Violation of the linearity condition at V ≤ 100 ml/sec caused shifts between methods with regard to the partition of exhaled NO into alveolar (C(A)NO: P > T) and bronchial (J(aw)NO: T > P) components. Both methods gave similar results in the linear range of 150-250 ml/sec: The mean ratios P/T and limits of agreement calculated in AA and AR patients were 1.03 (0.49-1.56) and 1.07 (0.55-1.59) for C(A)NO and 1.03 (0.73-1.33) and 0.99 (0.90-1.10) for J(aw)NO, respectively. No significant differences between AA and AR were found in C(A)NO and J(aw)NO calculated in the linear range by the T method {medians (inter-quartile ranges): 1.7 ppb (0.9-3.9) vs. 2.3 ppb (0.8-3.7), P = 0.91; 1,800 pl/sec (950-3,560) vs. 1,180 pl/sec (639-1,950), P = 0.061}. However, the flow-dependency of the estimates was markedly higher in AA than in AR patients: C(A) NO was decreased 2.8-fold vs. 1.5-fold and J(aw) NO was increased 1.5-fold vs. 1.2-fold in the linear range as compared to the range of 50-250 ml/sec. In both groups, the median standard errors (SE) of the J(aw) NO estimates were similar for the metods P and T and small (<15%) regardless of the range for expiratory flows. The precision of C(A) NO estimates was less in all ranges. For both methods, the SE of the estimates obtained in the range of 150-250 ml/sec exceeded 50% in asthmatics and 30% in AR patients, respectively. The results show that FE(NO) has to be measured at several expiratory flows ≥100 ml/sec for the accurate estimation of C(A) NO and J(aw) NO using linear methods P and T in children and adolescents with AA and AR. A stepwise procedure for detecting nonlinearity and evaluating the quality of FE(NO) measurements is suggested.
A rat model of early sepsis induced by lipopolysaccharide (LPS) combined with interleukin-2 (IL-2) was developed. The primary aim was to assess the pharmacokinetics of gentamicin and sepsis-induced pathophysiological changes. Moreover, the effects on the glomerular filtration rate and tubular function were studied in septic and control rats. First, an intravenous (i.v.) bolus of LPSIL-2 (1 mg/kg-Pseudomonas aeruginosa, 15 µg/ kg IL-2) or saline (controls, C) was administred. The Wistar rats were treated 30 min after LPSIL-2 with gentamicin as a 3 mg/kg i.v. bolus followed 10 min later by an i.v. 170-min infusion (GE, 0.09 mg/kg·min 1 ). The monitoring of vital functions, biochemistry and GE concentrations was performed. Creatinine clearance was 2-3 times lower and fractional urea excretion was 3-4 times less in septic rats as compared to controls(p<0.05), although urine flow was comparable. Capillary leakage caused a 55% elevation in the volume of distribution (V c ) in the LPSIL GE group vs. C GE (p<0.05). The renal CL ge was less (2.2 0.59 vs. 3.8 0.53 mL/min·kg 1 , p<0.05), while the total CL ge was comparable (5.9 1.5 vs. 6.7 1.1 mL/min·kg 1 ; p 0.30). In the LPSIL GE group relative to C GE, the half-life (t 1/2 ) was 79% higher (p<0.05) and GE concentrations detected at the end of the study in the plasma and kidney were elevated 2.5-fold (p 0.09) and 2.2-fold (p<0.05), respectively. The model reproduced several consequences of early sepsis like in patients such as capillary leak, a decreased glomerular filtration rate (GFR) and the changes in pharmacokinetics of GE (increased values of V c and t 1/2 and a drop in renal CL ge proportional to that of CL cr ). Nonrenal routes which, for the most part, compensate the reduced renal CL ge in septic rats deserve further study.
Hypothermia was shown to attenuate ventilator-induced lung
injury due to large tidal volumes. It is unclear if the protective
effect of hypothermia is maintained under less injurious
mechanical ventilation in animals without previous lung injury.
Tracheostomized rats were randomly allocated to non-ventilated
group (group C) or ventilated groups of normothermia (group N)
and mild hypothermia (group H). After two hours of mechanical
ventilation with inspiratory fraction of oxygen 1.0, respiratory
rate 60 min-1, tidal volume 10 ml·kg-1, positive end-expiratory
pressure (PEEP) 2 cm H2O or immediately after tracheostomy in
non-ventilated animals inspiratory pressures were recorded, rats
were sacrificed, pressure-volume (PV) curve of respiratory
system constructed, bronchoalveolar lavage (BAL) fluid and aortic
blood samples obtained. Group N animals exhibited a higher rise
in peak inspiratory pressures in comparison to group H animals.
Shift of the PV curve to right, higher total protein and interleukin6 levels in BAL fluid were observed in normothermia animals in
comparison with hypothermia animals and non-ventilated
controls. Tumor necrosis factor-α was lower in the hypothermia
group in comparison with normothermia and non-ventilated
groups. Mild hypothermia attenuated changes in respiratory
system mechanics and modified cytokine concentration in
bronchoalveolar lavage fluid during low lung volume ventilation in
animals without previous lung injury.
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