Intra- and extracellular measurement of reactive oxygen species produced during heat stress in diaphragm muscle.
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Skeletal muscles are exposed to increased temperatures during intense exercise, particularly in high environmental temperatures. We hypothesized that heat may directly stimulate the reactive oxygen species (ROS) formation in diaphragm (one kind of skeletal muscle) and thus potentially play a role in contractile and metabolic activity. Laser scan confocal microscopy was used to study the conversion of hydroethidine (a probe for intracellular ROS) to ethidium (ET) in mouse diaphragm. During a 30-min period, heat (42 degrees C) increased ET fluorescence by 24 +/- 4%, whereas in control (37 degrees C), fluorescence decreased by 8 +/- 1% compared with baseline (P < 0.001). The superoxide scavenger Tiron (10 mM) abolished the rise in intracellular fluorescence, whereas extracellular superoxide dismutase (SOD; 5,000 U/ml) had no significant effect. Reduction of oxidized cytochrome c was used to detect extracellular ROS in rat diaphragm. After 45 min, 53 +/- 7 nmol cytochrome c. g dry wt(-1). ml(-1) were reduced in heat compared with 22 +/- 13 nmol. g(-1). ml(-1) in controls (P < 0.001). SOD decreased cytochrome c reduction in heat to control levels. The results suggest that heat stress stimulates intracellular and extracellular superoxide production, which may contribute to the physiological responses to severe exercise or the pathology of heat shock. (+info)
No evidence for long-term facilitation after episodic hypoxia in spontaneously breathing, anesthetized rats.
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Repeated electrical or hypoxic stimulation of peripheral chemoreceptors has been shown to cause a persistent poststimulus increase in respiratory motoneuron activity, termed long-term facilitation (LTF). LTF after episodic hypoxia has been demonstrated most consistently in anesthetized, vagotomized, paralyzed, artificially ventilated rats. Evidence for LTF in spontaneously breathing animals and humans after episodic hypoxia is equivocal and may have been influenced by the awake state of the subjects in these studies. The present study was designed to test the hypothesis that LTF is evoked in respiratory-related tongue muscle and inspiratory pump muscle activities after episodic hypoxia in 10 spontaneously breathing, anesthetized, vagotomized rats. The animals were exposed to three (5-min) episodes of isocapnic hypoxia, separated by 5 min of hyperoxia (50% inspired oxygen). Genioglossus, hyoglossus, and inspiratory intercostal EMG activities, along with respiratory-related tongue movements and esophageal pressure, were recorded before, during, and for 60 min after the end of episodic isocapnic hypoxia. We found no evidence for LTF in tongue muscle (genioglossus, hyoglossus) or inspiratory pump muscle (inspiratory intercostal) activities after episodic hypoxia. Rather, the primary poststimulus effect of episodic hypoxia was diminished respiratory frequency, which contributed to a reduction in ventilatory drive. (+info)
Nasal proportional assist ventilation unloads the inspiratory muscles of stable patients with hypercapnia due to COPD.
