1,721,019 research outputs found
Ossigeno : dall’aria all’alveolo
No full textIl gradiente alveolo arterioso di ossigeno è calcolato, in ambito clinico, in base alla misura delle pressioni parziali di ossigeno e di anidride carbonica nel sangue arterioso, e ad alcune semplificazioni e assunzioni (ad esempio che il quoziente respiratorio sia uguale a circa 0.8 o che la pressione parziale di anidride carbonica nel sangue arterioso sia uguale a quella nel gas alveolare). In questo intervento è stato discussa l'entità dell'errore inevitabilmente introdotto da queste assunzioni nella stima del gradiente alveolo arterioso di ossigeno in varie situazioni cliniche
Weibel: l’importanza della morfometria polmonare
No full textCalcolo della capacità di diffusione polmonare per l'ossigeno su basi morfometriche
Assessment of airway occlusion by single breath N2 test and deflation lung PL-V curve in healthy subjects and COPD patients
No full textCyclic airway closing and opening may induce lung injury in both normal and diseased lung. During tidal breathing this phenomenon occurs when closing volume (CV) exceeds the expiratory reserve volume. In humans, CV is currently assessed from the onset of phase IV of the single breath nitrogen test (CVSBN), but this method fails in severe chronic obstructive pulmonary disease (COPD) patients in whom phase IV can be absent, even if the amount of airway closure should be substantial. At present, no agreement exists whether an another potential indicator of airways closure, the inflection point on the transpulmonary pressure–volume curve (CVPL-V) can be used as a surrogate of CVSBN, when phase IV is not detectable. The comparison of CVSBN with CVPL-V assessed during the same slow deflation showed that both in healthy subjects and in COPD patients, when CVSBN was present, it coincided with CVPL-V. In the young subjects in whom CVSBN was absent, CVPL-V was not detectable, in accordance to the notion that in these subjects lung recoil can be high enough to prevent airway closure in the whole vital capacity range. On the other hand, in the COPD patients with no phase IV, CVPL-V was constantly present, as expected. These results suggest that measurement of CVPL-V is a reliable method for closing volume assessment in both normal and COPD subjects. In the latter group, the measurement of CVSBN can lead to heavily underestimate the extent of the airway collapse
Pathophysiology of chronic obstructive pulmonary disease
No full textIn normal animals, cyclic airway closure and reopening during prolonged mechanical ventilation at low lung volumes causes histological damage of small airways, characterized by epithelial sloughing and lesion and/or rupture of alveolar-bronchiolar attachments, with a concurrent increase in airway resistance that persists after restoration of physiological end-expiratory lung volume. Peripheral airway injury should be therefore expected to occur when the closing capacity exceeds the functional residual capacity and tidal airway closure is regularly present during spontaneous breathing. On these basis, it is proposed that in smokers the transition from peripheral airway disease to chronic obstructive pulmonary disease is characterized by three sequential stages: Stage I, during which the closing capacity eventually exceeds the functional residual capacity, i.e. airway closure and reopening occur cyclically with breathing; Stage II, during which tidal expiratory flow limitation is eventually exhibited; and Stage III, during which dynamic hyperinflation progressively increases leading to dyspnea and exercise limitation. In this perspective, it is tidal airway closure and, probably, tidal expiratory flow limitation that promote peripheral airway injury, accelerate the abnormalities of lung function, and may determine which smoker is destined to develop chronic obstructive pulmonary disease
Motor control of the diaphragm in anesthetized rabbits
Full text linkDiaphragmatic regions are recruited in a specialized manner either as part of a central motor program during non-respiratory maneuvers, e.g. vomiting, or because of reflex responses, e.g. esophageal distension. Some studies in cats and dogs suggest that crural and costal diaphragm may be differentially activated also in response to respiratory stimuli from chemoreceptors or lung and chest wall mechanoreceptors. To verify whether this could occur also in other species, the EMG activity from the sternal, costoventral, costodorsal, and crural diaphragm was recorded in 42 anesthetized rabbits in response to various respiratory maneuvers, such as chemical stimulation, mechanical loading, lung volume and postural changes before and after vagotomy, or a non-respiratory maneuver such as esophageal distension. Regional activity was evaluated from timing of the raw EMG signal, and amplitude and shape of the moving average EMG. In all animals esophageal distension caused greater inhibition of the crural than sternal and costal diaphragm, whereas under all the other conditions differential diaphragmatic activation never occurred. These results indicate that in response to respiratory stimuli the rabbit diaphragm behaves as a single unit under the command of the central respiratory control system
Dependence of lung injury on surface tension during low-volume ventilation in normal open-chest rabbits
