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Biomedical subjects

B Lachmann

Publications and source records attributed to B Lachmann.

At least 55 records · Page 3Linked to original sources
PubMed1999

Different ventilation strategies affect lung function but do not increase tumor necrosis factor-alpha and prostacyclin production in lavaged rat lungs in vivo.

BACKGROUND: Using an in vivo animal model of surfactant deficiency, the authors compared the effect of different ventilation strategies on oxygenation and inflammatory mediator release from the lung parenchyma. METHODS: In adult rats that were mechanically ventilated with 100% oxygen, acute lung injury was induced by repeated lung lavage to obtain an arterial oxygen partial pressure < 85 mmHg (peak pressure/positive end-expiratory pressure [PEEP] = 26/6 cm H2O). Animals were then randomly assigned to receive either exogenous surfactant therapy, partial liquid ventilation, ventilation with high PEEP (16 cm H2O), ventilation with low PEEP (8 cm H2O), or ventilation with an increase in peak inspiratory pressure (to 32 cm H2O; PEEP = 6 cm H2O). Two groups of healthy nonlavaged rats were ventilated at a peak pressure/PEEP of 32/6 and 32/0 cm H2O, respectively. Blood gases were measured. Prostacyclin (PGI2) and tumor necrosis factor-alpha (TNF-alpha) concentrations in serum and bronchoalveolar lavage fluid (BALF) as well as protein concentration in BALF were determined after 90 and 240 min and compared with mechanically ventilated and spontaneously breathing controls. RESULTS: Surfactant, partial liquid ventilation, and high PEEP improved oxygenation and reduced BALF protein levels. Ventilation with high PEEP at high mean airway pressure levels increased BALF PGI2 levels, whereas there was no difference in BALF TNF-alpha levels between groups. Serum PGI2 and TNF-alpha levels did not increase as a result of mechanical ventilation when compared with those of spontaneously breathing controls. CONCLUSIONS: Although alveolar protein concentration and oxygenation markedly differed with different ventilation strategies in this model of acute lung injury, there were no indications of ventilation-induced systemic PGI2 and TNF-alpha release, nor of pulmonary TNF-alpha release. Mechanical ventilation at high mean airway pressure levels increased PGI2 levels in the bronchoalveolar lavage-accessible space.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Purine in bronchoalveolar lavage fluid as a marker of ventilation-induced lung injury.

OBJECTIVE: To investigate in a rat model of ventilation-induced lung injury whether metabolic changes in the lung are reflected by an increased purine concentration (adenosine, inosine, hypoxanthine, xanthine, and urate; an index of adenosine-triphosphate breakdown) of the bronchoalveolar lavage fluid and whether purine can, thus, indirectly serve as a marker of ventilation-induced lung injury. DESIGN: Prospective, randomized, controlled trial. SETTING: Research laboratory. SUBJECTS: Forty-two male Sprague-Dawley rats. INTERVENTIONS: Five groups of Sprague-Dawley rats were subjected to 6 mins of mechanical ventilation. One group was ventilated at a peak inspiratory pressure of 7 cm H2O and a positive end-expiratory pressure of 0 cm H2O. A second group was ventilated at a peak inspiratory pressure of 45 cm H2O and a positive end-expiratory pressure of 10 cm H2O. Three groups of Sprague-Dawley rats were ventilated at a peak inspiratory pressure of 45 cm H2O without positive end-expiratory pressure. Before mechanical ventilation, two of these groups received intratracheal administration of saline or exogenous surfactant at a dose of 100 mg/kg and one group received no intratracheal administration. A sixth group served as the nonventilated controls. MEASUREMENTS AND MAIN RESULTS: Bronchoalveolar lavage fluid was collected in which both purine concentration (microM; mean +/- SD) and protein concentration (mg/mL; mean +/- SD) were determined. Statistical differences were analyzed using the one-way analysis of variance (ANOVA) with a Student-Newman-Keul's post hoc test. Purine and protein concentrations were different between groups (ANOVA p value for purine and protein, <.0001). Both purine and protein concentrations in bronchoalveolar lavage fluid were increased in Group 45/0 (3.2 +/- 1.9 and 4.2 +/- 1.6, respectively) compared with Group 7/0 (0.4 +/- 0.1 [p < .05] and 0.4 +/- 0.2 [p < .001]) and controls (0.2 +/- 0.2 [p < .01] and 0.2 +/- 0.1 [p < .001]) and in Group 45/Na (5.8 +/- 2.5 and 4.2 +/- 0.5) compared with Group 7/0 (purine and protein, p < .001) and the controls (purine and protein, p < .001). Positive end-expiratory pressure prevented an increase in purine and protein concentrations in bronchoalveolar lavage fluid (0.4 +/- 0.3 and 0.4 +/- 0.2, respectively) compared with Group 45/0 (purine, p < .01; protein, p < .001) and Group 45/Na (purine and protein, p < .001). Surfactant instillation preceding lung overinflation reduced purine and protein concentration in bronchoalveolar lavage fluid (2.1 +/- 1.6 and 2.7 +/- 1.0) compared with Group 45/Na (purine, p < .001; protein (p < .01). Surfactant instillation reduced protein concentration compared with Group 45/0 (p < .01). CONCLUSIONS: This study shows that metabolic changes in the lung as a result of ventilation-induced lung injury are reflected by an increased level of purine in the bronchoalveolar lavage fluid and that purine may, thus, serve as an early marker for ventilation-induced lung injury. Moreover, the study shows that both exogenous surfactant and positive end-expiratory pressure reduce protein infiltration and that positive end-expiratory pressure decreases the purine level in bronchoalveolar lavage fluid after lung overinflation.

