 to 97.4 +/- 36.5 ml/100 g, but except for the brain, there was no change in blood flow to other organs. With tamponade (mean BP = 79 +/- 16 mmHg), flow decreased to all organs, whereas Qdi (39.0 +/- 19.4) did not change. QTR decreased, but not significantly, to 88.6 +/- 49.5. With more tamponade (mean BP = 53 +/- 13 mmHg), flow to all vital organs decreased as well as QTR (57.9 +/- 47.18), but Qdi did not significantly decrease and had the same relationship to respiratory force as with normal BP. Thus, with severe inspiratory elastic loading and severe hypotension, the diaphragm and external intercostal muscles did most of the respiratory work, and their flow was maintained at the expense of other vital organs.

Animals↗
PubMed1988

Lung function disturbances versus respiratory muscle fatigue in patients with systemic lupus erythematosus.

In 23 consecutive patients (mean age, 38.6 years) with systemic lupus erythematosus (SLE) and in 17 healthy subjects (mean age, 37.5 years) fatigue of respiratory (diaphragm, musculi intercostales externi) and leg muscles (musculus gastrocnemius) was determined comparatively by electromyography. Additionally, routine lung function parameters, including maximum inspiratory (PImax) and expiratory (PEmax) mouth pressures, were measured. The SLE patients showed lower values of vital capacity (VC), total lung capacity (TLC), thoracic gas volume (TGV), FEV1, PImax and PEmax than the healthy controls, while FEV1/VC, residual volume and specific airway conductance were not significantly different in either group. Lung compliance, corrected for TGV, was normal in the SLE group. Breathing through stenoses with increasing resistances resulted in fatigue of the diaphragm in 73% of the SLE group and in 41% of the control group. The corresponding values of the external intercostal muscles were 74% (SLE group) and 29% (control group). Electromyographic signs of respiratory and leg muscle fatigue occurred at lower loads in the SLE group than in the healthy subjects. The pattern of lung function data in patients with SLE was characteristic neither of lung restriction nor of airway obstruction. Respiratory muscle weakness can explain the decrease in TLC, VC, TGV, FEV1, PImax and PEmax.

Adult↗
PubMed1987

Expiratory neurons in the region of the retrofacial nucleus: inhibitory effects of intercostal tendon organs.

Intercostal muscle tendon organs have an inhibitory effect on the medullary neurons driving all inspiratory muscles, and on a subpopulation of medullary bulbospinal expiratory neurons. Results from this study showed that the activity of expiratory related neurons in the region of the retrofacial nucleus (Botzinger complex) decreases during tendon organ afferent stimulation; the response is similar to that of caudal bulbospinal expiratory neurons. We conclude that these expiratory neurons do not mediate the tendon organ inhibition of medullary inspiratory neuronal activity.

Action Potentials↗
PubMedDate not supplied

Neural prostheses in the respiratory system.

Approximately 5% of spinal cord-injured individuals suffer from respiratory muscle paralysis and require chronic mechanical ventilation. Unfortunately, this form of life support is associated with a number of undesirable side effects and discomforts. The only available alternative to mechanical ventilation is diaphragm pacing via bilateral phrenic nerve stimulation. This technique can provide patients with marked improvements in life quality and offers significant advantages compared to mechanical ventilation. Many patients, however, do not have bilateral phrenic function or are not willing to accept the risks inherent with phrenic nerve pacing and therefore are not candidates for this technique. Two alternative methods to ventilate patients with ventilator-dependent tetraplegia are reviewed in this paper. In patients with only a single functional phrenic nerve who are therefore not candidates for phrenic nerve pacing, combined intercostal muscle and unilateral phrenic nerve stimulation has recently been shown to maintain ventilatory support. In patients with bilateral phrenic nerve function, on-going studies suggest that intramuscular diaphragm pacing may be a useful alternative to direct phrenic nerve pacing. With the electrodes placed into the diaphragm laparoscopically, this method allows for the diaphragm to be activated without manipulation of the phrenic nerve, need for thoracotomy, or hospitalization. Both techniques provide benefits similar to that derived from bilateral phrenic nerve pacing and hold promise as alternative methods of ventilatory support in selected populations groups.

Animals↗
PubMed1995

Histamine-induced end-tidal inspiratory activity and lung receptors in cats.

