1,721,249 research outputs found
Airway inflammation in chronic obstructive pulmonary disease
No full textCigarette smoking causes an inflammatory process in the central airways, peripheral airways, and lung parenchyma, even in smokers with normal lung function. The characteristics of this inflammatory process differ between smokers who develop chronic airflow limitation (COPD) and those who do not develop chronic airflow limitation: there is an increased infiltration of CD8- positive T lymphocytes in smokers with COPD. We examine whether airway inflammation alters with increasing severity of disease. When the disease becomes severe, a prominent neutrophilia occurs. The precise roles of the CD8+ T lymphocyte and the neutrophil in the pathogenesis of COPD still remain to be determined
Mechanisms of bronchial obstruction in COPD and emphysema: From anatomopathology to respiratory function
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Airway pathology in asthma
No full textAbstract
This review focuses on the major cellular and structural changes present in the airways and lung parenchyma in asthma in comparison with chronic obstructive pulmonary disease (COPD) in an attempt to underline the possible mechanisms contributing to airflow limitation in these two diseases. Both asthma and COPD are characterized by a thickening of the airway wall and by the presence of an inflammatory process, but the inflammatory cells infiltrating the airway wall differ between the two diseases. In asthma, the most striking feature is the eosinophilic infiltration, whereas, in COPD, it is the CD8 T-lymphocytic infiltration of the airway wall. In the lung parenchyma, both diseases are characterized by an inflammatory process, whereas destruction and fibrosis of the alveolar walls occur in COPD but not in asthma. These cellular and structural changes may contribute to the development of airflow limitation (that characterizes both asthma and chronic obstructive pulmonary disease) by inducing either an increase in resistance or a decrease in driving pressure
Interaction of hypoxic and hypercapnic stimuli on breathing pattern in the newborn rat.
No full textAbstract
We aimed to investigate whether newborn rats respond to acute hypoxia with a biphasic pattern as other newborn species, the characteristics of their ventilatory response to hypercapnia, and the ventilatory response to combined hypoxic and hypercapnic stimuli. First, we established that newborn unanesthetized rats (2-4 days old) exposed to 10% O2 respond as other species. Their ventilation (VE), measured by flow plethysmography, immediately increased by 30%, then dropped and remained around normoxic values within 5 min. The drop was due to a decrease in tidal volume, while frequency remained elevated. Hence, alveolar ventilation was about 10% below normoxic value. At the same time O2 consumption, measured manometrically, dropped (-23%), possibly indicating a mechanism to protect vital organs. Ten percent CO2 in O2 breathing determined a substantial increase in VE (+47%), indicating that the respiratory pump is capable of a marked sustained hyperventilation. When CO2 was added to the hypoxic mixture, VE increased by about 85%, significantly more than without the concurrent hypoxic stimulus. Thus, even during the drop in VE of the biphasic response to hypoxia, the respiratory control system can respond with excitation to a further increase in chemical drive. Analysis of the breathing patterns suggests that in the newborn rat in hypoxia the inspiratory drive is decreased but the inspiratory on-switch mechanism is stimulated, hypercapnia increases ventilation mainly through an increase in respiratory drive, and moderate asphyxia induces the most powerful ventilatory response by combining the stimulatory action of hypercapnia and hypoxia
Exponential analysis of the lung pressure-volume curve in newborn mammals.
No full textAbstract
The compliance of the lung (per unit of lung weight) is less in newborn mammals than in adults. This could result from a smaller volume of airspaces per unit weight and/or a lower lung distensibility. The isolated role of lung distensibility was evaluated by using a mathematical description of the pressure-volume (P-V) curve during lung deflation. Deflation limbs of static P-V curves in newborns of six species (four experimentally obtained and two taken from the literature) ranging from total lung capacity to the resting volume (Vr) were fitted by a monoexponential function of the type V = B - Ae-KP, where B equals Vmax at infinite P, A equals the difference between Vmax and V at P = O, and K is a constant representing lung distensibility. Unlike in adults, in newborns the monoexponential fitting provided an adequate description of the P-V curve for only a relatively small range of transpulmonary pressure (from P at Vr to 10-15 cm H2O). The K value of this portion of the curve was similar among species but higher than in adult mammals, averaging 0.240 cm H2O-1. This suggests a similar lung structure in the different species. Since lung distensibility in newborns is larger than in adults, the fact that a unit mass of lung in the newborn is less compliant should be due to the smaller volume of its airspaces
Breathing pattern and CO2 response in newborn rats before and during anesthesia.
No full textAbstract
We have studied the breathing pattern (minute ventilation VE, tidal volume VT, and respiratory rate f) in newborn rats before and during barbiturate (20-30 mg/kg ip) or ketamine anesthesia (40-80 mg/kg ip). Animals were intact and prone in a flow plethysmograph in thermoneutral conditions. Before anesthesia, CO2 breathing (5 min in 5% and 5 min in 10% CO2 in O2) resulted in a substantial increase in VE (169 and 208%, respectively), which was maintained throughout the entire CO2 breathing period. This indicates that, despite the extremely large VE per kilogram at rest, in these small animals there is still a large reserve for a sustained increase in VE. During barbiturate, the resting VE dropped to 45% of control, due to a reduction in VT (83%) and f (59%). This latter result was due to a prolongation of the expiratory time (214%) with no significant changes in inspiratory time. CO2 response was also much depressed, to approximately 63% of the control. The late portion of the expiratory flow-volume curves, the slope of which represents the expiratory time constant of the system, was similar before and during anesthesia in approximately 50% of the animals, whereas it increased during anesthesia in the remaining animals. Although compliance of the respiratory system was generally unaltered, the increased impedance during anesthesia probably reflected an increased resistance. Qualitatively similar results were obtained during ketamine anesthesia. Therefore, as observed in adult mammals, anesthesia in newborn rats has a marked depressant effect on resting breathing pattern and CO2 response, occasionally accompanied by an increase in the expiratory impedance of the respiratory system
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