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Acid Aspiration
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Torsten Richter – One of the best experts on this subject based on the ideXlab platform.
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Causative treatment of Acid Aspiration induced acute lung injury – Recent trends from animal experiments and critical perspective.
Clinical hemorheology and microcirculation, 2018Co-Authors: Johannes Gramatté, Jens Pietzsch, Ralf Bergmann, Torsten RichterAbstract:Aspiration of low-pH gastric fluid leads to an initial pneumonitis, which may become complicated by subsequent pneumonia or acute respiratory distress syndrome. Current treatment is at best supportive, but there is growing experimental evidence on the significant contribution of both neutrophils and platelets in the development of this inflammatory pulmonary reaction, a condition that can be attenuated by several medicinal products. This review aims to summarize novel findings in experimental models on pathomechanisms after an Acid–Aspiration event. Given the clinical relevance, specific emphasis is put on deduced potential experimental therapeutic approaches, which make use of the characteristic alteration of microcirculation in the injured lung.
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Effects of pulmonary Acid Aspiration on the regional pulmonary blood flow within the first hour after injury: An observational study in rats1
Clinical hemorheology and microcirculation, 2015Co-Authors: Torsten Richter, Ralf Bergmann, Jens Pietzsch, Michael P. Mueller, Thea KochAbstract:INTRODUCTION Gastric Aspiration events are recognized as a major cause of pneumonitis and the development of acute respiratory distress syndrome. The first peak in the inflammatory response has been observed one hour after Acid-induced lung injury in rats. The spatial pulmonary blood flow (PBF) distribution after an Acid Aspiration event within this time frame has not been adequately studied. We determined therefore PBF pattern within the first hour after Acid Aspiration. METHODS Anesthetized, spontaneous breathing rats (n = 8) underwent unilateral endobronchial hydrochlorid Acid instillation so that the PBF distributions between the injured and non-injured lungs could be compared. The signal intensity of the lung parenchyma after injury was measured by magnetic resonance tomography. PBF distribution was determined by measuring the concentration of [68Ga]-radiolabeled microspheres using positron emission tomography. RESULTS Following Acid Aspiration, magnetic resonance images revealed increased signal intensity in the injured regions accompanied by reduced oxygenation. PBF was increased in all injured lungs (171 [150; 196], median [25%; 75%]) compared to the blood flow in all uninjured lungs (141 [122; 159], P = 0.0078). CONCLUSIONS From the first minute until fifty minutes after Acid-induced acute lung injury, the PBF was consistently increased in the injured lung. These blood flow elevation was accompanied by significant hypoxemia.
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Reduced pulmonary blood flow in regions of injury 2 hours after Acid Aspiration in rats
BMC Anesthesiology, 2015Co-Authors: Torsten Richter, Ralf Bergmann, Guido Musch, Jens Pietzsch, Thea KochAbstract:Background Aspiration-induced lung injury can decrease gas exchange and increase mortality. Acute lung injury following Acid Aspiration is characterized by elevated pulmonary blood flow (PBF) in damaged lung areas in the early inflammation stage. Knowledge of PBF patterns after Acid Aspiration is important for targeting intravenous treatments. We examined PBF in an experimental model at a later stage (2 hours after injury). Methods Anesthetized Wistar-Unilever rats (n = 5) underwent unilateral endobronchial instillation of hydrochloric Acid. The PBF distribution was compared between injured and uninjured sides and with that of untreated control animals (n = 6). Changes in lung density after injury were measured using computed tomography (CT). Regional PBF distribution was determined quantitatively in vivo 2 hours after Acid instillation by measuring the concentration of [^68Ga]-radiolabeled microspheres using positron emission tomography. Results CT scans revealed increased lung density in areas of Acid Aspiration. Lung injury was accompanied by impaired gas exchange. Acid Aspiration decreased the arterial pressure of oxygen from 157 mmHg [139;165] to 74 mmHg [67;86] at 20 minutes and tended toward restoration to 109 mmHg [69;114] at 110 minutes ( P
Elie Fadel – One of the best experts on this subject based on the ideXlab platform.
