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 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of guinea pigs were exposed to respirable particles of cotton dust obtained from opening and carding rooms of a textile mill. The bulk cotton dust was resuspended with a modified sonic sifter. Exposures were conducted 6 hr/day at concentrations varying between 16 and 25 mg/m3. The particle size for these exposures varied around a 3 micron aerodynamic equivalent diameter. In animals exposed for 5 days, a pulmonary effect began to develop 3 hr after the start of exposure on the first day and was maximal 18 hr postexposure. The pulmonary effect faded during the ensuing weekdays as daily exposures continued. In one group exposed for 6 weeks, 5 days/week, the pulmonary effect was apparent on each Monday and faded during the week. The pulmonary response can best be characterized as a reflex restriction of breathing from stimulation of vagal nerve endings, resulting in rapid shallow breathing. This effect was exaggerated upon challenge of the animals with air containing 10% CO2. In humans this pattern of rapid shallow breathing is associated with symptoms of shortness of breath, dyspnea, breathlessness, and fatigue upon exertion. Such symptoms are characteristic of those reported by workers exposed to cotton dust. This animal model is proposed for further evaluation of the possible relationship between the acute responses to cotton dust and the development of a chronic response.
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PMID:Pulmonary reactions to inhaled cotton dust: an animal model for byssinosis. 642 99

When the ventilatory muscles are unable to develop the required force as it occurs during fatigue, hypercapnic respiratory failure ensues. We present evidence that when the respiratory muscles work in a fatiguing load domain the central controllers respond at an early stage with tachypnea, while when the muscles fail bradypnea ensues which is followed by apnea. Although bradypnea and apnea in addition to muscle inability to develop force may reduce alveolar ventilation by virtue of reducing the total minute ventilation, tachypnea may also be followed by hypercapnia at constant total minute ventilation by virtue of a reduction in tidal volume (VT). Such a strategy will increase the ratio of dead space (VD) to tidal volume (VD/VT) and PCO2 will rise. It is argued that this mechanism could satisfactorily explain the high levels of CO2 in patients with chronic obstructive lung disease, as well as the CO2 retention at an early stage in acute cases of fatigue during, for example, the weaning period of a patient from the respirator. Bradypnea and apnea contribute to CO2 retention at a later stage, when the muscles are exhausted and total ventilation decreases. This sequence in frequency of breathing is explained as an advantageous strategy adopted for the respiratory muscles, because it allows the muscles to operate at an optimal length. It is also hypothesized that muscle afferents, probably via the small fibers III and IV and/or Golgi and tendon organs, are responsible for this interaction of CNS and respiratory muscles.
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PMID:Ventilatory muscle fatigue governs breathing frequency. 650 21

The major effects of breathing dense gas during physical exercise in hyperbaric environments can be traced to high airway resistance during inspiration and expiration and especially to an increased tendency for lung airways to become "choked" during expiration. The body's responses to the high resistance include decrease of alveolar ventilation, which leads to CO2 retention. This hypoventilation is aggravated by poor mixing in the lung because of low diffusivity of gases in the dense environment. Also, there is a tendency for the person to let the end-expired volume of the lung enlarge; this causes a marked increase of work against elastic recoil of pulmonary structures. Because the elastic work occurs during the inspiratory phase of a breath, there is a disproportionate increase of the work of the inspiratory muscles that may lead to fatigue of inspiratory musculature and consequent aggravation of the hypoventilation.
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PMID:Mechanical and physical factors in lung function during work in dense environments. 663 48

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.
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PMID:Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors. 680 50

temporaria (0.9-2.5degrees C) were stimulated to produce a 1 s isometric tetanus at regular intervals until constant mechanical responses were attained. Various degrees of force depression ("fatigue") were produced by decreasing the contraction interval from 30 or 15 min (control to 120, 60, 30 and 15s, respectively. In this was the steady-state tetanic force could be reversibly reduced to approximately 70% of the control value. The velocity of shortening at zero load, V0, was determined at each level of fatigue using an approach for direct measurement of V0. V0 was not significantly affected as long as the decrease in force was less than 10%. With further reduction of the isometric tension there was a progressive decline of V0 according to the following empirical relationship between percentage depression of force (delta P0) and maximum speed (delta V0) of shortening: delta V0 = 0.006 delta P02.48- 1.0 (correlation coefficient, 0.86). Cine photographic recording of nylon markers on the fibre surface provided evidence that fatigue developed uniformly along the fibre with no sign of failure of excitation in any segment. The change in mechanical performance during fatigue could be reproduced inthe non-fatigued fibre by reducing the pH of the external medium within the range 8.0-6.6 using a bicarbonate-CO2 buffer. A decrease in pH thus reduced both the rate of rise and the total amplitude of isometric force and prolonged the relaxation phase. Furthermore, there was a drop in V0 that was related to the force decline in approximately the same way as observed during fatigue. The results support the idea the fatigue involves both a reduced state of activation of the contractile system and a specific (activation independent) inhibition of crossbridge turnover. Increased intracellular H+ concentration is likely to contribute to the development of both these effects during fatigue.
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PMID:Effects of fatigue and altered pH on isometric force and velocity of shortening at zero load in frog muscle fibres. 697 40