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This study was undertaken to assess the physiological effects of proportional assist ventilation (PAV), administered noninvasively through a nose mask, on ventilatory pattern, arterial blood gases, lung mechanics, and inspiratory muscle effort in stable, hypercapnic patients with chronic obstructive pulmonary disease. In 15 patients, PAV was set by adjusting volume assist (VA) and flow assist (FA) according to the "run-away" technique and the patient's comfort respectively. The level of support was fixed at 80% of the total possible assistance and averaged 13.9+/-4.1 cmH2O x L(-1) and 4.1+/-1.3 cmH2O x L(-1) x s for VA and FA, respectively. Continuous positive airway pressure (CPAP) was established at 2 cmH2O and then increased to 5 cmH2O. Physiological measurements were made during spontaneous breathing (SB), after more than 40 min of PAV, and 20 min after the rise in CPAP. On average, PAV improved ventilation (10.3+/-2.1 to 12.5+/-2.0 L x m(-1)), tidal volume (0.60+/-0.11 to 0.76+/-0.24 L), arterial oxygen tension and arterial carbon dioxide pressure (from 6.7+/-0.7 to 7.1+/-0.9 and from 7.6+/-1.0 to 7.2+/-1.2 kPa, respectively). During SB, pulmonary resistance and dynamic lung elastance averaged 15.0+/-7.6 cmH2O x L(-1) s and 15.8+/-8.0 cmH2O x L(-1), respectively. Assuming a normal chest wall elastance (5 cmH2O x L(-1)), VA and FA relieved respectively approximately 70% of the elastic and 30% of the resistive burden, with PAV set with the procedure of this study. The overall magnitude of the patients' inspiratory effort, measured by means of the oesophageal and diaphragmatic pressure time product in 10 patients was significantly reduced by PAV, on average, 328+/-122 to 226+/-118 (-31%) and 361+/-119 to 254+/-126 (-30%) cmH2O x min(-1), respectively. In 10 patients the electrical activity of the diaphragm (Edi) was also reduced by PAV to approximately 70%, on average, of the SB activity. The rise of CPAP 25 cmH2O did not cause any further significant change in the physiological variables. In all instances there was a good patient-ventilator interaction, the ventilatory breath never entering into the patient's neural expiratory time. These data show that nasal proportional assist ventilation can provide physiological benefits to the stable hypercapnic chronic obstructive pulmonary disease patients. In fact, proportional assist ventilation, which was well tolerated by all patients, unloaded the inspiratory muscles and improved arterial blood gases. Further studies can clarify whether these beneficial physiological effects of nasal proportional assist ventilation can bear profitable consequences in the overall clinical management of chronic obstructive pulmonary disease patients with chronic carbon dioxide retention. (+info)
Thixotropy of rib cage respiratory muscles in normal subjects.
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In this study, we searched for signs of thixotropic behavior in human rib cage respiratory muscles. If rib cage respiratory muscles possess thixotropic properties similar to those seen in other skeletal muscles in animals and humans, we expect resting rib cage circumference would be temporarily changed after deep rib cage inflations or deflations and that these aftereffects would be particularly pronounced in trials that combine conditioning deep inflations or deflations with forceful isometric contractions of the respiratory muscles. We used induction plethysmography to obtain a continuous relative measure of rib cage circumference changes during quiet breathing in 12 healthy subjects. Rib cage position at the end of the expiratory phase (EEP) was used as an index of resting rib cage circumference. Comparisons were made between EEP values of five spontaneous breaths immediately before and after six types of conditioning maneuvers: deep inspiration (DI); deep expiration (DE); DI combined with forceful effort to inspire (FII) or expire (FEI); and DE combined with forceful effort to inspire (FIE) or expire (FEE), both with temporary airway occlusion. The aftereffects of the conditioning maneuvers on EEP values were consistent with the supposition that human respiratory muscles possess thixotropic properties. EEP values were significantly enhanced after all conditioning maneuvers involving DI, and the aftereffects were particularly pronounced in the FII and FEI trials. In contrast, EEP values were reduced after DE maneuvers. The aftereffects were statistically significant for the FEE and FIE, but not DE, trials. It is suggested that respiratory muscle thixotropy may contribute to the pulmonary hyperinflation seen in patients with chronic obstructive pulmonary disease. (+info)
Effects of phrenicotomy and exercise on hypoxia-induced changes in phrenic motor output.
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To investigate models of plasticity in respiratory motor output, we determined the effects of chronic unilateral phrenicotomy and/or exercise on time-dependent responses to episodic hypoxia in the contralateral phrenic nerve. Anesthetized (urethane), ventilated, and vagotomized rats were presented with three, 5-min episodes of isocapnic hypoxia (11% O(2)), separated by 5 min of hyperoxia (50% O(2)). Integrated phrenic (and hypoglossal) nerve discharge were recorded before and during each hypoxic episode, for the first 5 min after the first hypoxic episode, and at 30 and 60 min after the final episode. Of 36 rats, one-half were sedentary while the other one-half had free access to a running wheel; each of these groups was split into three subgroups: 1) unoperated, 2) chronic left phrenicotomy (27-37 days), and 3) sham operated. Neither unilateral phrenicotomy nor running wheel activity influenced the short-term hypoxic phrenic response (during hypoxia) or long-term facilitation (posthypoxia). Posthypoxia frequency decline was exaggerated in phrenicotomized-sedentary rats relative to unoperated-sedentary rats (change in burst frequency = -23+/-4 vs. -11 +/-5 bursts/min, respectively; 5 min posthypoxia; P<0.05), an effect that was eliminated by spontaneous exercise. The results indicate that neither voluntary running nor unilateral phrenicotomy has major effects on time-dependent hypoxic phrenic responses, with the exception of an unexpected effect of phrenicotomy on posthypoxia frequency decline in sedentary rats. (+info)
Effect of expiratory resistive loading on the noninvasive tension-time index in COPD.
