(1/1124) Modulation of the thermoregulatory sweating response to mild hyperthermia during activation of the muscle metaboreflex in humans.
1. To investigate the effect of the muscle metaboreflex on the thermoregulatory sweating response in humans, eight healthy male subjects performed sustained isometric handgrip exercise in an environmental chamber (35 C and 50 % relative humidity) at 30 or 45 % maximal voluntary contraction (MVC), at the end of which the blood circulation to the forearm was occluded for 120 s. The environmental conditions were such as to produce sweating by increase in skin temperature without a marked change in oesophageal temperature. 2. During circulatory occlusion after handgrip exercise at 30 % MVC for 120 s or at 45 % MVC for 60 s, the sweating rate (SR) on the chest and forearm (hairy regions), and the mean arterial blood pressure were significantly above baseline values (P < 0.05). There were no changes from baseline values in the oesophageal temperature, mean skin temperature, or SR on the palm (hairless regions). 3. During the occlusion after handgrip exercise at 30 % MVC for 60 s and during the occlusion alone, none of the measured parameters differed from baseline values. 4. It is concluded that, under mildly hyperthermic conditions, the thermoregulatory sweating response on the hairy regions is modulated by afferent signals from muscle metaboreceptors. (+info)
(2/1124) A pilot study on the human body vibration induced by low frequency noise.
To understand the basic characteristics of the human body vibration induced by low frequency noise and to use it to evaluate the effects on health, we designed a measuring method with a miniature accelerometer and carried out preliminary measurements. Vibration was measured on the chest and abdomen of 6 male subjects who were exposed to pure tones in the frequency range of 20 to 50 Hz, where the method we designed was proved to be sensitive enough to detect vibration on the body surface. The level and rate of increase with frequency of the vibration turned out to be higher on the chest than on the abdomen. This difference was considered to be due to the mechanical structure of the human body. It also turned out that the measured noise-induced vibration negatively correlated with the subject's BMI (Body Mass Index), which suggested that the health effects of low frequency noise depended not only on the mechanical structure but also on the physical constitution of the human body. (+info)
(3/1124) Radiation induced endothelial cell retraction in vitro: correlation with acute pulmonary edema.
We determined the effects of low dose radiation (<200 cGy) on the cell-cell integrity of confluent monolayers of pulmonary microvascular endothelial cells (PMEC). We observed dose- and time-dependent reversible radiation induced injuries to PMEC monolayers characterized by retraction (loss of cell-cell contact) mediated by cytoskeletal F-actin reorganization. Radiation induced reorganization of F-actin microfilament stress fibers was observed > or =30 minutes post irradiation and correlated positively with loss of cell-cell integrity. Cells of irradiated monolayers recovered to form contact inhibited monolayers > or =24 hours post irradiation; concomitantly, the depolymerized microfilaments organized to their pre-irradiated state as microfilament stress fibers arrayed parallel to the boundaries of adjacent contact-inhibited cells. Previous studies by other investigators have measured slight but significant increases in mouse lung wet weight >1 day post thoracic or whole body radiation (> or =500 cGy). Little or no data is available concerning time intervals <1 day post irradiation, possibly because of the presumption that edema is mediated, at least in part, by endothelial cell death or irreversible loss of barrier permeability functions which may only arise 1 day post irradiation. However, our in vitro data suggest that loss of endothelial barrier function may occur rapidly and at low dose levels (< or =200 cGy). Therefore, we determined radiation effects on lung wet weight and observed significant increases in wet weight (standardized per dry weight or per mouse weight) in < or =5 hours post thoracic exposure to 50 200 cGy x-radiation. We suggest that a single fraction of radiation even at low dose levels used in radiotherapy, may induce pulmonary edema by a reversible loss of endothelial cell-cell integrity and permeability barrier function. (+info)
(4/1124) External thoracic restriction, respiratory sensation, and ventilation during exercise in men.
