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PubMed1982

Acetylcholine receptors at the rat neuromuscular junction as revealed by deep etching.

Collagenase treatment of rat intercostal muscles yielded single muscle fibres in which the nerve terminals and basal lamina were removed allowing an unimpeded view of the external surface of the postsynaptic membrane. This was revealed by deep etching of freeze-fractured preparations and appeared as a maze of folds separated by deep troughs, showing on the crests of the folds a densely packed population of protrusions about 8.5 nm in diameter. These densely packed protrusions (ca. 9000 microns-2) are mainly confined to the postsynaptic regions of the sarcolemma and presumably represent the acetylcholine receptor molecules, which are highly concentrated in these areas. The protrusions are generally tightly packed without obvious regular arrangement, but in some areas, usually on the tops of the crests, they are arranged into irregular rows normal to the long axis of the folds.

Animals↗
PubMed1994

Modeling current density distributions during transcutaneous cardiac pacing.

We developed a two-dimensional finite element model of a cross-section of the human thorax to study the current density distribution during transcutaneous cardiac pacing. The model comprises 964 nodes and 1842 elements and accounted for the electrical properties of eight different tissues or organs and also simulated the anisotropies of the intercostal muscles. The finite element software employed was a version for electrokinetics problems of Finite Element for Heat Transfer (FEHT) and we assessed the effects upon the efficacy of transcutaneous cardiac pacing of several electrode placements and sizes. To minimize pain in the chest wall and still be able to capture the heart, we minimized the ratio, R, between the current density in the thoracic wall (which causes pain) and the current density in the heart wall (which captures the heart). The best placement of the negative electrode was over the cardiac apex. The best placement of the positive electrode was under the right scapula, although other placements were nearly as good. The efficiency of pacing increased as electrode size increased up to 70 cm2 and showed little improvement for larger areas. Between different configurations of the precordial electrodes V1, V2, ..., V6 the most efficient configuration to pace with was V1 and V2 positive and V5 and V6 negative. A more efficient configuration uses an auxiliary electrode located at the right subscapular region.

Anisotropy↗
PubMed1994

Effect of polylactic acid on osteoinduction of demineralized bone: preliminary study of the usefulness of polylactic acid as a carrier of bone morphogenetic protein.

To evaluate the usefulness of polylactic acid (PLA), a bioabsorbable and plastic polymer, as a carrier of bone morphogenetic protein (BMP), a preliminary study has been carried out to investigate any negative effect of PLA on osteoinduction of demineralized bone (DB). PLA (10,600 mol. wt) was mixed with DB particles (1-1.5 mm square) prepared from rat femurs and laid subcutaneously on the intercostal muscle of 4-week-old Wistar rats. The PLA/DB pellets were harvested at 2, 4, 8 and 24 weeks after the operation, and prepared for light microscopic examination. Histological examination revealed cartilage formation at 2 weeks and new bone formation at 4 weeks. Extensive bone and marrow formation were observed at 24 weeks. PLA was gradually absorbed and completely disappeared at 24 weeks to be replaced by connective tissue. These results demonstrate that PLA does not have a negative influence on the osteoinductive activity and that PLA could well be a promising bioabsorbable carrier of BMP.

Animals↗
PubMed1986

Respiratory effects of high thoracic epidural anaesthesia.

The respiratory effects of high thoracic epidural anaesthesia (TEA) were studied in nine healthy volunteers by means of spirometry, nitrogen single-breath test and flow-volume loop. After the baseline measurements an epidural catheter was inserted at T4 level, and 5 ml of 0.5% bupivacaine were injected. This volume led to sensory block within dermatomes T1-T5. Total lung capacity, vital capacity and inspiratory capacity decreased slightly but significantly during TEA. Expiratory reserve volume was not affected. Maximal inspiratory flow at 50% VC decreased 24%. Maximal expiratory flow at 75% VC and peak expiratory flow were not changed. N2 difference during a constant flow rate of 0.5 l/s and forced expiratory volume in 1 s were not changed, which indicates that there were no changes of bronchial tone. The respiratory effects of high TEA in this study were caused by the motor block of the intercostal muscles.

