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PubMed1978

Metabolic control of the circulation. Effects of acetate and pyruvate.

Chloralose-anesthetized dogs were infused intravenously with either Tris-acetate or Tris-pyruvate at 0.0375, 0.075, and 0.15 mmol/kg per min successively, each for 20 min. Acetate infusion increased cardiac output, left ventricular dP/dt and dP/dt/P, and coronary blood flow, while pyruvate infusion did not. Infusions of either substance increased arterial blood and skeletal muscle concentrations of citrate and malate, but only acetate infusion increased the tissue AMP content and decreased the ATP:AMP ratio. The increase in cardiac output produced by acetate was accompanied by an increase in total body oxygen consumption and a decrease in the difference between arterial and mixed venous blood oxygen. Myocardial oxygen consumption increased during acetate infusion, but the decrease in myocardial oxygen extraction and the increase in coronary sinus blood oxygen saturation suggest that an active coronary vasodilation which was not a result of the increased cardiac work, occurred. The concentration of hypoxanthine in the coronary sinus and the content of myocardial adenosine increased, which suggests that the increase in coronary blood flow was caused by the vasodilator action of adenosine released from the myocardium, and that adenosine production is not necessarily tied to PO(2). These systemic and coronary hemodynamic changes also occurred when acetate (0.075 mmol/kg per min) was infused into conscious dogs. Acetate infusion also increased blood flow to the gastrointestinal tract, kidneys, intercostal muscle, and diaphragm. These changes were not affected by propranolol pretreatment, but were abolished by pretreatment with fluoroacetate which reduced acetate oxidation. These results suggest that the circulatory stimulation produced by acetate was not caused by increases in tricarboxylic acid cycle intermediates. Instead, it was probably related to the increased cleavage of ATP to AMP that accompanies activation of acetate to acetyl CoA, and was not mediated via beta-adrenergic receptors. It is speculated that hemodynamic changes may occur in patients who undergo hemodialysis with acetate-containing dialysate. Hemodynamic changes of ethanol may also be brought about by acetate, which is one of the intermediates that accumulates during ethanol metabolism.

Acetates↗

PubMed2003

[Electromyographic activity of human triangularis sterni muscles during thoracic rotation].

The triangularis sterni muscles (TS) have been recognized as expiratory muscles, but there is no information on their postural activity or their phasic electromyographic (EMG) activity during thoracic rotation. We examined the EMG activity of the right TS using fine-wire electrodes, in 5 healthy male subjects. With subjects breathing through a mouthpiece, airflow, raw and moving-averaged EMG signals were sampled with a computer during thoracic rotation and resting, accompanied by breathing with or without voluntary thoracic rotation. Maximum EMG (EMGmax) was defined as the greatest moving-averaged EMG activity recorded from each subject during the slow expiratory maneuver from functional residual capacity to residual volume. With leftward thoracic rotation without breathing, the tonic EMG activity of the right TS was observed in all subjects. During resting breathing without thoracic rotation, there were respiration-related phasic activities on TS EMG during expiration in all subjects. With leftward thoracic rotation, the respiration-related phasic activities on TS EMG significantly increased from 8.2 +/- 3.5 (mean +/- SE) %EMGmax to 15.2 +/- 6.1 %EMGmax. On the other hand, with rightward thoracic rotation, it decreased to 3.0 +/- 1.0 %EMGmax. We concluded that 1) TS has a postural function like that of the intercostal muscles, and that 2) the respiratory function of TS is affected by thoracic rotation.

Adult↗

PubMed1988

An EMG analysis on regulation of the diaphragm and abdominal muscles.