Multiple factors may contribute to the dyspnea associated with restrictive ventilatory disease (RVD). Simple models that examine specific features of this problem are likely to provide insight into the mechanisms. Previous models of RVD utilizing elastic loads may not represent completely the impact on pulmonary and chest wall receptors derived from breathing at low thoracic volumes. The purpose of this study was to investigate the sensory consequences of breathing at low lung volumes induced by external thoracic restriction in an attempt to further elucidate the etiology of dyspnea in this setting. Ten men were studied, with and without an inelastic corset applied at residual volume (restriction resulted in mean reductions in vital capacity, functional residual capacity, residual volume, and forced expired volume in 1 s of 44, 31, 12.5, and 42%, respectively). During 10-min steady-state exercise tests (at a workload set to achieve approximately 65% maximum heart rate), restriction resulted in significant increases, compared with control, in minute ventilation (61 vs. 49 l/min), respiratory frequency (43 vs. 23 breaths/min), and visual analog scale measurements of respiratory discomfort (65 vs. 20 mm). Alveolar hyperventilation (end-tidal PCO2 = 39 vs. 44 Torr for control) and mild O2 desaturation (arterial blood O2 saturation = 93 vs. 95% for control) occurred. Hypoxemia, atelectasis, increased work and effort of breathing, or a decrease in the volume-related feedback from chest wall and/or lungs could be responsible for the increased dyspnea reported. External thoracic restriction provides a useful model to study mechanisms of dyspnea in RVD. (+info)
(5/1124) Core temperature and sweating onset in humans acclimated to heat given at a fixed daily time.
The thermoregulatory functions of rats acclimated to heat given daily at a fixed time are altered, especially during the period in which they were previously exposed to heat. In this study, we investigated the existence of similar phenomena in humans. Volunteers were exposed to an ambient temperature (Ta) of 46 degrees C and a relative humidity of 20% for 4 h (1400-1800) for 9-10 consecutive days. In the first experiment, the rectal temperatures (Tre) of six subjects were measured over 24 h at a Ta of 27 degrees C with and without heat acclimation. Heat acclimation significantly lowered Tre only between 1400 and 1800. In the second experiment, six subjects rested in a chair at a Ta of 28 degrees C and a relative humidity of 40% with both legs immersed in warm water (42 degrees C) for 30 min. The Tre and sweating rates at the forearm and chest were measured. Measurements were made in the morning (0900-1100) and afternoon (1500-1700) on the same day before and after heat acclimation. Heat acclimation shortened the sweating latency and decreased the threshold Tre for sweating. However, these changes were significant only in the afternoon. The results suggest that repeated heat exposure in humans, limited to a fixed time daily, alters the core temperature level and thermoregulatory function, especially during the period in which the subjects had previously been exposed to heat. (+info)
(6/1124) A chest wall restrictor to study effects on pulmonary function and exercise. 1. Development and validation.
Chest wall-restrictive loading reduces a person's ability to expand the chest wall during inhalation and results in decrements in lung capacities, resting pulmonary function, and ultimately, exercise performance. Chest wall restriction is observed in some forms of skeletal and pulmonary diseases (e.g., scoliosis) as well as in occupational situations (e.g., bulletproof vests). We have designed a constant-pressure chest wall-restrictive device that provides a quantifiable and reproducible load on the chest. This paper describes the device and the initial pulmonary function tests conducted. Ten subjects participated in this study. Subjects wore the restrictive device while performing pulmonary function tests at four externally added restrictive loads on three separate occasions. A two-way repeated-measures multivariate analysis of variance revealed significant decreases in forced expiratory vital capacity (FVC) and forced expiratory volume in 1 s (FEV1.0) at each load while the ratio of FEV1.0 to FVC (FEV1.0%) was maintained. No significant differences in any variable were found across time or between the seated and standing position. These results indicate that this chest wall-restrictive device provides a quantifiable added inspiratory load in the breathing cycle that results in reproducible decrements in pulmonary function representative of those seen in some restrictive pulmonary disease and occupational situations. (+info)
(7/1124) A chest wall restrictor to study effects on pulmonary function and exercise. 2. The energetics of restrictive breathing.