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Exogenous surfactant attenuates lung injury from gastric-Acid Aspiration during ex vivo reconditioning in pigs.
Transplantation, 2014Co-Authors: Theresa Khalifé-hocquemiller, Edouard Sage, Peter Dorfmüller, Sacha Mussot, Daniel Le Houérou, Saadia Eddahibi, Elie FadelAbstract:BACKGROUND Lung injury (LI) due to gastric-Acid Aspiration is associated with poor posttransplantation outcomes. We investigated the effects of ex vivo lung perfusion (EVLP) reconditioning and surfactant administration on LI due to gastric-Acid Aspiration. METHODS Thirty piglets were allocated at random to five groups: the lungs were studied 24 hr after gastric juice-induced LI of the left lower lobe (LLL), LI followed by EVLP (4 hr), or LI followed by LLL surfactant lavage immediately before EVLP; sham animals were studied 24 hr after saline infusion alone or followed by EVLP. Gross anatomy, hemodynamics, and aerodynamics were evaluated; neutrophil and bacterial counts were determined in bronchoalveolar lavage (BAL) fluid and blood. LLLs were evaluated based on a semi-quantitative histologic score, apoptotic cell death (TUNEL), and inflammatory cytokine levels. RESULTS The sham and sham-EVLP groups were not significantly different. Compared with sham, LI animals had irreversible atelectasis, higher lung infection rates (P
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exogenous surfactant attenuates lung injury from gastric Acid Aspiration during ex vivo reconditioning in pigs
Transplantation, 2014Co-Authors: Theresa Khalifehocquemiller, Edouard Sage, Peter Dorfmüller, Sacha Mussot, Daniel Le Houérou, Saadia Eddahibi, Elie FadelAbstract:BACKGROUND Lung injury (LI) due to gastric-Acid Aspiration is associated with poor posttransplantation outcomes. We investigated the effects of ex vivo lung perfusion (EVLP) reconditioning and surfactant administration on LI due to gastric-Acid Aspiration. METHODS Thirty piglets were allocated at random to five groups: the lungs were studied 24 hr after gastric juice-induced LI of the left lower lobe (LLL), LI followed by EVLP (4 hr), or LI followed by LLL surfactant lavage immediately before EVLP; sham animals were studied 24 hr after saline infusion alone or followed by EVLP. Gross anatomy, hemodynamics, and aerodynamics were evaluated; neutrophil and bacterial counts were determined in bronchoalveolar lavage (BAL) fluid and blood. LLLs were evaluated based on a semi-quantitative histologic score, apoptotic cell death (TUNEL), and inflammatory cytokine levels. RESULTS The sham and sham-EVLP groups were not significantly different. Compared with sham, LI animals had irreversible atelectasis, higher lung infection rates (P<0.0001) and BAL neutrophil percentages (P<0.0001), lower PaO2 (P=0.0006), higher IL-1 (P=0.022) and IL-8 (P=0.006), higher apoptotic cell percentages (P=0.007), and worse histologic severity scores (P<0.0001). EVLP alone did not improve these findings. Adding surfactant before EVLP returned PaO2, pulmonary vascular resistance, and apoptotic-cell percentage to sham-EVLP values but only partially improved the histologic severity score. CONCLUSION Local surfactant infusion immediately before EVLP improved the function of donor lungs injured by gastric juice Aspiration. This strategy may hold promise for decreasing the shortage of donor lungs.