Neural mechanisms regulating activities of diaphragm and abdominal muscles were investigated on anesthetized, tracheostomized and spontaneously breathing dogs. EMGs of costal diaphragm and external oblique (EO)abdominal muscle were recorded by fine-wire electrodes. The electrodes for diaphragm-EMG were implanted without opening abdominal cavity using laparoscopy. During quiet breathing the mean firing frequency of diaphragm-EMG was 7.6 +/- 0.7 (S.D.) Hz. The discharge spikes of diaphragm-EMG observed in early-inspiration or in post-inspiratory phase, were low in amplitudes, consistent with previous reports that phrenic motoneurons were comprised of two populations. During quiet breathing spikes were not observed in EO-EMG in a half of the animals, and were tonically-firing in the remaining dogs. Hypercapnia increased firing frequency of diaphragm-EMG, but did not recruit spikes of high amplitude. On the other hand, hypercapnia recruited EO-spikes of higher amplitude, and increased firing frequency. When spikes fired tonically in EO-EMG, hypercapnia suppressed these spikes during inspiration. Airway occlusion gradually recruited EO units of higher amplitude. Mechanical stimulation of upper airway suppressed tonic-EO activity during inspiration. In conclusion, we demonstrated that 1) abdominal wall is not related with control mechanism of diaphragm; 2) the control mechanism of dog's EO differs from cat's internal intercostal muscles; and 3) the tonic component of EO is affected by respiratory commands from higher neuronal architecture.

Abdominal Muscles↗

PubMed2001

Clinical electrophysiology of the upper and lower motor neuron in amyotrophic lateral sclerosis.

Electrophysiology is important in amyotrophic lateral sclerosis (ALS). It helps in the assessment of disease severity and rate of progression, and it plays a role in evaluating the efficacy of therapeutic trials. Presently, electrophysiology is the only means of confirming suspected ALS, and this has been incorporated into the El Escorial criteria. Needle electromyography identifies disease in clinically "unaffected muscles" including bulbar musculature, confirms involvement of anterior horn cells, and can detect early involvement of respiratory muscles (intercostals and diaphragm). Conduction studies are imperative to rule out motor neuropathy with multifocal conduction block. Various techniques (cortical threshold, cortical silent period, double stimulation) employing transcranial magnetic stimulation have demonstrated that the motor cortex in ALS is hyperexcitable. Central motor conduction is normal in ALS but uniquely slow in the D9OA SOD1 mutation. Using peristimulus time histograms (PSTHs) it is possible to estimate the size of a unitary excitatory postsynaptic potential (EPSP). In ALS the EPSP is typically desynchronized. With time it becomes reduced in amplitude and a slow conducting component becomes recognizable in the primary peak of the PSTH. This reflects conduction through a slow motor pathway. Abnormalities of the PSTH are not seen in Kennedy's disease, implying that the changes seen in ALS are due to supraspinal mechanisms.

Amyotrophic Lateral Sclerosis↗

PubMed2007

Stimulation-induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals.

To investigate mitochondrial responses to repetitive stimulation, we measured changes in NADH fluorescence and mitochondrial membrane potential (Psi(m)) produced by trains of action potentials (50 Hz for 10-50 s) delivered to motor nerve terminals innervating external intercostal muscles. Stimulation produced a rapid decrease in NADH fluorescence and partial depolarization of Psi(m). These changes were blocked when Ca2+ was removed from the bath or when N-type Ca2+ channels were inhibited with omega-conotoxin GVIA, but were not blocked when bath Ca2+ was replaced by Sr2+, or when vesicular release was inhibited with botulinum toxin A. When stimulation stopped, NADH fluorescence and Psi(m) returned to baseline values much faster than mitochondrial [Ca2+]. In contrast to findings in other tissues, there was usually little or no poststimulation overshoot of NADH fluorescence. These findings suggest that the major change in motor terminal mitochondrial function brought about by repetitive stimulation is a rapid acceleration of electron transport chain (ETC) activity due to the Psi(m) depolarization produced by mitochondrial Ca2+ (or Sr2+) influx. After partial inhibition of complex I of the ETC with amytal, stimulation produced greater Psi(m) depolarization and a greater elevation of cytosolic [Ca2+]. These results suggest that the ability to accelerate ETC activity is important for normal mitochondrial sequestration of stimulation-induced Ca2+ loads.

Action Potentials↗

PubMed1975

Guanidine and neuromuscular transmission. I. Effect on transmitter release occurring spontaneously and in response to single nerve stimuli.

