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Extraintestinal migration of Pharyngostomum cordatum metacercariae in experimental rodents.

Extraintestinal migration patterns of Pharyngostomum cordatum (Digenea: Neodiplostomidae) were studied in experimental rodents such as mice, rats, and hamsters. When metacercariae isolated from grass snakes were infected orally to rodents, they penetrated the intestinal wall at days 2-3 post-infection (p.i.) and were discovered mainly in the diaphragm, intercostal muscles, and vital organ such as the lungs at days 7-28 p.i., without morphological changes. Interestingly, from several rodents which died suddenly at days 2-9 p.i., small to considerable numbers of metacercariae were found, not only in the lungs, but also in the heart and brain. Within the tissues, worms were freely motile until day 7 p.i., but later they were surrounded by host cells, and finally tissue cysts were formed. When metacercariae harvested from the snakes and intercostal muscles of rodents were infected orally to cats, they developed into adult flukes in the small intestine. The results show that P. cordatum undergoes considerable extraintestinal migration including the vital organs of its rodent hosts.

Animals↗

Effects of pulmonary and intercostal denervation on the response of breathing frequency to varying inspiratory flow.

In mechanically ventilated awake and sleeping humans, it has been shown that increasing inspiratory flow rate (V'I) exerted a reflex excitatory effect on respiratory output. Mechanoreceptors located in intercostal muscles or within the lung have been suggested as possible pathways that may mediate the excitatory effect of V'I. To test this, five patients with bilateral lung transplantation (LTP) and eight quadriplegics with spinal cord transection at the level of C6-C7 (QP) were studied. Patients were connected to a volume cycle ventilator in the assist volume-control mode and V'I was randomly changed. V'I pattern was square and all breaths were patient-triggered. V'I values of 30, 60 and 90 L x min(-1) were studied. Each level of V'I was sustained for 15 breaths. Airway pressures, end-tidal partial pressure of carbon dioxide (PCO2), airflows and volumes were measured breath by breath. Thirty seven trials in LTP and sixty in QP, where V'I was randomly changed between 30 and 90 L x min(-1), were analysed. In both groups of patients, minute ventilation increased and total breath duration decreased significantly as V'I increased. These changes were complete in the first breath after V'I transition, without evidence of adaptation of the response. The magnitude of the response did not differ between the two groups of patients and was comparable to that observed previously in conscious normal subjects. We conclude that the excitatory effect of inspiratory flow rate on breathing frequency persists in patients who have pulmonary or intercostal denervation. These results do not favour receptors located within the lung (below the resection lines) or in the intercostal muscles to mediate the response of breathing frequency to flow rate.

Denervation↗

Hypoventilation after acute phrenicotomy of the urethane anaesthetized rats.

The aim of this study was to explore the mechanism resulting in hypoventilation in rats with denervated diaphragm. Bilateral cervical phrenicotomy (PX) was performed in 15 male rats anaesthetized with urethane (1.3 g/kg i.p.); other 8 rats were sham operated (SX). Ventilation, PaCO2 and the integrated EMG of the external intercostal muscles (iEMG) were measured before and after the surgery, at regular intervals, up to 4 hours postoperatively. During the 4 hours after PX there was a progressive decrease in minute ventilation and an increase in PaCO2 compared with the control values and with that in the SX rats. The increase in PaCO2 was accompanied by an increase in the peak amplitude of the iEMG to 155 +/- 18% of control values after PX and to 228 +/- 33% 4 hours later. Despite the augmented EMG activity tidal volume gradually decreased. The iEMG of the intercostal muscles, however, did not reach a maximum because the shortlasting stimulation of breathing by acute hypercapnia and hypoxia as the result of added dead space (0.5 ml) increased the iEMG still further. These results indicate that both the central and peripheral mechanisms contribute to hypoventilation in anaesthetized rats with denervated diaphragm.

Anesthesia↗

Late complications of collapse therapy for pulmonary tuberculosis.