Adult↗
PubMed2005

Unilateral bronchospasm following interpleural analgesia with bupivacaine.

The interpleural block (IPB) is a relatively safe procedure and is commonly practised to provide analgesia. A local anaesthetic injected into the interpleural space spreads widely to block various neural structures. The IPB can initiate bronchospasm by interrupting the sympathetic outflow but sparing the parasympathetic outflow to the lungs. In addition, unilateral reduction of intercostal muscle tone with consequential selective reduction of the functional residual capacity of that lung may also mimic airflow obstruction. We report a case of unilateral bronchospasm encountered following IPB.

Aged↗
PubMed1983

Transplacental transmission of experimental autoimmune myasthenia gravis. A morphological study.

Using neonates born from experimental autoimmune myasthenic rabbits, the authors demonstrated antibodies to acetylcholine receptor (AChR) in the newborn sera. By radioimmunoassay, antibody titers of 1-day-old neonates were roughly one seventh to one ninth of the mothers. At 8 weeks postpartum, the antibody was no longer detectable. Ultrastructural observations of the intercostal muscles of the neonates revealed two types of changes. The first type was degenerative alterations in the postsynaptic membrane. The second type of change, which was morphometrically analyzed, was immaturity of postsynaptic membrane structure with underdeveloped secondary synaptic clefts. After 28 days postpartum, these changes were not visible, thereby indicating that the process is reversible as the antibody titer decreases. These results suggested the possibility that the antibody to AChR, transferred transplacentally, arrested the development of postsynaptic structure, although reversible, by blocking of the receptor sites in the end-plate.

Animals↗
PubMed1997

Assessment and management of dyspnoea.

The terms 'dyspnoea' or 'breathlessness' refer to an individual's subjective awareness of discomfort related to the act of breathing. Elevations in CO2 above normal levels have been shown to cause breathlessness although it is unlikely to be the sole cause of breathlessness in a clinical setting. Several studies suggest that supplemental O2 during exercise will diminish the sensation of breathlessness although not all work has confirmed this finding. Much about the role of gas exchange in dyspnogenesis remains controversial. Phrenic blockade can abolish dyspnoea in response to breath-holding, while work in quadriplegics suggests that the intercostal muscles are not involved. A separate and direct pathway from the respiratory centre to the sensory cortex has also be implicated. Threshold discrimination has established that patients with chronic airflow limitation (CAL) have a blunted response to the addition of resistive loads to breathing, while category scaling methods (e.g. the Borg scale) have added descriptive terms to these physiological measures. Questionnaires often appear limited by their subjectivity and lack of correlation with physiological changes, but remain a useful tool in the clinical setting. In regard to therapy of dyspnoea high fat diets have a theoretical advantage in the CAL group but are generally not well tolerated. Resistive training devices and exercise training in CAL have been widely researched but in general, measures of lung remain unaltered and many of the studies would suggest that they have little, if any, inpact on functional status. Beta-agonists have been widely shown to be useful in CAL patients, despite the fact that bronchodilatation is not always demonstrable. Anticholinergics have be shown to be effective bronchodilators, but whether there is an improvement in dyspnoea above that expected from improvement in lung function is unclear. Animal studies and work in normal individuals would suggest that methylxanthines have a theoretical role in CAL possibly by increasing diaphragmatic muscle strength and decaying fatigue, but toxicity and lack of clear benefit in this group suggest that they should not be used as monotherapy. There is little evidence to support the use of opioids in chronic CAL although their role in the acute dyspnoea of end-stage CAL remains defined. The use of benzodiazepines has also been disappointing. Bullectomy remains widely accepted in clinical practice. New techniques such as 'reduction surgery' for diffuse emphysema are showing promise, although still in need of further testing and validation.

Carotid Body↗
PubMed2006

Obstructive sleep apnoea syndrome: translating science to clinical practice.