Hyperinflation in acute asthma has been associated with inspiratory muscle activity, which persist during expiration. The main objective of the present study was to evaluate the role of rapidly adapting receptors (RARs), slowly adapting receptors (SARs) and C-fibre endings in generating end-tidal inspiratory activity (ETIA). ETIA was induced by intravenous administration of histamine and continuous negative airway pressure (CNAP) in anaesthetized, spontaneously breathing cats. To differentiate between reflex activities from the three types of lung receptors, both vagus nerves were cooled to eight different temperatures (Tvg) between 4 and 37 degrees C. It is known that CNAP stimulates RARs and inhibits SARs. Histamine was used to stimulate RARs, and this was combined with continuous positive airway pressure (CPAP) to further stimulate SARs. ETIA was evoked in the diaphragm and in parasternal intercostal muscles by both stimuli (histamine and CNAP) in 8 out of 18 cats. After vagotomy, neither histamine nor CNAP evoked ETIA any more. At Tvg = 37 degrees C, CPAP suppressed histamine-induced ETIA; whereas, this suppression was diminished at Tvg between 14 and 8 degrees C. ETIA sharply declined for Tvg between 8 degrees and 4 degrees C, and at Tvg = 4 degrees C ETIA had virtually disappeared. At Tvg = 37 degrees and 22 degrees C values of ETIA during CNAP were larger than those in response to histamine; whereas, at Tvg = 10 degrees C comparable ETIA values were obtained. It was shown that ETIA is a vagal reflex activity in which C-fibre endings are not involved. Histamine-induced ETIA originates from stimulation of RARs, and is inhibited by stimulation of SARs. Mechanical stimulation of RARs is a forceful stimulus to induce ETIA. This suggests that hyperinflation in acute asthma might be due, at least in part, to ETIA resulting from an imbalance between SAR and RAR activity.

Animals↗
PubMed1993

The effect of opioids on inspiratory muscle fatigue during inspiratory resistive loading.

The effect of opioids on inspiratory muscle function under high mechanical load is still unknown. Even less clear is the extent to which opioids influence the shift of the electromyographic power spectrum of the inspiratory muscles to lower frequencies during ventilatory stress. We studied seven healthy subjects breathing against high inspiratory threshold loads until exhaustion while keeping the minute ventilation constantly high. We compared runs with and without administration of 0.2 mg kg-1 of morphine sulphate intramuscularly; two subjects were given 30 mg morphine sulphate so that we could study the effect of higher opioid concentration. The endurance time (Tlim), the diaphragmatic electromyogram (EMG), the transdiaphragmatic pressures (Pdi) and the ventilatory effort sensation were analysed. Morphine did not have any effect on Tlim or on the effort sensation elicited by the inspiratory resistance in both concentrations. Analysing the spectral shifts of the diaphragmatic EMG, we did not find any significant difference in the decrease of the centroid frequency between drug and control runs. Furthermore, the activation pattern of the diaphragm and the intercostal muscles, evaluated from the percentage contribution of oesophageal and gastric pressures on the transdiaphragmatic pressure swings, did not change following the administration of morphine. Our study shows that morphine does not change the function of the inspiratory muscles during high-resistive breathing. Morphine does not affect the electromyographic power spectrum of the diaphragm during those resistive breathing runs, either. This points out that during stressful ventilatory situations, the shift of the electromyographic power spectrum is attributed to a peripheral (muscular) event consequent to muscle fatigue and not to the elaboration of endogenous opioids.

Adult↗
PubMed1994

Modification in activity of medullary respiratory-related neurons for vocalization and swallowing.