STUDY OBJECTIVES: Collapse therapy for pulmonary tuberculosis involved placement of various materials to occupy space and keep the lung collapsed. Complications are encountered decades later. PATIENTS AND METHODS: Between 1980 and 1997, we treated 31 patients with a history of pulmonary tuberculosis in whom collapse therapy had been used and who later developed complications related to their treatment. Pyogenic empyema was present in 24 patients, pleural calcifications with bronchopleural fistula was present in 3 patients, pleural calcification with nonresolvable pneumothorax was present in 1 patient, and migration of a foreign body with formation of subcutaneous mass occurred in 3 patients. All patients with empyema were treated with antibiotics and tube drainage of pus. In addition, Lucite balls were extracted in 4 patients, lung decortication was performed in 6 patients, thoracoplasty was performed in 2 patients, and fenestration was performed in 16 patients. Bronchopleural fistulas were closed with sutures and reinforced with intercostal muscle flap in three patients; in one patient with pleural calcification and nonresolvable pneumothorax, tube drainage was attempted. In three patients with subcutaneous mass due to paraffin migration, paraffin was extracted. RESULTS: Pulmonary decortication (six patients) and thoracoplasty (two patients) resulted in elimination of empyema. Extraction of Lucite balls resulted in lung expansion and elimination of empyema in three of four patients; draining sinus remains in one patient. Fenestration resulted in elimination of empyema in 12 of 16 patients, with 3 patients with residual draining sinuses and 1 patient with remaining empyema. All bronchopleural fistulas closed with intercostal muscle flap remained closed. Following extraction of paraffin blocks, infection developed in one patient. During the follow-up period, three patients died, all of unrelated causes. CONCLUSIONS: Delayed complications of collapse therapy for tuberculosis should be treated without delay. Pressure on adjacent structures or their erosion presents danger and mandates immediate extraction; however, there is no need for routine removal of every residual plombe. Further increase in the number of multiple-drug resistant strains may force the return of collapse therapy.

Adult↗

Chest wall motion of infants during spinal anesthesia.

To test the extent to which diaphragmatic contraction moves the rib cage in awake supine infants during quiet breathing, we studied chest wall motion in seven prematurely born infants before and during spinal anesthesia for inguinal hernia repair. Infants were studied at or around term (postconceptional age 43 +/- 8 wk). Spinal anesthesia produced a sensory block at the T2-T4 level, with concomitant motor block at a slightly lower level. This resulted in the loss of most intercostal muscle activity, whereas diaphragmatic function was preserved. Rib cage and abdominal displacements were measured with respiratory inductance plethysmography before and during spinal anesthesia. During the anesthetic, outward inspiratory rib cage motion decreased in six infants (P less than 0.02, paired t test); four of these developed paradoxical inward movement of the rib cage during inspiration. One infant, the most immature in the group, had inward movement of the rib cage both before and during the anesthetic. Abdominal displacements increased during spinal anesthesia in six of seven infants (P less than 0.05), suggesting an increase in diaphragmatic motion. We conclude that, in the group of infants studied, outward rib cage movement during awake tidal breathing requires active, coordinated intercostal muscle activity that is suppressed by spinal anesthesia.

Anesthesia, Spinal↗

A structural model of the thoracic cage in the cat.

A homogeneous shell model of the mechanical characteristics of the thoracic cage in the cat is presented. The global characterization proposed parallels the characterization--presented elsewhere--of the motor control of the intercostal musculature in terms of a conceptual spatially continuous control function, that underlies the discretely distributed muscular activity and reflects an inferred global dynamic control of the intercostal muscles during breathing. Proposing a static, homogeneous shell characterization of the thoracic cage, which is heterogeneous and composed of an assembly of mobile structures, implies assuming that other elements are indirectly giving this system features that make it resemble, from a structure analysis point of view, a homogeneous, static one. The pattern of the lines of stress along the shell structure proposed as a model compares favourably with the shape of the ribs. In agreement with previous findings, supporting the need for muscular activity to satisfy demands of purely structural character, it is suggested that this global shell-like functional character is achieved by neuromuscular global dynamic integration of the components of the rib cage by the nervous control of the intercostal muscles.

Animals↗

Effects of exercise in normoxia and acute hypoxia on respiratory muscle metabolites.

We determined changes in rat plantaris, diaphragm, and intercostal muscle metabolites following exercise of various intensities and durations, in normoxia and hypoxia (FIO2 = 0.12). Marked alveolar hyperventilation occurred during all exercise conditions, suggesting that respiratory muscle motor activity was high. [ATP] was maintained at rest levels in all muscles during all normoxic and hypoxic exercise bouts, but at the expense of creatine phosphate (CP) in plantaris muscle and diaphragm muscle following brief exercise at maximum O2 uptake (VO2max) in normoxia. In normoxic exercise plantaris [glycogen] fell as exercise exceeded 60% VO2max, and was reduced to less than 50% control during exhaustive endurance exercise (68% VO2max for 54 min and 84% for 38 min). Respiratory muscle [glycogen] was unchanged at VO2max as well as during either type of endurance exercise. Glucose 6-phosphate (G6P) rose consistently during heavy exercise in diaphragm but not in plantaris. With all types of exercise greater than 84% VO2max, lactate concentration ([LA]) in all three muscles rose to the same extent as arterial [LA], except at VO2max, where respiratory muscle [LA] rose to less than half that in arterial blood or plantaris. Exhaustive exercise in hypoxia caused marked hyperventilation and reduced arterial O2 content; glycogen fell in plantaris (20% of control) and in diaphragm (58%) and intercostals (44%). We conclude that respiratory muscle glycogen stores are spared during exhaustive exercise in the face of substantial glycogen utilization in plantaris, even under conditions of extreme hyperventilation and reduced O2 transport. This sparing effect is due primarily to G6P inhibition of glycogen phosphorylase in diaphragm muscle. The presence of elevated [LA] in the absence of glycogen utilization suggests that increased lactate uptake, rather than lactate production, occurred in the respiratory muscles during exhaustive exercise.