OSA syndrome is characterized by recurring episodes of upper airway (UA) obstruction during sleep. The UA is subjected to collapse when the negative airway pressure generated by inspiratory activity of the diaphragm and intercostal muscles exceeds the force produced by the UA dilating muscles. Factors that reduce UA calibre lead to increased UA resistance with the generation of a more negative pharyngeal pressure during inspiration, and thereby predispose to UA occlusion during sleep. As a consequence, UA dilating muscles must contract more forcefully to maintain a patent UA, which may predispose to fatigue. Nasal CPAP counteracts these collapsing forces and is associated with resting of the UA muscles. The more recent development of auto-adjusting CPAP (APAP) is a reflection of the understanding that the pressure required to prevent UA collapse fluctuates throughout the night and results in a lower mean pressure that may be more comfortable for some patients. The predominant morbidity of the OSA syndrome is cardiovascular and there is growing understanding of the basic mechanisms involved. Intermittent hypoxia appears to play a central role by activating transcription factors that predispose to atherogenesis, particularly NFkappaB. Sympathetic overactivity also appears to play an important role but the mechanisms involved are unclear.

Airway Resistance↗
PubMed1997

Evidence from motoneurone synchronization for disynaptic pathways in the control of inspiratory motoneurones in the cat.

1. Motoneurone synchronization was measured by cross-correlation between paired inspiratory discharges in external and internal intercostal nerves or their intramuscular branches (T3 to T8) or in the phrenic nerve (C5 root or both C5 and C6 roots independently) in anaesthetized, paralysed cats. 2. All cross-correlation histograms showed central peaks, for which the durations at half-amplitude (half-widths) from internal nerve pairs in adjacent segments were all less than for external nerve pairs in adjacent segments or within a segment (means, 1.6 ms vs. 3.4 ms for adjacent segments). Values for external-internal pairs covered the ranges for both these two. Lowest values came from two phrenic pairs (1.2 and 1.4 ms). 3. The peaks from ipsisegmental external-internal pairs were usually asymmetric and the maximum of the peak was often displaced to a lag of about -1 ms (external nerve providing the reference spikes), whereas peaks from external-external pairs were always symmetrical and centred on zero. Phrenic-internal peaks gave maxima with lags about 1 ms less than for phrenic-external peaks from the same segments. 4. Two explanations were considered possible for the differences in duration and timing: an extra synapse on the pathway to the external nerve motoneurones, or a correlation kernel for a monosynaptic connection to the external nerve motoneurones that had a slower time course than that for the internal or phrenic nerve motoneurones. Computer simulations, assuming the extra synapse, gave a good fit to the observed time courses of the correlation peaks for all categories of nerve pairs using single values of parameters (e.g. EPSP rise time) consistent with those in the literature. This could not be achieved with the different correlation kernel model. The timing of high-frequency oscillation (HFO), which was sometimes present in the correlations, was also better predicted with the extra synapse model. 5. It is concluded that most of the synchronization between external nerve motoneurones is derived from disynaptic common inputs and that any motoneurone synchronization peak with a half-width greater than about 2.2 ms should be assumed to be likely to contain di- or oligosynaptically derived components.

Animals↗
PubMed2001

Respiratory activity in glossopharyngeal, vagus and accessory nerves and pharyngeal constrictors in newborn rat in vitro.

