PubMed · 12588719
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Peter D Bridge, Sheila A McKenzie. 2003-02-15. Time for standardization.. https://doi.org/10.1164/ajrccm.167.4.957
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Carbon monoxide (CO) in expired gas has been shown to be elevated with asthma; however, its function is not known, and there is some potential that it may serve a bronchoprotective role to decrease airway hyperresponsiveness (AHR). Thus the ability of CO to reverse methacholine (MCh)-induced bronchoconstriction was evaluated in C57BL/6 (C57) and A/J mice with and without airway inflammation produced by ovalbumin (OVA). Acutely administered CO (1% in air, 10 min) reduced MCh-driven increases in lung resistance in OVA-challenged C57 mice by an average of 50% (from 14.5 to 7.1 cmH2O.ml-1.s-1), whereas no effect was observed in naïve C57 mice or OVA-challenged C57 mice inhaling air alone. Acutely inhaled CO (500 ppm = 0.05%, for 10 min) reduced MCh-induced airway reactivity (AR) by 20-60% in airway hyperresponsive naïve A/J mice, whereas repeated 10-min administrations of 500 ppm CO over a 5-day period decreased AR by 50%. Repeated administration of low-dose CO [250 (0.025%) and (0.05%) 500 ppm, 1 h/day, 5 days] to A/J mice with airway inflammation likewise resulted in a drop of AR by 50%, compared with those not receiving CO. Inhibition of guanylyl cyclase/guanosine 3',5'-cyclic monophosphothioate (cGMP) using 1H-[1,2,4] oxydiazolo[4,3-a]quinoxalin-1-one or a competitive inhibitor, Rp diastereomers of 8-bromo-cGMP, resulted in inhibition of the effect of CO on AHR, suggesting that the effects of CO were mediated through this mechanism. These results indicate that low-dose CO can effectively reverse AHR in the presence and absence of airway inflammation in mice and suggest a potential role for CO in the modulation of AHR.
OBJECTIVE: To determine the effect of forced deflation maneuvers on respiratory mechanics and to assess the reproducibility of such measurements in intubated infants with lung disease. DESIGN AND SETTING: Prospective study in the pediatric intensive care unit of a university children's hospital. PATIENTS: Ten clinically stable infants requiring mechanically assisted ventilation for acute pulmonary disease, mean age 5.9 months (1-18), mean weight 5.8 kg (3.2-13). INTERVENTIONS: Two sets of measurements of compliance (Crs) and resistance (Rrs) were obtained at 20-min intervals both before and after +40/-40 cmH(2)O forced deflation maneuvers. Forced deflation measurements were repeated at the end of the study. RESULTS: . Forced deflation caused a significant increase in Crs from 0.53+/-0.09 and 0.58+/-0.11 ml/cmH(2)O/kg to 0.71+/-0.11 and 0.68+/-0.11 ml/cmH(2)O/kg. Rrs measurements did not differ. The low coefficients of variation for repeated measures of the baseline measurements (Crs 4.2+/-0.5%, Rrs 7.1+/-0.8%, for forced vital capacity 8.6+/-2.5%, maximum expiratory flows at 25% vital capacity 16.0%+/-3.3%) confirmed the good reproducibility during stable conditions. CONCLUSIONS: Inflation and deflation maneuvers affect subsequent measurements of respiratory system compliance but not measurements of maximum expiratory flow-volume relationships in intubated infants, probably through recruitment of lung volume. Careful interpretation and planning of the sequence of infant pulmonary function testing is necessary to reassure that changes are not related to short-term alterations in volume history.
Mechanical distortion of blood vessels is known to activate endothelial cells. Whether airway distension likewise activates the vascular endothelium within the airway wall is unknown. Using intravital microscopy in the rat trachea, we investigated if airway distention with the application of positive end-expiratory pressure (PEEP) caused leukocyte recruitment to the airway. Tracheal postcapillary venules were visualized and leukocyte kinetics monitored in anesthetized, mechanically ventilated rats (80 breaths/minute, 6 ml/kg VT, 1 cm H(2)O PEEP). Leukocyte rolling velocity (Vwbc) and the number of adherent cells were not altered with normal ventilation over the course of 2 hours. Ventilation with sustained PEEP (8 cm H(2)O for 1 hour reduced Vwbc and increased adhesion, reaching a maximum at 1 hour of PEEP. Intermittent (2x and 5x) 8 cm H(2)O PEEP also induced a similar reduction in Vwbc, accompanied by an increase in adhesion. However, leukocyte recruitment after airway distension is localized to the airways because increased PEEP did not induce leukocyte recruitment in the mesenteric microcirculation or when PEEP was applied to the lung distal to the site of measurement. Pretreatment with endothelin receptor and selectin inhibitors blocked the effects of distension on leukocyte recruitment, suggesting their involvement in the proinflammatory response.