Animals↗

Fine-needle aspiration cytology in fibromatoses.

Fine-needle aspiration (FNA) cytology was performed in seven cases of fibromatosis of variable types with tumorous clinical presentation. These included: four cases of musculoaponeurotic fibromatosis, two in posterior neck muscles, one in anterior neck muscles and one in intercostal muscles; one case of fibromatosis of the breast; and two cases of fibromatosis colli in neonates. In all cases the specimens contained connective tissue with many fibroblast-like cells, lacking features which could indicate a malignant lesion. The findings in these cases indicate that, although by FNA cytology in fibromatoses a specific diagnosis for each pathologic entity may not be easily reached, in the proper clinical setting the cytologic findings can be of sufficient relevance to offset the need for an open tissue biopsy, where there are valid reasons against a surgical intervention.

Aged↗

Normal and abnormal US findings at the mastectomy site.

Evaluation of a mastectomy site is more effective with ultrasonography (US) than with either mammography or chest computed tomography because abnormalities are usually small and close to the skin surface. US does not involve the use of ionizing radiation and has a multiplanar scanning capability. The technique is readily available and inexpensive, and it allows real-time monitoring of needle tip placement during biopsy of a lesion. Normal US anatomy of the chest wall after mastectomy usually consists of four layers: skin, subcutaneous fat, pectoral muscles, and rib and intercostal muscle. The axilla is changed in appearance after lymph node dissection, but it remains the same in patients who have undergone simple mastectomy. US can accurately depict benign and malignant conditions in the mastectomy site, including fluid collection, fibrosis, local recurrent tumor, and metastatic lymphadenopathy, and can enable accurate diagnosis based on findings at fine needle aspiration biopsy.

Adult↗

Upper airway muscle activity during sustained hypoxia in awake humans.

To examine the effects of sustained hypoxia on upper airway and chest wall muscle activity in humans, we measured genioglossus muscle (GG) activity, inspiratory intercostal muscle (IIM) activity, and ventilation during sustained hypoxia in 17 normal subjects and 17 patients with obstructive sleep apnea (OSA). The trial of sustained hypoxia was performed as follows: after an equilibration period of 3 min, isocapnic hypoxia (arterial O2 saturation = 80 +/- 2%) was maintained for 20 min. GG EMG was measured with a fine-wire electrode inserted percutaneously, and IIM EMG was measured with surface electrodes. Ventilatory response to sustained hypoxia was initially increased and subsequently decreased. Stable phasic GG activity during spontaneous tidal breathing was observed in 6 normal subjects and 10 patients with OSA. Responses of GG and IIM activities to sustained hypoxia showed a biphasic response qualitatively similar to the ventilatory response in these 16 subjects. The absolute value of the subsequent decline in GG activity was similar to that of the initial increase, whereas the subsequent decline in IIM activity was smaller than that of the initial increase. Percent GG activity was significantly lower than both percent IIM activity and percent minute ventilation during the decline and plateau phases. There were no significant differences in ventilatory and EMG responses between the normal subjects and the patients with OSA. We conclude that, during wakefulness, upper airway muscle activity declined to a greater extent than inspiratory pump muscle activity during sustained hypoxia.

Adult↗

Myotonia of the respiratory muscles in myotonic dystrophy.