Chest wall restriction, whether caused by disease or mechanical constraints such as protective outerwear, can cause decrements in pulmonary function and exercise capacity. However, the study of the oxygen cost associated with mechanical chest restriction has so far been purely qualitative. The previous paper in this series described a device to impose external chest wall restriction, its effects on forced spirometric volumes, and its test-retest reliability. The purpose of this experiment was to measure the oxygen cost associated with varied levels of external chest wall restriction. Oxygen uptake and electromyogram (EMG) of the external intercostals were recorded during chest restriction in 10 healthy males. Subjects rested for 9 min before undergoing volitional isocapnic hyperpnea for 6 min. Subjects breathed at minute ventilations (V.I) of 30, 60, and 90 liters/min with chest wall loads of 0, 25, 50 and 75 mm Hg applied. Frequency of breathing was set at 15, 30, and 45 breaths per minute with a constant tidal volume (VT) of 2 liters. Oxygen uptake was measured continuously at rest and throughout the hyperventilation bouts, while controlling V.I and VT. Integrated EMG (IEMG) from the 3rd intercostal space was recorded during each minute of rest and hyperventilation. Two-way ANOVA with repeated measures revealed that chest wall loading and hyperpnea significantly increased V.O2 values (p < 0.01). External intercostal IEMG levels were significantly increased (p < 0.05) at higher restrictive load (50 and 75 mm Hg) and at the highest minute ventilation (90 liters/min). These data suggest that there is a significant and quantifiable increase in the oxygen cost associated with external chest wall restriction which is directly related to the level of chest wall restriction. (+info)
(8/1124) Lung and chest wall mechanics in ventilated patients with end stage idiopathic pulmonary fibrosis.
BACKGROUND: Idiopathic pulmonary fibrosis is an inflammatory disease which leads to chronic ventilatory insufficiency and is characterised by a reduction in pulmonary static and dynamic volumes. It has been suggested that lung elastance may also be abnormally increased, particularly in end stage disease, but this has not been systematically tested. The aim of this study was to assess the respiratory mechanics during mechanical ventilation in patients affected by end stage disease. METHODS: Respiratory mechanics were monitored in seven patients with idiopathic pulmonary fibrosis being ventilated for acute respiratory failure (PaO2/FiO2 5.8 (0.3); pH 7. 28 (0.02); PaCO2 8.44 (0.82) kPa; tidal volume 3.4 (0.2) ml/kg; respiratory rate 35.1 (8.8) breaths/min) using an oesophageal balloon and airway occlusion during constant flow inflation. The total respiratory system mechanics (rs) was partitioned into lung (L) and chest wall (w) mechanics to measure static intrinsic positive end expiratory pressure (PEEPi), static (Est) and dynamic (Edyn) elastances, total respiratory resistance (Rrs), interrupter respiratory resistance (Rint,rs), and additional respiratory resistance (DeltaRrs). RESULTS: PEEPi was negligible in all patients. Edyn,rs and Est,rs were markedly increased (60.9 (7.3) and 51.9 (8. 0) cm H2O/l, respectively), and this was due to abnormal lung elastance (dynamic 53.9 (8.0) cm H2O/l, static 46.1 (8.1) cm H2O/l) while chest wall elastance was only slightly increased. Rrs and Rint, rs were also increased above the normal range (16.7 (4.5) and 13.7 (3.5) cm H2O/l/s, respectively). RL and Rint,L contributed 88% and 89%, on average, to the total. Edyn,rs, Est,rs, Rrs and Rint,rs were significantly correlated with the degree of hypercapnia (r = 0.64 (p<0.01), r = 0.54 (p<0.05), r = 0.84 (p<0.001), and r = 0.72 (p<0. 001), respectively). CONCLUSIONS: The elastances and resistances of the respiratory system are significantly altered in ventilated patients with end stage idiopathic pulmonary fibrosis. These features are almost totally due to abnormalities in lung mechanics. These profound alterations in elastic and resistive mechanical properties at this stage of the disease may be responsible for the onset of hypercapnia. (+info)