scholarly journals Lung ventilation injures areas with discrete alveolar flooding, in a surface tension-dependent fashion

2014 ◽  
Vol 117 (7) ◽  
pp. 788-796 ◽  
Author(s):  
You Wu (吴右) ◽  
Angana Banerjee Kharge ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Tidal Volume ◽  
Lung Ventilation ◽  
Transpulmonary Pressure ◽  
Exogenous Surfactant ◽  
Control Group ◽  
Positive End Expiratory Pressure ◽  
Lung Inflation ◽  
Surfactant Activity ◽  
Theoretical Considerations

With proteinaceous-liquid flooding of discrete alveoli, a model of the edema pattern in the acute respiratory distress syndrome, lung inflation over expands aerated alveoli adjacent to flooded alveoli. Theoretical considerations suggest that the overexpansion may be proportional to surface tension, T. Yet recent evidence indicates proteinaceous edema liquid may not elevate T. Thus whether the overexpansion is injurious is not known. Here, working in the isolated, perfused rat lung, we quantify fluorescence movement from the vasculature to the alveolar liquid phase as a measure of overdistension injury to the alveolar-capillary barrier. We label the perfusate with fluorescence; micropuncture a surface alveolus and instill a controlled volume of nonfluorescent liquid to obtain a micropunctured-but-aerated region (control group) or a region with discrete alveolar flooding; image the region at a constant transpulmonary pressure of 5 cmH2O; apply five ventilation cycles with a positive end-expiratory pressure of 0–20 cmH2O and tidal volume of 6 or 12 ml/kg; return the lung to a constant transpulmonary pressure of 5 cmH2O; and image for an additional 10 min. In aerated areas, ventilation is not injurious. With discrete alveolar flooding, all ventilation protocols cause sustained injury. Greater positive end-expiratory pressure or tidal volume increases injury. Furthermore, we determine T and find injury increases with T. Inclusion of either plasma proteins or Survanta in the flooding liquid does not alter T or injury. Inclusion of 2.7–10% albumin and 1% Survanta together, however, lowers T and injury. Contrary to expectation, albumin inclusion in our model facilitates exogenous surfactant activity.

scholarly journals Surface tension in situ in flooded alveolus unaltered by albumin

2014 ◽  
Vol 117 (5) ◽  
pp. 440-451 ◽  
Author(s):  
Angana Banerjee Kharge ◽  
You Wu ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Plasma Proteins ◽  
Lung Surfactant ◽  
Exogenous Surfactant ◽  
Surfactant Activity ◽  
Interfacial Surfactant ◽  
Isolated Rat Lung ◽  
Alveolar Liquid

In the acute respiratory distress syndrome, plasma proteins in alveolar edema liquid are thought to inactivate lung surfactant and raise surface tension, T. However, plasma protein-surfactant interaction has been assessed only in vitro, during unphysiologically large surface area compression (%Δ A). Here, we investigate whether plasma proteins raise T in situ in the isolated rat lung under physiologic conditions. We flood alveoli with liquid that omits/includes plasma proteins. We ventilate the lung between transpulmonary pressures of 5 and 15 cmH2O to apply a near-maximal physiologic %Δ A, comparable to that of severe mechanical ventilation, or between 1 and 30 cmH2O, to apply a supraphysiologic %Δ A. We pause ventilation for 20 min and determine T at the meniscus that is present at the flooded alveolar mouth. We determine alveolar air pressure at the trachea, alveolar liquid phase pressure by servo-nulling pressure measurement, and meniscus radius by confocal microscopy, and we calculate T according to the Laplace relation. Over 60 ventilation cycles, application of maximal physiologic %Δ A to alveoli flooded with 4.6% albumin solution does not alter T; supraphysiologic %Δ A raise T, transiently, by 51 ± 4%. In separate experiments, we find that addition of exogenous surfactant to the alveolar liquid can, with two cycles of maximal physiologic %Δ A, reduce T by 29 ± 11% despite the presence of albumin. We interpret that supraphysiologic %Δ A likely collapses the interfacial surfactant monolayer, allowing albumin to raise T. With maximal physiologic %Δ A, the monolayer likely remains intact such that albumin, blocked from the interface, cannot interfere with native or exogenous surfactant activity.