The effect of guanidine on neuromuscular transmission was studied in human intercostal muscle and mouse diaphragm preparations in vitro. Guanidine greatly increased the number of acetylcholine (ACh) quanta released by a single motor nerve action potential. This effect of guanidine was greater at junctions with a low quantum content. The spontaneous release of ACh quanta was not substantially changed by guanidine. No change was found in the postsynaptic sensitivity to ACh released from the motor nerve or iontophoretically applied to the muscle fiber. Effects of the drug had slow onset and were very long-lasting and resistant to wash.

Acetylcholine↗

PubMed1975

End-plate morphology in amyotrophic lateral sclerosis.

Intercostal muscle end-plates were measured in patients with amyotrophic lateral sclerosis (ALS) and more benign motor neuron disease (MND). The length of the intact end-plates in ALS and MND was not different from the controls. Segmented end-plates were increased in both ALS and benign MND, and the end-plate length was greatest in ALS. In individual ALS cases, no correlation was found between the end-plate abnormalities and relevant clinical variables.

Adult↗

PubMed1977

Neuropathy presenting as prolonged dyspnea. Case report and review of literature.

Polyneuropathy presented as isolated respiratory muscular paralysis. Transdiaphragmatic pressure measurements, nerve conduction studies, electromyography, and biopsy of intercostal muscle confirmed the nature of the process. Patients with unexplained respiratory insufficiency must be carefully evaulated for underlying neuromuscular disease.

Adult↗

PubMed1995

Successful treatment of invasive thoracopulmonary mucormycosis in a patient with acute lymphoblastic leukemia.

BACKGROUND: Pulmonary mucormycosis associated with hematologic malignancy is an uncommon, but important opportunistic fungal pneumonia that is usually a fatal infection. Only a few survivors of pulmonary mucormycosis have been reported. METHODS: A case report of invasive thoracopulmonary mucormycosis during remission-induction therapy for acute lymphoblastic leukemia and a review of the literature are presented. RESULTS: The fungal lesions extended to both lungs, the left ribs, and intercostal muscles. Percutaneous needle biopsy and immunostaining of the fungal hyphae established the diagnosis of thoracopulmonary mucormycosis. The patient was treated with granulocyte-colony stimulating factor (G-CSF) and intravenous amphotericin B for 9 weeks and the lesions in the right lung disappeared. Left pneumonectomy and partial resection of the chest wall were later performed. The left lung was grossly necrotic and contained a large cavity and bronchopulmonary fistula. Thereafter, antileukemic therapy was resumed and completed without recurrence of mucormycosis or leukemia. CONCLUSIONS: In the management of mucormycosis, the addition of G-CSF to the conventional treatment may substantially improve outcome.

Adolescent↗

PubMed2005

Time-related interdependence between low-frequency cortical electrical activity and respiratory activity in lizard, Gallotia galloti.

Electroencephalograms of medial cortex and electromyograms of intercostal muscles (EMG-icm) were simultaneously recorded in the lizard, Gallotia galloti, during two daily time periods (at daytime, DTP: 1200-1600 h; by night, NTP: 0000-0400 h), to investigate whether a relationship exists between the respiratory and cortical electrical activity of reptiles, and, if so, how this relationship changes during the night rest period. Testing was carried out by studying interdependence between cortical electrical and respiratory activities, by means of linear and nonlinear signal analysis techniques. Both physiological activities were evaluated through simultaneous power signals, derived from the power of the low-frequency band of the electroencephalogram (pEEG-LF), and from the power of the EMG-icm (pEMG-icm), respectively. During both DTP and NTP, there was a significant coherence between both signals in the main frequency band of pEMG-icm. During both DTP and NTP, the nonlinear index N measured significant linear asymmetric interdependence between pEEG-LF and pEMG-icm. The N value obtained between pEEG-LF vs. pEMG-icm was greater than the one between pEMG-icm vs. pEEG-LF. This means that the system that generates the pEEG-LF is more complex than the one that generates the pEMG-icm, and suggests that the temporal variability of power in the low-frequency cortical electrical activity is driven by the power of the respiratory activity.

Animals↗

PubMed1985

A method for localizing high-resolution NMR spectra from human subjects.

