scholarly journals Effects of pumpless extracorporeal lung assist on hemodynamics, gas exchange and inflammatory cascade response during experimental lung injury

2017 ◽  
Author(s):  
Zhihai Ju ◽  
Jinhui Ma ◽  
Chen Wang ◽  
Jie Yu ◽  
Yeru Qiao ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Lung Injury ◽  
Inflammatory Cascade ◽  
Extracorporeal Lung Assist ◽  
Pumpless Extracorporeal Lung Assist

The contribution of arterio-venous extracorporeal lung assist to gas exchange in a porcine model of lavage-induced acute lung injury

Perfusion ◽  
2006 ◽  
Vol 21 (5) ◽  
pp. 277-284 ◽  
Author(s):  
Jörg Brederlau ◽  
Ralf Muellenbach ◽  
Markus Kredel ◽  
Ulrich Schwemmer ◽  
Martin Anetseder ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Porcine Model ◽  
Extracorporeal Lung Assist

Pumpless extracorporeal lung assist for protective mechanical ventilation in experimental lung injury*

2007 ◽  
Vol 35 (10) ◽  
pp. 2359-2366 ◽  
Author(s):  
Rolf Dembinski ◽  
Nadine Hochhausen ◽  
Sandra Terbeck ◽  
Stefan Uhlig ◽  
Constanze Dassow ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Extracorporeal Lung Assist ◽  
Protective Mechanical Ventilation ◽  
Pumpless Extracorporeal Lung Assist

Pumpless extracorporeal lung assist in severe blunt chest trauma

2004 ◽  
Vol 18 (6) ◽  
pp. 777-779 ◽  
Author(s):  
Joerg Brederlau ◽  
Martin Anetseder ◽  
Richard Wagner ◽  
Thomas Roesner ◽  
Alois Philipp ◽  
...  
Keyword(s):  
Blunt Chest Trauma ◽  
Chest Trauma ◽  
Extracorporeal Lung Assist ◽  
Pumpless Extracorporeal Lung Assist

Effects of Vaporized Perfluorocarbon on Pulmonary Blood Flow and Ventilation/Perfusion Distribution in a Model of Acute Respiratory Distress Syndrome

2001 ◽  
Vol 95 (6) ◽  
pp. 1414-1421 ◽  
Author(s):  
Matthias Hübler ◽  
Jennifer E. Souders ◽  
Erin D. Shade ◽  
Nayak L. Polissar ◽  
Carmel Schimmel ◽  
...  
Keyword(s):  
Blood Flow ◽  
Oleic Acid ◽  
Gas Exchange ◽  
Lung Injury ◽  
Repeated Measures ◽  
Pulmonary Blood Flow ◽  
Analysis Of Covariance ◽  
Inert Gas ◽  
Low Flow ◽  
Repeated Measures Analysis

Background Perfluorocarbon (PFC) liquids are known to improve gas exchange and pulmonary function in various models of acute respiratory failure. Vaporization has been recently reported as a new method of delivering PFC to the lung. Our aim was to study the effect of PFC vapor on the ventilation/perfusion (VA/Q) matching and relative pulmonary blood flow (Qrel) distribution. Methods In nine sheep, lung injury was induced using oleic acid. Four sheep were treated with vaporized perfluorohexane (PFX) for 30 min, whereas the remaining sheep served as control animals. Vaporization was achieved using a modified isoflurane vaporizer. The animals were studied for 90 min after vaporization. VA/Q distributions were estimated using the multiple inert gas elimination technique. Change in Qrel distribution was assessed using fluorescent-labeled microspheres. Results Treatment with PFX vapor improved oxygenation significantly and led to significantly lower shunt values (P < 0.05, repeated-measures analysis of covariance). Analysis of the multiple inert gas elimination technique data showed that animals treated with PFX vapor demonstrated a higher VA/Q heterogeneity than the control animals (P < 0.05, repeated-measures analysis of covariance). Microsphere data showed a redistribution of Qrel attributable to oleic acid injury. Qrel shifted from areas that were initially high-flow to areas that were initially low-flow, with no difference in redistribution between the groups. After established injury, Qrel was redistributed to the nondependent lung areas in control animals, whereas Qrel distribution did not change in treatment animals. Conclusion In oleic acid lung injury, treatment with PFX vapor improves gas exchange by increasing VA/Q heterogeneity in the whole lung without a significant change in gravitational gradient.