Response of slowly adapting pulmonary stretch receptors to reduced lung compliance

1991 ◽  
Vol 71 (2) ◽  
pp. 425-431 ◽  
Author(s):  
J. Yu ◽  
T. E. Pisarri ◽  
J. C. Coleridge ◽  
H. M. Coleridge
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Time Constant ◽  
Transpulmonary Pressure ◽  
Lung Compliance ◽  
Steady State Response ◽  
Positive End Expiratory Pressure ◽  
State Response ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

We examined the steady-state response of slowly adapting pulmonary stretch receptors (SAPSRs) to reduced lung compliance in open-chest cats with lungs ventilated at eupneic rate and tidal volume (VT) and with a positive end-expiratory pressure (PEEP) of 3–4 cmH2O. Transient removal of PEEP decreased compliance by approximately 30% and increased transpulmonary pressure (Ptp) by 1–2.5 cmH2O. Reduction of compliance significantly decreased SAPSR discharge in deflation and caused a small increase in discharge at the peak of inflation; it had little effect on discharge averaged over the ventilatory cycle. Increasing VT to produce a comparable increase in Ptp significantly increased peak discharge. Thus unlike rapidly adapting receptors, whose discharge is increased more effectively by reduced compliance than by increased VT, SAPSRs are stimulated by increased VT but not by reduced compliance. We speculate that the most consistent effect of reduced compliance on SAPSRs (the decrease in deflation discharge) was due to the decreased time constant for deflation in the stiffer lung. This alteration in firing may contribute to the tachypnea evoked as the lungs become stiffer.

scholarly journals Comparative analysis of changes in the lungs of experimental animals’ induced conventional and lung protective ventilation

2018 ◽  
Vol 69 (1) ◽  
pp. 771
Author(s):  
N. VIDENOVIC ◽  
J. MLADENOVIC ◽  
V. VIDENOVIC ◽  
R. ZDRAVKOVIC
Keyword(s):  
Mechanical Ventilation ◽  
Tidal Volume ◽  
Protective Ventilation ◽  
Lung Protective Ventilation ◽  
Control Group ◽  
Histological Structure ◽  
Positive End Expiratory Pressure ◽  
Acid Base ◽  
Acid Base Status ◽  
The Impact

Mechanical ventilation has long been the leader in the treatment of critically ill and injured patients in an intensive care unit. The aim of this study was to examine the impact of the application of positive end-expiratory pressure on histopathological findings and on the parameters of ventilation, oxygenation and acid-base status. The experimental study included 42 animals (piglets), which were divided into of tree groups, each containing 14. The animals of the control group (conventional ventilation) were ventilated with the tidal volume of 10-15 mL/kg. Tidal volume of 6 mL/kg was applied in the low tidal ventilation group, whereas the ventilation strategy in the lung protective ventilation group meant the application of a tidal volume of 6 mL/kg and the 7 mbar of positive end-expiratory pressure. Mechanical ventilation in each animal lasted for 4 hours. After conducting mechanical ventilation, samples were taken from the lung tissue, which were sent for histopathological examination. The parameters of ventilation, oxygenation and acid-base status were measured after each hour’s duration of mechanical ventilation. Application of positive end-expiratory pressure 5-10 mbar during mechanical ventilation is a safe and useful method which is not followed by the occurrence of significant abnormalities in the structure of the ventilated lung. However, a low tidal volume without positive end-expiratory pressure causes significant changes in the histological structure of healthy lungs. Positive end-expiratory pressure keeps the alveoli open throughout the respiratory cycle which allows the lungs to maintain homeostasis in terms of adequate ventilation, oxygenation and acid-base status.

scholarly journals Sulforhodamine B and exogenous surfactant effects on alveolar surface tension under acute respiratory distress syndrome conditions

2020 ◽  
Author(s):  
Tam L. Nguyen ◽  
Carrie E. Perlman
Keyword(s):  
Surface Tension ◽  
Acute Respiratory Distress Syndrome ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Distress Syndrome ◽  
Exogenous Surfactant ◽  
Sulforhodamine B ◽  
Surfactant Activity ◽  
Isolated Lungs ◽  
Alveolar Surface