Full text linkIn order to evaluate the role of pulmonary surfactant in the prevention of lung injury caused by mechanical ventilation (MV) at low end-expiratory volumes, lung mechanics and morphometry were assessed in three groups of 8 normal, open-chest rabbits ventilated for 3-4 h at zero end-expiratory pressure (ZEEP) with physiologic tidal volumes (VT=10 ml(.)kg(-1)). One group was left untreated (group A), the other two received surfactant intratracheally (group B) or aerosolized dioctylsodiumsulfosuccinate (group C) before MV on ZEEP. Relative to initial MV on PEEP (2.3 cmH2O), quasi-static elastance (Est) and airway (Rint) and viscoelastic resistance (Rvisc) increased on ZEEP in all groups. After restoration of PEEP, only Rint (124%) remained elevated in group A, only Est (36%) was significantly increased in group B, whereas in group C Est, Rint and Rvisc were all markedly augmented (274, 253, and 343%). In contrast, prolonged MV on PEEP had no effect on lung mechanics of 8 open-chest rabbits (group D). Lung edema developed in group C (wet-to-dry ratio=7.1), but not in the other groups. Relative to group D, both group A and C but not B, showed histological indices of bronchiolar injury, while all groups exhibited an increased number of polymorphonuclear leukocytes in alveolar septa, which was significantly greater in group C. In conclusion, administration of exogenous surfactant largely prevents the histological and functional damage of prolonged MV at low lung volumes, whereas surfactant dysfunction worsen the functional alterations, also because of edema formation and, possibly, increased inflammatory response
Effects of low lung volume ventilation on respiratory mechanics and nitric oxide exhalation in normal rabbits
No full textExhaled NO (NOe), tumor necrosis factor α (TNF) in serum and bronchoalveolar lavage fluid (BALF), and lung mechanics were assessed in 8 closed and 8 open chest, normal anesthetized rabbits undergoing prolonged (3-4 h) mechanical ventilation (MV) at low volume with fixed tidal volume (10 ml/kg). Low volume ventilation increased lung quasi-static elastance (Est; 267 and 281%), airway (Rint; 471 and 382%) and viscoelastic resistance (Rvisc; 480 and 294%), and decreased NOe (-42 and -25%) in closed and open chest animals, respectively. After restoration of normal end-expiratory volume (EEV), Rvisc returned to control, Rint remained elevated (120 and 31%), and NOe low (-25 and -20%), whilst Est increased (23%) only in closed chest animals, being associated to interstitial edema. In contrast, after prolonged MV with normal EEV, there were no changes in lung mechanics and NOe in 16 additional closed and open chest rabbits. After prolonged MV, TNF was undetectable in serum, while its concentration in BALF was low (48 pg/ml) and similar in all groups of animals.
Thus, cyclic opening-closing of peripheral airways and uneven stresses with low volume MV, that cause epithelial damage and rupture of alveolar-bronchiolar attachments (D'Angelo, E. et al. J Applied Physiol 2004; 97:260-268), result in reduced NOe and increased Rint. These alterations are not mediated by a proinflammatory process as indexed by TNF levels
Understanding at-risk subgroups for lung function impairment in life-long nonsmokers with α1-antitrypsin deficiency
Full text linkLung-deflating ability of rib cage and abdominal muscles in rabbits
No full textAnesthetized, apneic, mechanically ventilated rabbits were placed into a tilting plethysmograph that a rubber diaphragm, tightly fitting the animal's body just below the xiphoid process, separated into a rib cage and abdominal chamber. Expired volumes (ΔV) and abdominal pressure changes (ΔPab) were assessed in supine and upright posture during maximal rib cage (RCC) and/or abdominal compression (ABC) by pressurizing either or both chambers, and during maximal stimulations of abdominal muscles (ABS). With RCC, ΔV supine and upright amounted to 16±4.9 (mean±S.D.) and 20.9±7% of the vital capacity in supine posture (VCs) and to 75.8±14.5 and 44.8±13.9% of the expiratory reserve volume (ERV) in corresponding posture, ΔPab being negligible. With ABC, ΔV was 13.7±2 and 38.9±7.3% VCs and 68.4±14.8 and 84.4±10.5% ERV, respectively. Both ΔV and ΔPab were similar with ABC and ABS, independent of posture. If this applies also to RCC and expiratory rib cage muscle contraction, maximal expiratory effects of the latter (a) are larger in upright than supine posture; (b) contribute to ERV more in supine than upright posture; and (c) are similar to those caused by ABS in supine, but substantially smaller in upright posture
Uso delle resistenze specifiche per la stima della risposta al broncodilatatore in pazienti BPCO
No full textNei pazienti affetti da broncopneumopatia cronica ostruttiva (BPCO), i broncodilatatori migliorano la funzione polmonare e alleviano la sintomatologia respiratoria nella misura in cui riducono la resistenza delle vie aeree durante la respirazione tidalica, prevenendo o riducendo l’iperinflazione dinamica (Barnes et al., 1981). Inoltre, la riduzione del tono broncomotore a livello delle piccole vie aeree può ridurre il volume residuo (RV) e aumentare la capacità vitale (VC).
Secondo le linee guida ATS/ERS (Pellegrino et al., 2005), un paziente BPCO risponde a un broncodilatatore se, dopo somministrazione del farmaco, l’aumento del volume espirato forzatamente in un secondo (FEV1) e/o della capacità vitale forzata (FVC) è uguale o maggiore del 12% del valore di controllo, e comunque uguale o maggiore di 200 ml.
Tuttavia è noto che a) FEV1 riflette solo parzialmente le resistenze polmonari (Pride, 1971;Skinner and Palmer, 1974), b) la misurazione di FEV1 e di FVC è ottenuta con una manovra di per sè in grado di modificare il calibro delle vie aeree (Barnes et al., 1981), c) FEV1 e FVC sono altamente correlate (Schermer et al., 2007), e d) le variazioni di FEV1 e di FVC nei pazienti BPCO di grado severo possono essere molto piccole (Deesomchok et al., 2010).
E’ possibile che le variazioni delle resistenze specifiche pletismografiche (sRAW), un parametro che riflette accuratamente le resistenze delle vie aeree periferiche (Bassiri et al., 1997), possano evidenziare l’azione dei broncodilatatori nei pazienti BPCO meglio di quanto possano fare le variazioni di FEV1 o di FVC
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