1. Previously, in a brainstem-spinal cord-rib preparation from neonatal rats we demonstrated that a decrement in extracellular pH (from about 7.4 to 7.1) caused expiratory activity in an internal intercostal muscle (IIM) during the first half of the expiratory phase (Ea). As the initial step in finding nerves or muscles firing during the second half of the expiratory phase (Eb), the patterns of activity in the glossopharyngeal, vagus and accessory nerves were examined in the present study. 2. Since the emerging motor rootlets of these three nerves (> 20; collected into about 10 bundles before the jugular foramen) are distributed in a continuous fashion from rostral to caudal levels of the brainstem, visual identification was impossible. Therefore, antidromic compound action potentials evoked by stimulation of the glossopharyngeal nerve (IX), the pharyngeal branch of the vagus nerve (PhX), the superior laryngeal nerve (SLN), the cervical vagus nerve (CX) and the accessory nerve (XI) were recorded from the peripheral stumps of the various rootlets. Nerve rootlets could be categorised into rostral, intermediate and caudal groups (rostIX-XI, intIX-XI, caudIX-XI). The rostIX-XI rootlets showed their largest potential on IX stimulation, while the intIX-XI and caudIX-XI rootlets showed their largest potentials on CX stimulation. The intIX-XI rootlets showed larger potentials on PhX and SLN stimulation than the caudIX-XI rootlets. 3. Activity was recorded simultaneously from the central stumps of the rootlets in the above three groups. Most rootlets showed inspiratory bursts. Under low pH conditions, all representatives of group rostIX-XI, most of intIX-XI and about half of caudIX-XI showed additional bursts during the Ea phase. Groups intIX-XI and caudIX-XI but not rostIX-XI also showed discrete bursts during the Eb phase in some preparations. In general, expiratory activity was prominent in intIX-XI. The spinal branch of XI showed no consistent respiratory activity. 4. Since the intIX-XI rootlets showed Eb bursts and large antidromic potentials on stimulation of PhX and SLN (which innervate the inferior pharyngeal constrictor muscle (IPC)), electromyograms were recorded from the rostral and caudal parts of IPC (rIPC and cIPC). Under low pH conditions, cIPC showed bursts during the Ea and Eb phases, while rIPC showed bursts predominantly during the Eb phase. 5. These results indicate that recording from rIPC would be a useful way of examining the neuronal mechanisms responsible for Eb phase activity.

Accessory Nerve↗
PubMed1989

Role of carboxylesterase in soman, sarin and tabun poisoning in rats.

TOCP (triorthocresyl phosphate) inhibits carboxylesterase (CarbE) activity in rat plasma and liver and significantly increases soman, sarin and tabun toxicity. Application of these agents after TOCP caused strong additional inhibition of CarbE and cholinesterases (ChE) in rat red blood cells, plasma, liver, brain, diaphragm and intercostal muscle. After phenobarbital pretreatment, which induced CarbE activity in plasma and liver by 80% and that of plasma ChE by 33%, acute toxicity of soman and tabun was greatly decreased, while that of sarin remained unaffected.

Animals↗
PubMed1982

The spatial distribution of synchronization of intercostal motoneurones in the cat.

1. The three different types of synchronization of intercostal motoneurones which were described in the preceding paper (Kirkwood, Sears, Tuck & Westgaard, 1982) were studied for motoneurones of the same segment or for different segmental separations (up to five segments) and for motoneurones on opposite sides of the same segment.2. The strength of synchronization declined with segmental separation for all three categories, although the rate of decline was more variable for broad-peak synchronization than for the two other types. Short-term synchronization was undetectable for separations greater than three or four segments but clear peaks were still visible in the cross correlation histograms for high-frequency oscillation (h.f.o.) or broad-peak synchronization at a segmental separation of five. Synchronization between motoneurones on opposite sides of the cord was generally weak although less so for broad-peak or h.f.o. components.3. The decline in strength of short-term synchronization with segmental separation could not be explained by temporal dispersion of impulses in presynaptic axons.4. A time shift was observed in the position of the cross-correlation histogram peak which was dependent on segmental separation and equivalent to a mean descending conduction velocity of 28 m/s in the assumed common input. This figure is similar to the mean conduction velocity of bulbospinal respiratory neurones derived from published values.5. We conclude that the short-term synchronization in these preparations is generated by the bulbospinal respiratory neurones and that the majority of their axons do not branch to make strong synaptic connexions to motoneurones over more than three to four segments.6. Interpretations of the different distributions of the other types of synchronization are discussed.

Action Potentials↗
PubMed1985

Electrical excitability of motor nerve terminals in the mouse.