Myotonic dystrophy is a muscle disorder in which there is a tendency to rapid shallow breathing and a reduced ventilatory response to chemical stimuli. Respiratory failure may occur when respiratory muscle weakness is not marked. One explanation proposed for these observations is that myotonia of the respiratory muscles reduces the compliance of the chest wall. However, direct electrical evidence of myotonia in the respiratory muscles with breathing is lacking. In 11 patients with myotonic dystrophy the scalene, sternocleidomastoid, a parasternal muscle, and a lateral intercostal muscle were studied using intramuscular bipolar wires. Five of the 11 patients had an elevated PaCO2. All patients had a FVC greater than 70% of predicted. Myotonia was sought with needle insertion, quiet tidal breathing, voluntary large breaths, and involuntary larger breaths with chemical stimulation. Two of the 11 patients demonstrated no myotonia. Myotonia on insertion of the needle was seen in four patients. Myotonia was rare in an isolated respiratory cycle during quiet breathing, and repetitive myotonia with consecutive breathing cycles was never noted. Voluntary big breaths produced myotonia in five patients, whereas chemically stimulated larger breaths produced myotonia in seven patients. In two of these seven patients, myotonic activity with consecutive respiratory cycles was seen at higher levels of ventilation. In conclusion, the rare occurrence of myotonia with tidal breathing would suggest myotonia in the muscles does not account for the respiratory failure and tachypneic breathing pattern found in myotonic dystrophy. Its occurrence at higher levels of ventilation may contribute to the reduced ventilatory response to chemical stimuli.

Adult↗

Organophosphate-induced intermediate syndrome: aetiology and relationships with myopathy.

The intermediate syndrome (IMS) following organophosphorus (OP) insecticide poisoning was first described in the mid-1980s. The syndrome described comprised characteristic symptoms and signs occurring after apparent recovery from the acute cholinergic syndrome. As the syndrome occurred after the acute cholinergic syndrome but before organophosphate-induced delayed polyneuropathy, the syndrome was called 'intermediate syndrome'. The IMS occurs in approximately 20% of patients following oral exposure to OP pesticides, with no clear association between the particular OP pesticide involved and the development of the syndrome. It usually becomes established 2-4 days after exposure when the symptoms and signs of the acute cholinergic syndrome (e.g. muscle fasciculations, muscarinic signs) are no longer obvious. The characteristic features of the IMS are weakness of the muscles of respiration (diaphragm, intercostal muscles and accessory muscles including neck muscles) and of proximal limb muscles. Accompanying features often include weakness of muscles innervated by some cranial nerves. It is now emerging that the degree and extent of muscle weakness may vary following the onset of the IMS. Thus, some patients may only have weakness of neck muscles whilst others may have weakness of neck muscles and proximal limb muscles. These patients may not require ventilatory care but close observation and monitoring of respiratory function is mandatory. Management is essentially that of rapidly developing respiratory distress and respiratory failure. Delays in instituting ventilatory care will result in death. Initiation of ventilatory care and maintenance of ventilatory care often requires minimal doses of non-depolarising muscle relaxants. The use of depolarising muscle relaxants such as suxamethonium is contraindicated in OP poisoning. The duration of ventilatory care required by patients may differ considerably and it is usual for patients to need ventilatory support for 7-15 days and even up to 21 days. Weaning from ventilatory care is best carried out in stages, with provision of continuous positive airway pressure prior to complete weaning. Continuous and close monitoring of respiratory function (arterial oxygen saturation, partial pressure of oxygen in arterial blood, partial pressure of carbon dioxide in arterial blood) and acid-base status are an absolute necessity. Prophylactic antibiotics are usually not required unless there has been evidence of aspiration of material into the lungs. Close monitoring of fluid and electrolyte balance is mandatory in view of the profuse offensive diarrhoea that most patients develop. Maintenance of nutrition, physiotherapy, prevention of bed sores and other routine measures to minimise discomfort during ventilatory care are necessary. Recovery from the intermediate syndrome is normally complete and without any sequelae. The usefulness of oximes during the IMS remains uncertain. In animal experiments, very early administration of oximes has prevented the occurrence of myopathy. There are reports from developed countries where administration of oximes at recommended doses and within 2 hours of ingestion of OP insecticide did not prevent the onset of the IMS. Controlled randomised clinical studies are necessary to evaluate the efficacy of oximes in combating the IMS. Electrophysiological studies following OP poisoning have revealed three characteristic phenomena: (i) repetitive firing following a single stimulus; (ii) gradual reduction in twitch height or compound muscle action potential followed by an increase with repetitive stimulation (the 'decrement-increment response'); and (iii) continued reduction in twitch height or compound muscle action potential with repetitive simulation ('decrementing response'). Of these, the decrementing response is the most frequent finding during the IMS, whilst repetitive firing is observed during the acute cholinergic syndrome. The distribution of the weakness in human cases of the IMS, in general, parallels the distribution of the myopathy observed in a number of studies in experimental animals. This has led to speculation that myopathy is involved in the causation of the IMS. However, while myopathy and the IMS have a common origin in acetylcholine accumulation, they are not causally related to one another.