Analysis of Variance↗
PubMed1999

Conventional ventilation modes with small pressure amplitudes and high positive end-expiratory pressure levels optimize surfactant therapy.

OBJECTIVE: High-frequency oscillation studies have shown that ventilation at high end-expiratory lung volumes combined with small volume cycles at high rates best preserves exogenous surfactant and gas exchange in lavaged lungs. We investigated whether surfactant composition and gas exchange can also be preserved by conventional modes of mechanical ventilation, which combine high levels of positive end-expiratory pressure (PEEP) with small pressure amplitudes. DESIGN: Prospective, randomized, nonblinded, controlled study. SETTING: Research laboratory. SUBJECTS: Thirty male Sprague-Dawley rats. INTERVENTIONS: Rats were lung-lavaged and treated with exogenous surfactant (100 mg/kg). After 5 mins, four different ventilator settings (F(IO)2 = 1.0) were applied for 3 hrs in four groups of rats [peak inspiratory pressure (cm H2O); static PEEP (cm H2O); inspiratory/expiratory ratio; frequency], as follows: 26/2/1:2/30 (group 26/2), 26/6/1:2/30 (group 26/6), 20/10/1:2/30 (group 20/ 10-static), and 20/6/7:3/130, creating an auto PEEP of 4 cm H2O (group 20/10-auto). MEASUREMENTS AND MAIN RESULTS: In all groups, Pao2 increased immediately to prelavage values after surfactant therapy. In group 26/2, Pao2 deteriorated to postlavage values within 30 mins when PEEP was decreased to 2 cm H2O, whereas Pao2 remained stable for 3 hrs in the other groups. The Paco2 increased in groups 26/2 and 20/10-static; Paco2 could not be reduced by increasing ventilation frequency to 130 in group 20/10-static. Groups 26/6 and 20/10-auto remained normocapnic. Bronchoalveolar lavage protein concentration was higher in groups 26/2 and 26/6 compared with groups 20/10-static and 20/10-auto. There was significantly more conversion of surface active large aggregates into nonactive small aggregates in group 26/2 compared with groups 20/10-static and 20/10-auto. CONCLUSIONS: We conclude that exogenous surfactant composition is preserved by conventional modes of mechanical ventilation that use small pressure amplitudes, and adequate oxygenation is maintained by high end-expiratory pressure levels. Effective carbon dioxide removal can be achieved by applying a ventilation mode that creates auto PEEP and not by a mode that applies the same level of PEEP by static PEEP only.

Animals↗
PubMed1999

Mechanisms of ventilation-induced lung injury: physiological rationale to prevent it.