Electrical activity of motor nerve terminals was recorded with focal extracellular electrodes under visual location with Nomarski optics in the intercostal muscle of the mouse. Following ionophoretic applications of tetrodotoxin (TTX) to the last three nodes of Ranvier, a nerve impulse jumped across the three inexcitable nodes and excited the heminodal region. When excitation at the last node of Ranvier and the heminodal region was blocked by TTX, the distal terminal revealed a small inward current in response to nerve stimulation. This inward current disappeared when TTX was applied to the distal terminal, indicating the presence of active inward currents in this region under normal conditions. When excitation at the last node, heminode and distal terminals was blocked by TTX, the transmitter release was still observed by nerve stimulation, suggesting substantial passive depolarization of the terminal by excitation of up-stream nodes of Ranvier. Local hyperpolarization of the distal terminal caused an increase in the amplitude of the TTX-sensitive inward current at the terminal, and the reverse effects were exerted by depolarization of the terminal. It is concluded that the mouse motor terminal is electrically excitable and that the TTX-sensitive inward current at the terminal is largely masked by passive depolarization due to excitation of up-stream nodes of Ranvier and the heminode under normal conditions.

Action Potentials↗
PubMed1991

Role of excitatory amino acids in the generation and transmission of respiratory drive in neonatal rat.

1. The involvement of excitatory amino acids in the generation and transmission of rhythmic respiratory drive was studied in an in vitro neonatal rat brain stem-spinal cord preparation. The subclasses of excitatory amino acid receptors studied included: (i) N-methyl-D-aspartate (NMDA) receptors, (ii) (R, S)-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid hydrobromide (AMPA) and kainate (non-NMDA) receptors and (iii) 2-amino-4-phosphonobutyric acid (AP-4)-sensitive receptors. Respiratory motoneurone population discharge was recorded from glossopharyngeal (IX), vagus (X), and hypoglossal (XII) cranial nerves, as well as cervical (C1-C5) and thoracic (T2-T5) spinal ventral roots. This activity is generated in the motoneurone pools that transmit respiratory drive to upper airway, accessory, diaphragm and intercostal muscles. Perturbations of motor nerve discharge were analysed after excitatory amino acid receptor antagonists or agonists were added to bathing solutions surrounding either the spinal cord or brain stem. The excitatory amino acid receptor antagonists included: (i) NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imin-H-maleate (MK-801) and (ii) non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The agonists included: (i) NMDA, (ii) non-NMDA receptor agonists AMPA and kainic acid. The effects of perturbations of AP-4-sensitive receptors with AP-4, and of inhibiting excitatory amino acid uptake with dihydrokainic acid (DHK) were also studied. 2. Block of non-NMDA receptors in the medulla by CNQX resulted in an antagonist concentration-dependent decrease in the respiratory motoneuronal burst frequency. Non-NMDA receptor activation with kainic acid or AMPA caused a concentration-dependent increase in burst frequency, with competitive interactions with CNQX. 3. Inhibition of excitatory amino acid uptake in the medulla with DHK resulted in a reversible, dose-dependent increase in respiratory frequency. A similar increase in respiratory frequency was induced by DHK when medullary NMDA receptors were blocked with MK-801, confirming that endogenously released excitatory amino acids act at non-NMDA receptors to modulate rhythm. 4. Non-NMDA receptor block reduced and ultimately abolished the amplitude of integrated cranial and spinal respiratory motoneuronal discharge when added to the solution bathing the medulla and spinal cord, respectively. 5. NMDA receptor block in the medulla with MK-801 did not perturb the spontaneous respiratory burst frequency, although bath application of NMDA produced a dose-dependent increase in frequency, with non-competitive interactions with MK-801. MK-801 also did not perturb the amplitude of cranial or bulbospinal premotoneurone discharge.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acids↗
PubMed2002

Sim2 mutants have developmental defects not overlapping with those of Sim1 mutants.