Animals↗

Myocardial injury in the mouse induced by transthoracic cauterization.

A simplified transthoracic procedure using electrocauterization was used to induce myocardial injury in mice. After a single small incision through the skin and dissection of the underlying musculature, a modified electrocautery probe consisting of an insulated 20-gauge blunt needle with a polyethylene sleeve was inserted through the interior intercostal muscle at the fourth intercostal space and positioned on the anterior surface of the heart. The placement of the probe on the heart was indicated by mechanical motion of the exterior section of the needle. Electrocautery was applied to the distal exposed end of the probe. Of 10 mice that underwent this procedure, nine survived. After 10 days, myocardial damage was assessed by visual and histologic examination of the heart. In eight of nine surviving mice, transmural injury was induced in the left ventricle. The region of myocardial tissue damage on the surface of the left ventricle was 4.6 +/- 0.5 mm in diameter. This method provides a simple, noninvasive technique using a transthoracic electrocautery procedure to induce myocardial injury in the mouse heart with a low incidence of postoperative mortality.

Animals↗

[Dyspnea and rib cage distortion in postural changes].

We studied the topographical ventilatory motion and electrical muscle activity (EMG) of intercostal muscle within the rib cage for the patients complaining dyspnea produced mostly by their postural changes. There were inappropriateness between the rib cage motion and EMG and this inappropriateness was closely related to a sensation of dyspnea. We could relieve partly dyspnea by applying the negative pressure ventilator, because of prevention of a distortion of rib cage. Based on these clinical observation, we concluded that one of mechanism to sense dyspnea was the inappropriateness between motion and electrical muscle activity within the rib cage.

Dyspnea↗

[Physiology and physiopathology of postnatal pulmonary adaptation. 1: Physiology].

The aim of the review consists of the help to understand the complex physiological mechanisms of the onset of breathing and the regulation of the respiration during the early newborn period. The lungs of the newborn contain nearly no alveoli. Postnatal formation of alveoli enlarges the gas exchange surface until the 20th year of life, the lung volume increases by a factor of 27. Immediately postnatal the aeration of the lungs is performed by several deep inspirations with breath hold and following crying. The fetal lung liquid is resorbed via both, lymph and blood vessels. Stability of the functional residual capacity is reached very rapidly. The inflation augmenting reflex and sighing support effectively this process. The significant importance of the surfactant for the successful begin of air breathing is described. Onset of respiration is combined with the decrease of the pulmonary arterial resistance and the remarkable increase of the pulmonary blood flow. The hypoxic response in the newborn is biphasic. An initial short hyperventilation is regularly followed by ventilatory depression. Neurophysiological causes are evident. Hyperventilation by inhalation of gas mixtures with higher CO2 concentrations is low, at least in preterm infants. The causes are believed to ly in the limitation of the efficiency of the respiratory muscles. Peripheral chemoreceptors in the glomus caroticum and in the bronchial mucosa, stretch receptors in the bronchial muscles, and muscle spindles in the intercostal muscles are functioning in newborns as well as in preterm infants.

Adaptation, Physiological↗

Structure of axon terminals and active zones at synapses on lizard twitch and tonic muscle fibers.

The freeze-fracture technique was used to study differences in membrane structure which could explain differences in the number of quanta released from axon terminals on twitch and tonic muscle fibers in Anolis intercostal muscles. The protoplasmic leaflets of axon terminals facing lizard twitch muscle fibers have intramembrane particle specializations characterized by two parallel linear particle arrays each composed of two particle rows which lie perpendicular to the axis of shallow ridges in the axolemma. During K+ depolarization, vesicles open between the arrays, confirming that these structures are the active zones for synaptic vesicle opening. Active zones at axon terminals on tonic fibers are defined by one linear particle array composed of two parallel particle rows oriented along the axis of a shallow presynaptic ridge; vesicles open beside these arrays. Thus, there are more particles near active zone vesicles in terminals on twitch fibers. Even though terminals on twitch and tonic muscle fibers seem to have similar numbers of synaptic vesicles associated with their active zones, a presynaptic action potential is reported to release at least 10 times more quanta from terminals on twitch fibers. We postulate that the differences in quantal output are related to the observed differences in the number of active zone particles flanking synaptic vesicles at the active zone. Indeed, the correlation between the distribution of these particles and the level of transmitter release provides additional support for the idea that they are the calcium channels which couple transmitter release to the action potential.

Animals↗