We compared the effects of a cardioselective beta-adrenergic blocking drug, metoprolol, with a nonselective beta-adrenergic blocker, propranolol, on the response of 10 normal men to dynamic treadmill exercise. The volunteers underwent a standard graded exercise test to exhaustion while receiving placebo; propranolol, 40 mg every 6 hours; propranolol, 80 mg every 6 hours; metoprolol, 50 mg every 6 hours; or metoprolol, 100 mg every 6 hours. The drugs were given in a double-blind fashion for 48 hours before exercise. Five days were allowed between successive drug administrations and the order of drug administration was randomized. Heart rate, arterial pressure, oxygen consumption, minute ventilation and CO2 production were monitored. Plasma drug concentrations were measured at the time of exercise. Judged by plasma levels, propranolol was about three times more potent than metoprolol in attenuating heart rate. Both drugs produced a wide variation in plasma levels after a given oral dose, and both drugs attenuated the systolic blood pressure response to exercise. Neither drug affected diastolic blood pressure or maximum oxygen consumption, maximum minute ventilation or the anaerobic threshold. We conclude that there is no evidence that the cardioselective drug metoprolol is superior to propranolol in terms of the ability to perform or respond to short-term maximal exercise. In addition, the fact that maximal oxygen consumption and the anaerobic threshold were unaffected implies that fatigue during exercise while on beta-adrenergic blocking drugs is not due to an effect of these drugs in limiting blood flow to the exercising extremities.
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PMID:The effects of a cardioselective (metoprolol) and a nonselective (propranolol) beta-adrenergic blocker on the response to dynamic exercise in normal men. 707 50

We describe the fabrication and characterization of an optical CO2 sensor based on the change in fluorescence lifetimes due to fluorescence resonance energy transfer from a pH-insensitive donor, sulforhodamine 101, to a pH-sensitive acceptor, either m-cresol purple or thymol blue, entrapped in an ethyl cellulose film. A phase transfer agent allows incorporation of the dyes and water into the film, while providing an initially basic environment for the acceptor. Diffusion of CO2 into the water entrapped in the film produced carbonic acid, causing a pH-dependent decrease in the spectral overlap of the acceptor absorbance with the donor emission, and decreased energy transfer, resulting in increased SR101 donor lifetimes. The lifetime changes were detected as a change in the phase of the emission, relative to the modulated excitation, and were insensitive to excitation intensities and emission signal levels. In addition to an externally modulated 442-nm light source, we excited the sensor with a directly modulated 635-nm laser diode and detected the anti-Stokes emission. The CO2 sensor is not fragile and can provide stable readings for weeks. The use of fluorescence resonance energy transfer, along with the simple entrainment procedure, allows facile change of the CO2 response range through change of the acceptor dye and the use of laser diode excitation sources.
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PMID:A lifetime-based optical CO2 gas sensor with blue or red excitation and stokes or anti-stokes detection. 757 52

The results from experiments in various modalities of evoked potentials are described in a subject with a complete large peripheral neuropathy below the neck. He has no tactile or position sensitivity below that level, but has retained fatigue, pain, and temperature sensation. Percutaneous electrical stimulation of peripheral nerves led to scalp recorded evoked potentials with thresholds and propagation velocities compatible with conduction along A-delta peripheral pathways. CO2 laser evoked potentials were similar to those seen in controls, further support for intact A-delta peripheral fibres. Movement-related cortical potentials (MRCPs) were recorded associated with active and passive movement of the middle finger. The former were normal, evidence that the termination of the MRCP is not dependent on peripheral feedback. By comparing passive MRCPs between controls and the subject it was possible to establish which parts of the potentials are visual and which are proprioceptive and to gain evidence of central reorganisation in the subject. Magnetic brain stimulation was used to show that the subject did not perceive induced movement, had a normal centrally originating silent period, and could focus his attention during real and imagined movement of the finger more successfully than could normal controls.
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PMID:Evoked potentials in a subject with a large-fibre sensory neuropathy below the neck. 762 62

Neuromuscular diseases cause many changes that affect ventilation and ventilatory control. The pattern of ventilation may become abnormal because of muscle disease. Muscle fatigue and discordant breathing can lead to hypoventilation and CO2 retention. Motoneuron destructive and demyelinating disorders inevitably lead to hypoventilation and hypercapnia. Changes in chest wall mechanics can lead to changes in level of ventilation and ventilatory drive. In many neuromuscular disorders, ventilatory response to CO2 is depressed, but this does not imply an abnormal central control mechanism in all instances. Many patients with neuromuscular diseases have a normal ventilatory drive as manifested by a normal P0.1 but have low ventilation because of abnormalities in muscle function and neuromuscular transmission. Central drive is diminished in some patients with neuromuscular disease but not in the majority of cases. Hypoventilation during sleep is a common problem in neuromuscular diseases. Thus, a combination of factors can lead to abnormal patterns of breathing and hypoventilation in these disorders; no single pathophysiologic mechanism can explain all the abnormalities. Clinically, it is important to appreciate the prevalence of ventilatory control disorders and include appropriate evaluations when assessing patients with neuromuscular diseases and offering therapeutic options.
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PMID:Central control of ventilation in neuromuscular disease. 786 78

Smoke inhalation injury is a complex of disease processes best understood and treated when defined in terms of the time period after injury. The early phase (0 to 36 hrs) is characterized by diagnosis and treatment of carbon monoxide and cyanide toxicity and by management of early airways edema, bronchorrhea, and bronchoconstriction with aggressive pulmonary toilet. Between 1 and 5 days, the major characteristic is airways mucosal slough, tracheobronchitis, and increasing lung water and impaired gas exchange. Pulmonary toilet and infection control, as well as close management of fluid shifts, is the major treatment. With onset of the inflammation-infection phase, the risk of nosocomial pneumonia increases markedly, as does the impairment in lung function as a result of marked increase in oxygen consumption and CO2 production. Nutrition, stress modification, avoidance of muscle fatigue, and control of infection are the key treatment modalities.
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PMID:Smoke inhalation injury. 792 21


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