It is being increasingly realized that modes of mechanical ventilation that result in end-inspiratory alveolar overstretching and/or repeated alveolar collapse and re-expansion disturb the normal fluid balance across the alveolocapillary membrane. The effects of this include disturbance of the integrity of the endothelium and epithelium and impairment of the surfactant system and are similar to those seen in acute respiratory distress syndrome (ARDS). There is now also evidence that these modes of mechanical ventilation may result in the translocation of bacteria from the lungs into the bloodstream and the release of inflammatory mediators from the lung tissue into the systemic circulation. It may thus be speculated that mechanical ventilation may contribute to the development of multiple organ failure (MOF). Therefore, during mechanical ventilation, alveolar overstretching and the repeated collapse and re-expansion of alveoli should be prevented by ventilation modes that open up the lung and keep the lung open and ventilate with the smallest possible pressure amplitude. For the future, monitoring techniques should be developed that can evaluate, on-line, whether or not these therapeutic directives are being achieved.

Animals↗
PubMed1998

Lung overinflation without positive end-expiratory pressure promotes bacteremia after experimental Klebsiella pneumoniae inoculation.

OBJECTIVE: To determine the effect of peak inspiratory pressure (PIP) and positive end-expiratory pressure (PEEP) on the development of bacteremia with Klebsiella pneumoniae after mechanical ventilation of intratracheally inoculated rats. DESIGN: Prospective, randomized, animal study. SETTING: Experimental intensive care unit of a University. SUBJECTS: Eighty male Sprague Dawley rats. INTERVENTIONS: Intratracheal inoculation with 100 microliters of saline containing 3.5-5.0 x 10(5) colony forming units (CFUs) K. pneumoniae/ml. Pressure-controlled ventilation (frequency 30 bpm; I/E ratio = 1:2; FIO2 = 1.0) for 180 min at the following settings (PIP/PEEP in cmH2O): 13/3 (n = 16); 13/0 (n = 16); 30/10 (n = 16) and 30/0 (n = 16), starting 22 h after inoculation. Arterial blood samples were obtained and cultured before and 180 min after mechanical ventilation and immediately before sacrifice in two groups of non-ventilated control animals (n = 8 per group). After sacrifice, the lungs were homogenized to determine the number of CFUs K. pneumoniae. MEASUREMENTS AND RESULTS: The number of CFUs recovered from the lungs was comparable in all experimental groups. After 180 min, 11 animals had positive blood cultures for K. pneumoniae in group 30/0, whereas only 2, 0 and 2 animals were positive in 13/3, 13/0 and 30/10, respectively (p < 0.05 group 30/0 versus all other groups). CONCLUSIONS: These data show that 3 h of mechanical ventilation with a PIP of 30 cmH2O without PEEP in rats promotes bacteremia with K. pneumoniae. The use of 10 cmH2O PEEP at such PIP reduces ventilation-induced K. pneumoniae bacteremia.

Animals↗
PubMed1998

Bronchoalveolar lavage with a diluted surfactant suspension prior to surfactant instillation improves the effectiveness of surfactant therapy in experimental acute respiratory distress syndrome (ARDS).

OBJECTIVE: To assess whether bronchoalveolar lavage (BAL) with a diluted surfactant suspension prior to surfactant instillation prevents the only transient improvement in lung function as reported after surfactant instillation in severe acute respiratory distress syndrome (ARDS). DESIGN: Randomized, prospective, experimental study. SETTING: Laboratory and animal facility of a large university. MATERIALS: Adult male Sprague-Dawley rats (280 +/- 30 g). INTERVENTIONS: All animals underwent repetitive whole lung saline lavage to induce acute lung injury. Then, animals were randomly divided into seven study groups: the first group received surfactant (150 mg/ kg) within 10 min after the last lavage (early treatment), whereas in the other six groups mechanical ventilation was continued for 3 h before treatment (late treatment). Treatment consisted of: surfactant instillation at a dose of 150 mg/kg; at a dose of 250 mg/kg; BAL with saline; BAL with a diluted surfactant suspension (2.5 mg/ml); BAL with saline, immediately followed by surfactant instillation (150 mg/kg) and BAL with a diluted surfactant suspension (2.5 mg/kg), immediately followed by surfactant instillation (150 mg/kg). MEASUREMENTS AND RESULTS: Blood gases were measured for 6 h and then BAL was performed to measure the protein concentration and surface tension properties. Mean PaO2 values increased immediately after surfactant instillation to pre-lavage values but remained stable only in the group that received surfactant immediately after the lavage procedure and the group that underwent BAL with a diluted surfactant suspension prior to surfactant instillation. CONCLUSION: BAL with a diluted surfactant suspension prior to surfactant instillation at a later time point in lung injury resulted in a stable improvement of lung function. This improvement is comparable with the results seen after surfactant instillation immediately after lung lavage.

