Increased sensitivity to mechanical ventilation after surfactant inactivation in young rabbit lungs

Coker, P. J.; Hernandez, L. A.; Peevy, Keith J.; Adkins, Keith; Parker, James C.

doi:10.1097/00003246-199205000-00015

Cited by 45 publications

(18 citation statements)

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“…Coker and colleagues (35) and Taskar and colleagues (36) both found that VILI only occurred in animal models when surfactant was inactivated. Bilek and colleagues (37) found that fluid forced between glass plates that were coated with epithelial cells and separated by a distance that was similar to the diameter of small airways generated large pressure gradients that damaged the cells.…”

Section: Increased Surface Tension Is Necessary and Sufficient To Caumentioning

confidence: 99%

The Role of Ventilation-induced Surfactant Dysfunction and Atelectasis in Causing Acute Respiratory Distress Syndrome

Albert

2012

Am J Respir Crit Care Med

122

105

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This Pulmonary Perspective describes a new pathophysiologic scenario by which the acute respiratory distress syndrome (ARDS) might develop, summarizes the literature on which this new scenario is based, and discusses the resulting implications with respect to patient management. Rather than ARDS occurring as a result of the inflammatory response associated with predisposing risk factors, the proposed scenario theorizes that the initiating problem is atelectasis that develops as a result of a surfactant abnormality that is caused by spontaneous or mechanical ventilation, together with our current approaches to patient positioning and sedation. The proposed pathophysiology implies that ventilation-induced lung injury occurs before, and causes, ARDS (rather than developing after the fact and only serving to magnify the existing injury) and that some instances of ARDS are iatrogenic. If the proposed scenario is correct, it also implies that at least some instances of ARDS might be prevented by implementing a number of simple, safe modifications in patient care.

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Section: Increased Surface Tension Is Necessary and Sufficient To Caumentioning

confidence: 99%

The Role of Ventilation-induced Surfactant Dysfunction and Atelectasis in Causing Acute Respiratory Distress Syndrome

Albert

2012

Am J Respir Crit Care Med

122

105

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“…Other models of acute lung injury have been described and have confirmed the effectiveness of the PV curve to study pulmonary mechanics (13,14). Both tension work and hysteresis loop were greater in the paraquat group, and the extent of alteration increased as larger doses were administered (Figure 4).…”

Section: Discussionmentioning

confidence: 58%

Paraquat poisoning: an experimental model of dose-dependent acute lung injury due to surfactant dysfunction

Silva

Saldiva

1998

Braz J Med Biol Res

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Since the most characteristic feature of paraquat poisoning is lung damage, a prospective controlled study was performed on excised rat lungs in order to estimate the intensity of lesion after different doses. Twenty-five male, 2-3-month-old non-SPF Wistar rats, divided into 5 groups, received paraquat dichloride in a single intraperitoneal injection (0, 1, 5, 25, or 50 mg/kg body weight) 24 h before the experiment. Static pressure-volume (PV) curves were performed in air-and salinefilled lungs; an estimator of surface tension and tissue works was computed by integrating the area of both curves and reported as work/ ml of volume displacement. Paraquat induced a dose-dependent increase of inspiratory surface tension work that reached a significant two-fold order of magnitude for 25 and 50 mg/kg body weight (P<0.05, ANOVA), sparing lung tissue. This kind of lesion was probably due to functional abnormalities of the surfactant system, as was shown by the increase in the hysteresis of the paraquat groups at the highest doses. Hence, paraquat poisoning provides a suitable model of acute lung injury with alveolar instability that can be easily used in experimental protocols of mechanical ventilation. Correspondence

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“…These latter studies might indicate that our experimental period might have been too short to cause damage due to mechanical trauma or due to hypocapnia. However, Faridy et al [17] showed in isolated dog lungs a decreased com pliance and increased minimum surface ten sions with increased tidal volumes for periods up to 4 h. Other studies [18][19][20][21][22] reported that mechanical high positive pressure ventilation accompanied by hypocapnia led to severe pul monary dysfunction earlier than 4 h. The mechanism of impaired lung function was un clear; lung edema caused by microvascular injury was mentioned as a responsible factor [20,21,23,24], However, in these experi ments higher ventilation settings were used than in our experiments.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Hypocapnia and Mechanical Pulmonary Stress on Lung Tissue in Newborn Lambs

Klöpping-Ketelaars¹,

Havenith²,

Maertzdorf³

et al. 1993

Neonatology

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Positive pressure ventilation, using high inspiratory pressures, often causes lung damage. When associated with hypocapnia, it can produce severe focal alveolar alkalosis and can cause damage in areas of low blood flow. A vein-to-vein extracorporeal membrane oxygenator (ECMO) system was used to control blood gases independently of mechanical ventilation in 12 healthy newborn lambs. After connection to the ECMO system, ventilation was started with a peak inspiratory pressure of 35 cm H₂O and a positive end-expiratory pressure of 5 cm H₂O; the ventilator rate was 40/min with I:E = 1.5 and FiO₂ = 1.0. In 6 of the 12 lambs sweep gases through the silicone membrane were regulated to assure arterial normocapnia. The other 6 were ventilated with the same settings and perfused with the same pump flow, but PaCO₂ was allowed to fall to hypocapnic levels. The lambs were ventilated for 4h. Average pH and PaCO₂ were 7.62 ± 0.14 and 2.11 ± 0.54 kPa, respectively, in the hypocapnic group and 7.39 ± 0.11 and 4.79 ± 0.51 kPa in the normocapnic group. After sacrificing the lambs, the lungs were inspected macroscopically and microscopically by computer-assisted morphometry to assess atelectasis and lung edema. Macroscopically there were no hemorrhages, barotrauma or widespread atelectasis of the lungs in either group. The thickness of interlobular lung septa in the right upper lobe was 32.5 ± 18.0 μm for the hypocapnic group and 29.7 ± 12.5 μm for the normocapnic group. The parenchymal-alveolar area ratio in the right upper lobe was 28.4 ± 5.04 and 24.6 ± 3.75% in the hypocapnic and normocapnic groups, respectively. Hypocapnia and mechanical stress for 4 h in initially healthy lungs did not produce alveolar epithelial damage.

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Increased sensitivity to mechanical ventilation after surfactant inactivation in young rabbit lungs

Cited by 45 publications

References 0 publications

The Role of Ventilation-induced Surfactant Dysfunction and Atelectasis in Causing Acute Respiratory Distress Syndrome

The Role of Ventilation-induced Surfactant Dysfunction and Atelectasis in Causing Acute Respiratory Distress Syndrome

Paraquat poisoning: an experimental model of dose-dependent acute lung injury due to surfactant dysfunction

The Effect of Hypocapnia and Mechanical Pulmonary Stress on Lung Tissue in Newborn Lambs

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