AbstractIn the acute respiratory distress syndrome (ARDS), alveolar surface tension, T, may be elevated. Elevated T should increase ventilation-induced lung injury. Exogenous surfactant therapy, intended to lower T, has not reduced mortality. Sulforhodamine B (SRB) might, alternatively, be employed to lower T. We test whether substances suspected of elevating T in ARDS raise T in the lungs and test the abilities of exogenous surfactant and SRB to reduce T. In isolated rat lungs, we micropuncture a surface alveolus and instill a solution of a purported T-raising substance: control saline, cell debris, secretory phospholipase A2 (sPLA2), acid or mucins. We test each substance alone; with albumin, to model proteinaceous edema liquid; with albumin and exogenous surfactant; or with albumin and SRB. We determine T in situ in the lungs by combining servo-nulling pressure measurement with confocal microscopy, and applying the Laplace relation. With control saline, albumin does not alter T, additional surfactant raises T and additional SRB lowers T. The experimental substances, without or with albumin, raise T. Excepting under aspiration conditions, addition of surfactant or SRB lowers T. Exogenous surfactant activity is concentration and ventilation dependent. Sulforhodamine B, which could be delivered intravascularly, holds promise as an alternative therapeutic.New and NoteworthyIn the acute respiratory distress syndrome (ARDS), lowering surface tension, T, should reduce ventilation injury yet exogenous surfactant has not reduced mortality. We show with direct T-determination in isolated lungs that substances suggested to elevate T in ARDS indeed raise T, and exogenous surfactant reduces T. Further, we extend our previous finding that sulforhodamine B (SRB) reduces T below normal in healthy lungs and show that SRB, too, reduces T under ARDS conditions.

Protective Ventilation Influences Systemic Inflammation after Esophagectomy

2006 ◽  
Vol 105 (5) ◽  
pp. 911-919 ◽  
Author(s):  
Pierre Michelet ◽  
Xavier-Benoît D’Journo ◽  
Antoine Roch ◽  
Christophe Doddoli ◽  
Valerie Marin ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Systemic Inflammation ◽  
Lung Ventilation ◽  
Protective Ventilation ◽  
Ventilation Strategy ◽  
Positive End Expiratory Pressure ◽  
One Lung Ventilation ◽  
Ventilatory Strategy ◽  
Protective Ventilation Strategy ◽  
Protective Strategy

Background Esophagectomy induces a systemic inflammatory response whose extent has been recognized as a predictive factor of postoperative respiratory morbidity. The aim of this study was to determine the effectiveness of a protective ventilatory strategy to reduce systemic inflammation in patients undergoing esophagectomy. Methods The authors prospectively investigated 52 patients undergoing planned esophagectomy for cancer. Patients were randomly assigned to a conventional ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung and one-lung ventilation; no positive end-expiratory pressure) or a protective ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung ventilation, reduced to 5 ml/kg during one-lung ventilation; positive end-expiratory pressure 5 cm H2O throughout the operative time). Results Plasmatic levels of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor alpha were measured perioperatively and postoperatively. Pulmonary function and postoperative evolution were also evaluated. Patients who received protective strategy had lower blood levels of IL-1beta, IL-6, and IL-8 at the end of one-lung ventilation (0.24 [0.15-0.40] vs. 0.56 [0.38-0.89] pg/ml, P < 0.001; 91 [61-117] vs. 189 [127-294] pg/ml, P < 0.001; and 30 [22-45] vs. 49 [29-69] pg/ml, P < 0.05, respectively) and 18 h postoperatively (0.18 [0.13-0.30] vs. 0.43 [0.34-0.54] pg/ml, P < 0.001; 54 [36-89] vs. 116 [78-208] pg/ml, P < 0.001; 16 [11-24] vs. 35 [28-53] pg/ml, P < 0.001, respectively). Protective strategy resulted in higher oxygen partial pressure to inspired oxygen fraction ratio during one-lung ventilation and 1 h postoperatively and in a reduction of postoperative mechanical ventilation duration (115 +/- 38 vs. 171 +/- 57 min, P < 0.001). Conclusion A protective ventilatory strategy decreases the proinflammatory systemic response after esophagectomy, improves lung function, and results in earlier extubation.

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