Analysis of Variance↗
PubMed1998

Surfactant impairment after mechanical ventilation with large alveolar surface area changes and effects of positive end-expiratory pressure.

We have assessed the effects of overinflation on surfactant function and composition in rats undergoing ventilation for 20 min with 100% oxygen at a peak inspiratory pressure of 45 cm H2O, with or without PEEP 10 cm H2O (groups 45/10 and 45/0, respectively). Mean tidal volumes were 48.4 (SEM 0.3) ml kg-1 in group 45/0 and 18.3 (0.1) ml kg-1 in group 45/10. Arterial oxygenation in group 45/0 was reduced after 20 min compared with group 45/10 (305 (71) vs 564 (10) mm Hg); maximal compliance of the P-V curve was decreased (2.09 (0.13) vs 4.16 (0.35) ml cm H2O-1 kg-1); total lung volume at a transpulmonary pressure of 5 cm H2O was reduced (6.5 (1.0) vs 18.8 (1.4) ml kg-1) and the Gruenwald index was less (0.22 (0.02) vs 0.40 (0.05)). Bronchoalveolar lavage fluid from the group of animals who underwent ventilation without PEEP had a greater protein concentration (2.18 (0.11) vs 0.76 (0.22) mg ml-1) and a greater minimal surface tension (37.2 (6.3) vs 24.5 (2.8) mN m-1) than in those who underwent ventilation with PEEP. Group 45/0 had an increase in non-active to active total phosphorus compared with nonventilated controls (0.90 (0.16) vs 0.30 (0.07)). We conclude that ventilation in healthy rats with peak inspiratory pressures of 45 cm H2O without PEEP for 20 min caused severe impairment of pulmonary surfactant composition and function which can be prevented by the use of PEEP 10 cm H2O.

Animals↗
PubMed1998

Exogenous surfactant preserves lung function and reduces alveolar Evans blue dye influx in a rat model of ventilation-induced lung injury.

BACKGROUND: Changes in pulmonary edema infiltration and surfactant after intermittent positive pressure ventilation with high peak inspiratory lung volumes have been well described. To further elucidate the role of surfactant changes, the authors tested the effect of different doses of exogenous surfactant preceding high peak inspiratory lung volumes on lung function and lung permeability. METHODS: Five groups of Sprague-Dawley rats (n = 6 per group) were subjected to 20 min of high peak inspiratory lung volumes. Before high peak inspiratory lung volumes, four of these groups received intratracheal administration of saline or 50, 100, or 200 mg/kg body weight surfactant; one group received no intratracheal administration. Gas exchange was measured during mechanical ventilation. A sixth group served as nontreated, nonventilated controls. After death, all lungs were excised, and static pressure-volume curves and total lung volume at a transpulmonary pressure of 5 cm H2O were recorded. The Gruenwald index and the steepest part of the compliance curve (Cmax) were calculated. A bronchoalveolar lavage was performed; surfactant small and large aggregate total phosphorus and minimal surface tension were measured. In a second experiment in five groups of rats (n = 6 per group), lung permeability for Evans blue dye was measured. Before 20 min of high peak inspiratory lung volumes, three groups received intratracheal administration of 100, 200, or 400 mg/ kg body weight surfactant; one group received no intratracheal administration. A fifth group served as nontreated, nonventilated controls. RESULTS: Exogenous surfactant at a dose of 200 mg/kg preserved total lung volume at a pressure of 5 cm H2O, maximum compliance, the Gruenwald Index, and oxygenation after 20 min of mechanical ventilation. The most active surfactant was recovered in the group that received 200 mg/kg surfactant, and this dose reduced minimal surface tension of bronchoalveolar lavage to control values. Alveolar influx of Evans blue dye was reduced in the groups that received 200 and 400 mg/kg exogenous surfactant. CONCLUSIONS: Exogenous surfactant preceding high peak inspiratory lung volumes prevents impairment of oxygenation, lung mechanics, and minimal surface tension of bronchoalveolar lavage fluid and reduces alveolar influx of Evans blue dye. These data indicate that surfactant has a beneficial effect on ventilation-induced lung injury.