Several methods are available for the localization of high-resolution spectra. When the sample is a human subject, it may be difficult to realize a viable experimental protocol because the size and geometry of the subject often conflict with efficient probe design. In this paper a spectroscopic localization method is described which is based on the method of rotating frame imaging. A novel surface-coil probe has been developed so that this experiment can be performed on a large sample. 31P spectra from the thorax of a human subject are presented in which signals from liver and intercostal muscle are resolved. These data demonstrate that spatially resolved spectra of metabolites in vivo may be obtained in a time that is acceptable for patient examination.

Humans↗

PubMedDate not supplied

Facilitatory effects of 4-aminopyridine on neuromuscular transmission in disease states.

The in vitro effects of 4-aminopyridine (4-AP) on neuromuscular transmission were determined by microelectrode techniques in intercostal muscles from patients with myasthenia gravis (MG) and the Eaton-Lambert syndrome (ELS), and in forelimb muscles from rats with experimental autoimmune myasthenia gravis (EAMG). In MG and EAMG, the amplitudes of miniature endplate potentials (MEPPs) and endplate potentials (EPPs) were reduced, and there was increased sensitivity to the blocking action of d-tubocurarine (dTc). In ELS, MEPP amplitude was normal but the average number of acetylcholine quanta released by nerve impulses was reduced, causing subthreshold EPPs. In EAMG muscle, 4-AP produced dose-dependent increases in EPP amplitude and in the duration of indirectly elicited muscle action potentials but no changes in MEPP amplitude and resting membrane potential. 4-AP completely reversed the postsynaptic blockade produced by dTc and EAMG. 4-AP appears to facilitate neuromuscular transmission in EAMG, MG, and ELS by increasing the neurally evoked transmitter release, thus overcoming either the pre- or the postsynaptic neuromuscular blockade.

Adult↗

PubMedDate not supplied

Congenital myasthenia: end-plate acetylcholine receptors and electrophysiology in five cases.

The nature of the defect in congenital myasthenia was investigated in biopsy specimens of intercostal muscle from 5 male patients whose symptoms presented between birth and 2 years of age. Miniature end-plate potentials were reduced in amplitude in all 5 patients. The number of acetylcholine receptors as determined by alpha-bungarotoxin binding was normal in case 1 and reduced in cases, 2, 4, and 5. The shape of the end-plates as shown by autoradiography and cholinesterase staining was normal in case 1 and elongated in cases 2, 4, and 5. In cases 3, alpha-bungarotoxin binding was slowly reversible, and there were some muscle fibers with multiple end-plate regions. The acetylcholine content of the muscle was normal in all 5 cases. None of the patients had serum antibody to human acetylcholine receptor as measured by immunoprecipitation or inhibition of alpha-bungarotoxin binding. We conclude that congenital myasthenia is a heterogeneous condition of nonimmune etiology in which both presynaptic and postsynaptic defects can be found.

Acetylcholine↗

PubMed1988

A myasthenic syndrome with congenital paucity of secondary synaptic clefts: CPSC syndrome.

Two cases of a newly recognized myasthenic syndrome were investigated (CPSC syndrome). The course of the disease was observed for periods of 6 and 3 years. In infancy, exacerbations of the symptoms occurred during febrile illness, but thereafter the clinical course was stable and the children appeared to be only slightly handicapped. Biopsies were taken from the intercostal muscle in both patients. Microelectrode studies revealed small Mepp amplitudes. Light microscopy demonstrated predominance of type I fibers and focal type-grouping. There was a lowered cholinesterase activity and frequent branching of preterminal axons. Electron microscopy revealed that there were few, if any, folds of the postsynaptic membrane and that there were no signs of degeneration. Methods for localization of acetylcholine receptors (AChR) revealed a deficiency and altered distribution of AChRs at these postsynaptic membranes and the occurrence of extrajunctional AChRs in some muscle fibers. It is concluded that the syndrome is a clinicopathological entity, characterized morphologically by a congenital paucity of secondary synaptic clefts (CPSC syndrome).

Child↗

PubMed1993

Congenital myasthenic syndromes: I. Deficiency and short open-time of the acetylcholine receptor.