Colloidal gold particles as a new in vivo marker of early acute lung injury

2004 ◽  
Vol 287 (4) ◽  
pp. L867-L878 ◽  
Author(s):  
Kai Heckel ◽  
Rainer Kiefmann ◽  
Martina Dörger ◽  
Mechthild Stoeckelhuber ◽  
Alwin E. Goetz
Keyword(s):  
Electron Microscopy ◽  
Acute Lung Injury ◽  
Gas Exchange ◽  
Lung Injury ◽  
Colloidal Gold ◽  
Microvascular Permeability ◽  
Arterial Oxygen ◽  
Control Group ◽  
Gold Particles

Permeability of the endothelial barrier to large molecules plays a pivotal role in the manifestation of early acute lung injury. We present a novel and sensitive technique that brings microanatomical visualization and quantification of microvascular permeability in line. White New Zealand rabbits were anesthetized and ventilated mechanically. Rabbit serum albumin (RSA) was labeled with colloidal gold particles. We quantified macromolecular leakage of gold-labeled RSA and thickening of the gas exchange distance by electron microscopy, taking into account morphology of microvessels. The control group receiving a saline solution represented a normal gas exchange barrier without extravasation of gold-labeled albumin. Infusion of lipopolysaccharide (LPS) resulted in a significant displacement of gold-labeled albumin into pulmonary cells, the lung interstitium, and even the alveolar space. Correspondingly, intravital fluorescence microscopy and digital image analysis indicated thickening of width of alveolar septa. The findings were accompanied by a deterioration of alveolo-arterial oxygen difference, whereas wet/dry ratio and albumin concentration in the bronchoalveolar lavage fluid failed to detect that early stage of pulmonary edema. Inhibition of the nuclear enzyme poly(ADP-ribose) synthetase by 3-aminobenzamide prevented LPS-induced microvascular injury. To summarize: colloidal gold particles visualized by standard electron microscopy are a new and very sensitive in vivo marker of microvascular permeability in early acute lung injury. This technique enabling detailed microanatomical and quantitative pathophysiological characterization of edema formation can form the basis for evaluating novel treatment strategies against acute lung injury.

scholarly journals Regional Gas Exchange and Cellular Metabolic Activity in Ventilator-induced Lung Injury

2007 ◽  
Vol 106 (4) ◽  
pp. 723-735 ◽  
Author(s):  
Guido Musch ◽  
Jose G. Venegas ◽  
Giacomo Bellani ◽  
Tilo Winkler ◽  
Tobias Schroeder ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Lung Injury ◽  
Metabolic Activity ◽  
Cell Activation ◽  
Test Lung ◽  
Ventilator Induced Lung Injury ◽  
Positron Emission ◽  
Cellular Metabolic Activity ◽  
The Right ◽  
Tissue Fraction

Background Alveolar overdistension and repetitive derecruitment-recruitment contribute to ventilator-induced lung injury (VILI). The authors investigated (1) whether inflammatory cell activation due to VILI was assessable by positron emission tomography and (2) whether cell activation due to dynamic overdistension alone was detectable when other manifestations of VILI were not yet evident. Methods The authors assessed cellular metabolic activity with [(18)F]fluorodeoxyglucose and regional gas exchange with [(13)N]nitrogen. In 12 sheep, the left ("test") lung was overdistended with end-inspiratory pressure of 50 cm H(2)O for 90 min, while end-expiratory derecruitment of this lung was either promoted with end-expiratory pressure of -10 cm H(2)O in 6 of these sheep (negative end-expiratory pressure [NEEP] group) or prevented with +10 cm H(2)O in the other 6 (positive end-expiratory pressure [PEEP] group) to isolate the effect of overdistension. The right ("control") lung was protected from VILI. Results Aeration decreased and shunt fraction increased in the test lung of the NEEP group. [(18)F]fluorodeoxyglucose uptake of this lung was higher than that of the control lung and of the test lung of the PEEP group, and correlated with neutrophil count. When normalized by tissue fraction to account for increased aeration of the test lung in the PEEP group, [(18)F]fluorodeoxyglucose uptake was elevated also in this group, despite the fact that gas exchange had not yet deteriorated after 90 min of overdistension alone. Conclusion The authors could detect regional neutrophil activation in VILI even when end-expiratory derecruitment was prevented and impairment of gas exchange was not evident. Concomitant end-expiratory derecruitment converted this activation into profound inflammation with decreased aeration and regional shunting.

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