Animals↗
PubMed1998

Surfactant therapy restores gas exchange in lung injury due to paraquat intoxication in rats.

Paraquat is a weed killer which causes often fatal lung damage in humans and other animals. There is evidence that the pulmonary surfactant system is involved in the pathophysiology of respiratory failure after paraquat intoxication and, therefore, the possible therapeutic effect of intratracheal surfactant administration on gas exchange in rats with progressive lung injury induced by paraquat poisoning was studied. In one group of rats, the time course of the development of lung injury due to paraquat intoxication was characterized. In a second group of rats, 72 h after paraquat intoxication, the animals underwent mechanical ventilation and only those animals in which the arterial oxygen tension/inspiratory oxygen fraction (Pa,O2/FI,O2) decreased to below 20 kPa (150 mmHg) received exogenous surfactant (200 mg x kg(-1) body weight). Within 3 days the rats in group 1 developed progressive respiratory failure, demonstrated not only by impaired gas exchange and lung mechanics but also by increased minimal surface tension and increased protein concentration in bronchoalveolar lavage fluid. In group 2, intratracheal surfactant administration increased Pa,O2/FI,O2 significantly within 5 min (14.4+/-2.4 kPa (108+/-18 mmHg)) to (55.2+/-53 kPa (414+/-40 mmHg)) and sustained this level for at least 2 h. It is concluded that intratracheal surfactant administration is a promising approach in the treatment of severe respiratory failure caused by paraquat poisoning.

Animals↗
PubMed1997

Combining partial liquid ventilation with nitric oxide to improve gas exchange in acute lung injury.

OBJECTIVE: To assess the effects of increasing concentrations of inhaled nitric oxide (NO) during incremental dosages of partial liquid ventilation (PLV) on gas exchange, hemodynamics, and oxygen transport in pigs with induced acute lung injury (ALI). DESIGN: Prospective experimental study. SETTING: Experimental intensive care unit of a university. SUBJECTS: 6 pigs with induced ALI. INTERVENTIONS: Animals were surfactant-depleted by lung lavage to a partial pressure of oxygen in arterial blood (PaO2) < 100 mmHg. They then received four incremental doses of 5 ml/kg perflubron (Liqui-Vent). Between each dose the animals received 0, 10, 20, 30, 40, and 0 parts per million (ppm) NO. MEASUREMENTS AND MAIN RESULTS: Blood gases, hemodynamic parameters, and oxygen delivery were measured after each dose of perflubron as well as after each NO concentration. Perflubron resulted in a dose-dependent increase in PaO2. At each perflubron dose, additional NO inhalation resulted in a further significant (ANOVA, p < 0.05) increase in PaO2, with a maximum effect at 30 +/- 10 ppm NO. The 5 ml/kg perflubron dose led to a significant decrease in mean pulmonary artery pressure, which decreased further with higher NO concentrations. CONCLUSIONS: PLV can be combined with NO administration and results in a cumulative effect on arterial oxygenation and to a decrease in pulmonary artery pressure, without having any deleterious effect on measured systemic hemodynamic parameters.

Administration, Inhalation↗
PubMed1997

Cardiac depression after experimental air embolism in pigs: role of addition of a surface-active agent.

OBJECTIVE: Air bubbles entering the coronary artery may have harmful effects on cardiac function. From the physical point of view it is the relatively high surface tension of the blood-air interface which causes bubbles to trap in small vessels. The aim of the present study was to reduce depression of myocardial function from air embolism by lowering the surface tension of air bubbles. METHODS: The effect of using antifoam as a surface-tension-reducing agent on air bubble entrapment and cardiac function was investigated in 6 anesthetized pigs (27 +/- 1 kg) and analyzed using a two-compartment diffusion model. Air bubbles with a diameter of 150 microns were selectively injected into the left anterior descending coronary artery (LADCA) in a carrying fluid in the presence or absence of antifoam. Myocardial systolic segment shortening in the LADCA region (SS-LADCA) was measured by sonomicrometry. Presence of emboli was detected by measuring the amount of reverberation of ultrasound scattered by trapped air bubbles. RESULTS: SS-LADCA transiently decreased after injections of air bubbles in both the absence and presence of antifoam. However, in the presence of antifoam the regional depression recovered to normal sooner, the average depth of the depression was reduced, and bubbles from the embolized area cleared faster. These observations can be explained by a model derived from Laplace's law.