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Expiratory resistive loading (ERL) is used by chronic obstructive pulmonary disease (COPD) patients to improve respiratory function. We, therefore, used a noninvasive tension-time index of the inspiratory muscles (TT(mus) = I/PI(max) x TI/TT, where I is mean inspiratory pressure estimated from the mouth occlusion pressure, PI(max) is maximal inspiratory pressure, TI is inspiratory time, and TT is total respiratory cycle time) to better define the effect of ERL on COPD patients. To accomplish this, we measured airway pressures, mouth occlusion pressure, respiratory cycle flow rates, and functional residual capacity (FRC) in 14 COPD patients and 10 normal subjects with and without the application of ERL. TT(mus) was then calculated and found to drop in both COPD and normal subjects (P<0.05). The decline in TT(mus) in both groups resulted solely from a prolongation of expiratory time with ERL (P<0.001 for COPD, P<0.05 for normal subjects). In contrast to the COPD patients, normal subjects had an elevation in I and FRC, thus minimizing the decline in TT(mus). In conclusion, ERL reduces the potential for inspiratory muscle fatigue in COPD by reducing TI/TT without affecting FRC and I. (+info)
Expiratory muscle pressure and breathing mechanics in chronic obstructive pulmonary disease.
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Expiratory muscle recruitment is common in stable chronic obstructive pulmonary disease (COPD) patients. Due to airway obstruction, there is little reason to believe that active expiration in COPD would be mechanically effective in lowering operating lung volume. The physiological significance of expiratory muscle recruitment in COPD, therefore, remains unknown. The purpose of this study was to assess, in COPD patients breathing at rest, the effect of expiratory muscle contraction on force generating ability of the diaphragm. The force generating ability of the diaphragm was evaluated from its pressure swing (Pdi) for a given diaphragm electrical activity (Edi), where Edi was normalized as % of its maximal value (Pdi/Edi/Edi,max). Phasic expiratory muscle contraction was measured as the total expiratory rise in gastric pressure (Pga,exp.rise). Nineteen seated patients with moderate to severe COPD, participated in the study and 10 exhibited phasic rise in Pga during expiration with a mean Pga,exp.rise of 1.91+/-0.89 cmH2O. The patients were thus divided into passive expiration (PE) and active expiration (AE) groups. There was no significant difference in various lung function and breathing pattern parameters between the two groups. Pdi/Edi/Edi,max was 0.63+/-0.07 and 0.54+/-0.07 cmH2O/% in PE and AE groups, respectively, and was not significantly different between each other. Compared with PE group, AE group not only recruited expiratory muscles, but also preferentially recruited inspiratory rib cage muscles and derecruited the diaphragm. The results do not support a significant improvement of the force-generating ability of the diaphragm by phasic contraction of expiratory muscles at rest in chronic obstructive pulmonary disease patients. (+info)
Myositis associated graft-versus-host-disease presenting as respiratory muscle weakness.
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Myositis associated with graft-versus-host-disease (GVHD) typically presents with proximal muscle weakness, myalgias, and a raised creatinine phosphokinase (CPK) level. We report a case of a 51 year old man who developed respiratory muscle weakness five years after an allogeneic bone marrow transplant for multiple myeloma. His symptoms included tachypnoea, abdominal paradox, and orthopnoea. Pulmonary function tests revealed diminished vital capacity and maximal inspiratory and expiratory pressures. Serum CPK levels were raised and a peripheral muscle biopsy specimen was consistent with GVHD. He improved with immunosuppressive therapy. (+info)