A 5.5-year-old girl had myasthenic symptoms since birth. Tests for antiacetylcholine receptor (AChR) antibodies were negative. To investigate the character of the neuromuscular transmission defect, an intercostal muscle specimen was obtained at age 27 months. Immune deposits were absent from the endplates. On electron microscopy, most postsynaptic regions appeared normal, but the density of AChR on the junctional folds was diffusely reduced. In vitro microelectrode studies revealed that the number of transmitter quanta released by nerve impulse was normal. The amplitude of miniature of endplate potentials and currents was abnormally low. A study of the kinetic properties of AChR by analysis of acetylcholine-induced current noise demonstrated a significant decrease in mean channel open-time; the mean channel conductance was normal. The safety margin of neuromuscular transmission in this disorder is likely to be compromised by the deficiency and abnormal kinetic properties of AChR. The findings are unique among those patients with congenital AChR deficiency described to date.

Acetylcholinesterase↗

PubMed1993

Congenital myasthenic syndromes: II. Syndrome attributed to abnormal interaction of acetylcholine with its receptor.

A 21-year-old woman had myasthenic symptoms since birth that responded poorly to anticholinesterase therapy. Tests for acetylcholine receptor (AChR) antibodies were negative. An intercostal muscle specimen was obtained to investigate the character of the neuromuscular transmission defect. There were no immune deposits at the endplates. The quantal content of the endplate potential was normal. Miniature endplate potentials and currents were very small, but the number of AChR per endplate was normal. On electron microscopy, the synaptic vesicles were of normal size, the junctional folds were intact, and the density and distribution of AChR on the folds was normal. The kinetic properties of AChR were studied by analysis of acetylcholine (ACh)-induced current noise. The mean single channel conductance was normal. The noise power spectrum was abnormal, containing two components of different time course. This could result from an abnormal interaction of ACh with AChR, or from two populations of AChR at the endplate. The second possibility is unlikely because if two populations of AChR were present at the endplate, then both would have to have low conductance to explain the small miniature endplate current, but the average conductance of the channels that did open was normal.

Acetylcholine↗

PubMed1988

Relative contribution of ribcage and abdomen during augmented breaths in infants.

Changes in the relative contribution of ribcage and abdomen during augmented breaths were assessed in two groups of infants (less than 2 weeks and 4-12 weeks old). In both groups ribcage and abdominal movements increased during augmented breaths in quiet sleep. In the older infants the relative increase was greater for the ribcage (P less than 0.05) when expressed either as a ribcage to abdominal movement ratio or as a percent of the respective movements during control breaths. In contrast, no significant change of the relative contribution was observed in the younger age group. During active sleep paradoxical movement of the ribcage, observed during tidal breaths, continued during the first phase of the augmented breath; however, during the second phase of inspiration, the ribcage moved outward in all but one infant. Our results show that marked increases in tidal volume are associated with greater increases in ribcage contribution in infants beyond the neonatal period. This may reflect differences in recruitment patterns of intercostal muscles during development.

Abdominal Muscles↗

PubMed1993

Upper cervical inspiratory neurons in the rat: an electrophysiological and morphological study.

Upper cervical inspiratory neurons from a distinct neuronal column located near the lateral edge of the intermediate grey matter in the rostral spinal segments. Previous studies conducted in cats have demonstrated synaptic inputs to these neurons from several respiratory-related regions of the medulla, and long descending axonal projections mainly towards the motoneurons supplying the intercostal muscles. The aim of this study was to examine the electrophysiological and morphological properties of this propriospinal system in the rat. Extracellular recordings were made from 127 cervical inspiratory units, mainly in the C1 and C2 segments. Eighty-two percent could be antidromically activated from the C7/C8 border. No evidence of monosynaptic connection was obtained by cross-correlating the activity of some of these units with the discharge of the phrenic nerve. Intracellular recordings were made from seven neurons, three of which were labelled with biotinamide (neurobiotin). Long "survival times" after intracellular injections (up to 23 h) resulted in staining of axons for long distances, at least to the C5 segment. Each of the three labelled axons issued only one short collateral which arborized in the region of the phrenic nucleus. These results demonstrate that upper cervical inspiratory neurons in the rat have features similar to those previously described in the cat, including only a limited projection to the phrenic nucleus. In addition, this study provides the first morphological identification of these neurons.

Animals↗