Animals↗
PubMed1997

Improved oxygenation by nitric oxide is enhanced by prior lung reaeration with surfactant, rather than positive end-expiratory pressure, in lung-lavaged rabbits.

OBJECTIVES: The inhalation of nitric oxide increases oxygenation by improving the ventilation/perfusion ratios in neonates with respiratory distress syndrome and those ratios in adults with acute respiratory distress syndrome. There is evidence that inhaled nitric oxide is ineffective when the lung remains atelectatic and poorly inflated. This study aimed to enhance nitric oxide delivery by improving lung aeration by means of exogenous surfactant or by increasing positive end-expiratory pressure. DESIGN: Experimental, comparative study. SETTING: Research laboratory of a large university. SUBJECTS: Twenty-eight adult New Zealand white rabbits, weighing 2.7 +/- 0.3 kg. INTERVENTIONS: Lung injury was induced by repeated whole-lung lavage with saline. The animals were mechanically ventilated with a tidal volume of 10 mL/kg, an FIO2 of 1.0, and a positive end-expiratory pressure of 6 cm H2O. Forty-five minutes after the last lavage, the animals were randomly assigned to five groups. In two groups, lung aeration was first increased either by instillation of a low dose of exogenous surfactant (25 mg/kg) or by increasing the positive end-expiratory pressure to 10 cm H2O, before inhalation of nitric oxide was started. In each of these animals, five different nitric oxide concentrations (4 to 20 parts per million) were inhaled for 30 mins, followed by a 30-min washout period. The other three groups served as controls and received only one treatment protocol: nitric oxide (4 to 20 parts per million), or surfactant (25 mg/kg), or positive end-expiratory pressure (10 cm H2O). MEASUREMENTS AND MAIN RESULTS: Before and after lavage, blood gases and lung mechanics were measured every 30 mins. Both strategies to increase lung aeration improved PaO2 values from 61 +/- 13 torr (8.1 +/- 1.7 kPa) to 200 to 300 torr (26.6 to 39.9 kPa) in 30 mins. After inhalation of nitric oxide, additional increases of oxygenation were seen only in the animals that received a low dose (25 mg/kg) of surfactant. The control group that inhaled nitric oxide showed no significant change in oxygenation, and four of the six animals did not survive the observation period. In the two groups in which positive end-expiratory pressure was increased to 10 cm H2O, half of the animals developed a pneumothorax during the observation period. CONCLUSION: These data indicate that inhaled nitric oxide is able to improve arterial oxygenation after alveolar recruitment by means of a low dose of exogenous surfactant, and not by increase of positive end-expiratory pressure from 6 to 10 cm H2O, in lung-lavaged rabbits.

Administration, Inhalation↗
PubMed1997

Pulmonary clearance of 99mTc-DTPA in experimental surfactant dysfunction treated with surfactant instillation.

BACKGROUND: Breakdown of the alveolo-capillary barrier is a characteristic feature of respiratory distress syndrome. Restoration of alveolo-capillary barrier function may be an important aspect of surfactant replacement therapy. We examined the effect of surfactant instillation on alveolo-capillary barrier function in an experimental model of surfactant dysfunction by measuring pulmonary clearance of 99mTc-DTPA. METHODS: Nineteen rabbits were tracheotomized and mechanically ventilated. Surfactant dysfunction was induced by administration of a synthetic detergent in aerosol form. Detergent was given to 13 rabbits; seven rabbits were then treated with instillation of natural surfactant, whereas six rabbits received saline. Six rabbits were used as untreated controls. An aerosol of 99mTc-DTPA was administered to all animals and the pulmonary clearance was measured with a gamma camera. RESULTS: 99mTc-DTPA cleared from the lungs with a half-life of 71 +/- 22 min in the control animals, 21.4 +/- 7.4 min in the surfactant-treated animals and 5.8 +/- 1.5 min in the saline-treated animals. The difference in half-life between groups was highly significant (P < 0.001). There was no change in arterial oxygenation or compliance in controls or in animals treated with saline. In animals treated with surfactant, a small transient reduction in arterial oxygen tension and a more long-standing reduction in compliance were observed. CONCLUSION: Surfactant treatment thus significantly attenuated the effect of detergent treatment but did not restore alveolo-capillary transfer of 99mTc-DTPA to normal.

Animals↗