1. The medullary ventral respiratory group (VRG) in and near the nucleus ambiguus contains neurons related to respiration. Also found here are neurons related to vocalization and swallowing as well as motoneurons of laryngeal, pharyngeal, palatal, and esophageal muscles. Previous reports in anesthetized animals have characterized discharge properties of neurons as they relate to a single behavior, e.g., respiration. Relatively few studies have documented discharge properties during more than one behavior, e.g., respiration and swallowing. Neurons were recorded extracellularly from awake Macaca nemestrina monkeys engaged in a vocalization task. The present paper describes how respiratory-related neurons (RRNs) modify their discharge during vocalization and swallowing. 2. The temporal relation between vocalization, subglottal pressure (SP), and diaphragm electromyogram (EMG) was established from recordings in anesthetized monkeys. Vocalization was elicited by electrical stimulation of the midbrain periaqueductal gray (PAG). Vocalization is preceded by deep inspiration and a brief pause in diaphragm EMG and begins with a rapid increase in positive SP. 3. Extracellularly recorded neural potential from the VRG in three awake monkeys were related to respiration by correlating their discharge with EMGs from the posterior cricoarytenoid or intercostal muscles during quiet respiration. Neurons were classified as inspiratory (INSP; N = 27), phase spanning (PS; N = 20), or expiratory (N = 6) on this basis. 4. A fourth category of cells was defined as a subgroup of INSP cells on the basis of their discharge during vocalization. This group, inspiratory-pause (INSP-PS; N = 10), paused for approximately 100 ms just before vocalization and resumed their activity during vocalization. 5. Of 63 fully analyzed RRNs, 40 (63%) also modulated their activity with vocalization and 3 (5%) with swallowing. Thirteen (21%) RRNs modulated with vocalization, respiration, and swallowing. Seven (11%) cells were modulated only with respiration. 6. Most cells demonstrated a shorter period of activity and a higher discharge rate associated with vocalization in comparison with quiet respiration. Six (30%) of the PS cells demonstrated an augmenting discharge pattern before vocalization, which was different from the other PS cells and different from their pattern during quiet respiration. Thirteen RRNs showed a pause in activity during vocal fold closure associated with swallowing, whereas three cells gave a burst at this time. 7. The higher discharge rate and shorter burst duration preceding vocalization, compared with quiet respiration, may be related to the greater positive SP necessary to support vocalization.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Effects of spontaneous breathing during airway pressure release ventilation on respiratory work and muscle blood flow in experimental lung injury.

STUDY OBJECTIVES: To evaluate the effects of spontaneous breathing at ambient airway pressure (Paw) and during airway pressure release ventilation (APRV) on respiratory work and respiratory muscle blood flow (RMBF) in experimental lung injury. DESIGN: Prospective experimental study. SETTING: Research laboratory of a university hospital. SUBJECTS: Twelve hemodynamically stable, analgosedated, and tracheotomized domestic pigs. MEASUREMENTS: Respiratory work was estimated by the inspiratory pressure time product (PTPinsp) of esophageal pressure, and RMBF was measured with colored microspheres. Lung injury was induced with IV boli of oleic acid. The first set of measurements was performed before induction of lung injury while pigs were breathing spontaneously at ambient Paw, the second after induction of lung injury while breathing spontaneously at ambient Paw, and the third with lung injury and spontaneous breathing with APRV. RESULTS: After induction of lung injury PTPinsp increased from 138 +/- 14 to 214 +/- 32 cm H2O s/min when pigs breathed spontaneously at ambient Paw (p < 0.05) and returned to 128 +/- 27 cm H2O s/min during APRV. While systemic hemodynamics and blood flow to the psoatic and intercostal muscles did not change, diaphragmatic blood flow increased from 0.34 +/- 0.05 before to 0.54 +/- 0.08 mL/g/min after induction of lung injury and spontaneous breathing at ambient Paw (p < 0.05) and returned to 0.32 +/- 0.05 mL/g/min during APRV (p < 0.05 vs spontaneous breathing at ambient Paw [lung injury]). CONCLUSION: Respiratory work and RMBF are increased in acute lung injury when subjects breathe spontaneously at ambient Paw. Supporting spontaneous breathing with APRV decreases respiratory work and RMBF to physiologic values.

Animals↗
PubMed1991

[Intercostal nerve cross-anastomosis and DREZ-tomy in a patient with brachial plexus avulsion].

An 18-year-old male with a right brachial plexus injury caused by a motorcycle accident was admitted on October 13, 1988. A detailed examination revealed that the brachial plexus was totally injured. The axon reflex test suggested that the lesion sites were postganglionic in the C5 and C6 nerves, and preganglionic in the C7, C8 and Th1. On December 14, 1988, intercostal nerve cross-anastomosis was performed in the hope that a lost motor function of the right upper extremity could be restored as a first step. An electromyogram 6 months after this anastomotic operation demonstrated synkinesis between the biceps brachialis and the intercostal muscles during deep inspiration. Fifteen months after this operation, active voluntary muscle discharges which were higher than before in amplitude, were provoked. The right elbow flexion was gradually restored independently of respiration. On the other hand, intractable pain with a persistent severe tingling sensation appeared approximately one week after the injury on the lesioned upper extremity. The pain rapidly increased in severity. The DREZ-tomy from C5 to Th1 was performed on March 7, 1989. This has brought complete relief of the intractable pain. A brief discussion was given concerning some aspects of the brachial plexus avulsion and DREZ-tomy.

Adolescent↗