The mouse genome contains two Sim genes, Sim1 and Sim2. They are presumed to be important for central nervous system (CNS) development because they are homologous to the Drosophila single-minded (sim) gene, mutations in which cause a complete loss of CNS midline cells. In the mammalian CNS, Sim2 and Sim1 are coexpressed in the paraventricular nucleus (PVN). While Sim1 is essential for the development of the PVN (J. L. Michaud, T. Rosenquist, N. R. May, and C.-M. Fan, Genes Dev. 12:3264-3275, 1998), we report here that Sim2 mutant has a normal PVN. Analyses of the Sim1 and Sim2 compound mutants did not reveal obvious genetic interaction between them in PVN histogenesis. However, Sim2 mutant mice die within 3 days of birth due to lung atelectasis and breathing failure. We attribute the diminished efficacy of lung inflation to the compromised structural components surrounding the pleural cavity, which include rib protrusions, abnormal intercostal muscle attachments, diaphragm hypoplasia, and pleural mesothelium tearing. Although each of these structures is minimally affected, we propose that their combined effects lead to the mechanical failure of lung inflation and death. Sim2 mutants also develop congenital scoliosis, reflected by the unequal sizes of the left and right vertebrae and ribs. The temporal and spatial expression patterns of Sim2 in these skeletal elements suggest that Sim2 regulates their growth and/or integrity.

Animals↗
PubMed2004

Evidence for a conserved function in synapse formation reveals Phr1 as a candidate gene for respiratory failure in newborn mice.

Genetic studies using a set of overlapping deletions centered at the piebald locus on distal mouse chromosome 14 have defined a genomic region associated with respiratory distress and lethality at birth. We have isolated and characterized the candidate gene Phr1 that is located within the respiratory distress critical genomic interval. Phr1 is the ortholog of the human Protein Associated with Myc as well as Drosophila highwire and Caenorhabditis elegans regulator of presynaptic morphology 1. Phr1 is expressed in the embryonic and postnatal nervous system. In mice lacking Phr1, the phrenic nerve failed to completely innervate the diaphragm. In addition, nerve terminal morphology was severely disrupted, comparable with the synaptic defects seen in the Drosophila hiw and C. elegans rpm-1 mutants. Although intercostal muscles were completely innervated, they also showed dysmorphic nerve terminals. In addition, sensory neuron terminals in the diaphragm were abnormal. The neuromuscular junctions showed excessive sprouting of nerve terminals, consistent with inadequate presynaptic stimulation of the muscle. On the basis of the abnormal neuronal morphology seen in mice, Drosophila, and C. elegans, we propose that Phr1 plays a conserved role in synaptic development and is a candidate gene for respiratory distress and ventilatory disorders that arise from defective neuronal control of breathing.

Amino Acid Sequence↗
PubMed2005

Acute aortic dissection provoked by sneeze: a case report.

The response of the abdominal viscera and the contraction of the intercostal muscles during the respiratory phase of sneezing increases intrathoracic pressure, which may lead to several complications. However, there are no reports in the literature concerning aortic dissection after sneezing. We report a patient in whom the development of dissection was secondary to sneezing, although hypertension was present as a risk factor, and we discuss the relationship between sneezing and aortic dissection. To our knowledge, this is the first report of aortic dissection provoked by sneezing in the literature.

Acute Disease↗
PubMed1975

Alveolar hypoventilation and hyperosmnia in myotonic dystrophy.

A case of myotonic dystrophy accompanied by alveolar hypoventilation and hypersomnia is presented. Radiological studies and EMG examination of the intercostal muscles demonstrated that the respiratory muscles were affected by the disease, while polygraphic recordings showed that the alveolar hypoventilation and pulmonary hypertension worsened during sleep. The hypersomnia preceded the appearance of clinical signs of the muscular disease by many years and persisted even after treatment when the blood gas analysis values were greatly improved. During both diurnal and nocturnal sleep, the patient frequently fell asleep directly into a REM stage. The possibility is discussed that, concomitant with the respiratory musculature involvement, there is an alteration in the central nervous system in myotonic dystrophy which is at least partially responsible for both the alveolar hypoventilation and the hypersomnia.

Aminobutyrates↗