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Lung Injuries Induced by Gastric Acid Aspiration Are Attenuated by Exogenous Surfactant during Ex Vivo Reconditioning in Pigs
The Journal of Heart and Lung Transplantation, 2013Co-Authors: T. Khalife, Peter Dorfmüller, Edouard Sage, Saadia Eddahibi, Elie FadelAbstract:Purpose Gastric Acid Aspiration is a common reason for rejecting lungs for transplantation as it is associated with increased risks of graft dysfunction. We investigated Ex vivo lung perfusion (EVLP) reconditioning on lung injuries due to gastric Acid Aspiration and effects of surfactant administration. Methods and Materials 30 piglets were allocated to 5 groups. Aspiration lung injury (LI) was induced by infusing 1 ml/kg of autologous gastric juice into the left lower lobe (LLL). 24 hours later, the lungs were studied (LI group) or reconditioned using EVLP for 4 hours without additional treatment (LI-EVLP group) or after surfactant lavage (curosurf 100 mg/kg) in the LLL (Surf-EVLP group). Sham animals were studied 24 h after saline infusion and Sham-EVLP animals 24 h after saline infusion followed by 4 h of EVLP. Gross anatomy, hemodynamics, and aerodynamics were evaluated; neutrophil and bacterial counts in bronchoalveolar lavage (BAL) fluid and blood were determined. LLLs were evaluated by tissue wet/dry ratio; histology (semi-quantitative severity score); apoptotic cell using TUNEL; and IL-1, IL-6, IL-8, IL-10, and TNFa protein levels. Results There were no significant differences between the Sham and Sham-EVLP groups. Compared to Sham, LI animals had irreversible atelectasis, a higher lung infection rate (P 2 (P=0.0006), higher IL1 (P=0.022) and IL8 (P=0.006) levels and apoptotic cell percentage (P=0.007), and worse histology severity score (P Conclusions Although 4 hours EVLP worsened LI due to gastric Acid Aspiration, when preceded by local infusion of surfactant it allowed complete PaO2 and partial histology recovery.
Thea Koch – One of the best experts on this subject based on the ideXlab platform.
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Effects of pulmonary Acid Aspiration on the regional pulmonary blood flow within the first hour after injury: An observational study in rats1
Clinical hemorheology and microcirculation, 2015Co-Authors: Torsten Richter, Ralf Bergmann, Jens Pietzsch, Michael P. Mueller, Thea KochAbstract:INTRODUCTION Gastric Aspiration events are recognized as a major cause of pneumonitis and the development of acute respiratory distress syndrome. The first peak in the inflammatory response has been observed one hour after Acid-induced lung injury in rats. The spatial pulmonary blood flow (PBF) distribution after an Acid Aspiration event within this time frame has not been adequately studied. We determined therefore PBF pattern within the first hour after Acid Aspiration. METHODS Anesthetized, spontaneous breathing rats (n = 8) underwent unilateral endobronchial hydrochlorid Acid instillation so that the PBF distributions between the injured and non-injured lungs could be compared. The signal intensity of the lung parenchyma after injury was measured by magnetic resonance tomography. PBF distribution was determined by measuring the concentration of [68Ga]-radiolabeled microspheres using positron emission tomography. RESULTS Following Acid Aspiration, magnetic resonance images revealed increased signal intensity in the injured regions accompanied by reduced oxygenation. PBF was increased in all injured lungs (171 [150; 196], median [25%; 75%]) compared to the blood flow in all uninjured lungs (141 [122; 159], P = 0.0078). CONCLUSIONS From the first minute until fifty minutes after Acid-induced acute lung injury, the PBF was consistently increased in the injured lung. These blood flow elevation was accompanied by significant hypoxemia.
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Reduced pulmonary blood flow in regions of injury 2 hours after Acid Aspiration in rats
BMC Anesthesiology, 2015Co-Authors: Torsten Richter, Ralf Bergmann, Guido Musch, Jens Pietzsch, Thea KochAbstract:Background Aspiration-induced lung injury can decrease gas exchange and increase mortality. Acute lung injury following Acid Aspiration is characterized by elevated pulmonary blood flow (PBF) in damaged lung areas in the early inflammation stage. Knowledge of PBF patterns after Acid Aspiration is important for targeting intravenous treatments. We examined PBF in an experimental model at a later stage (2 hours after injury). Methods Anesthetized Wistar-Unilever rats (n = 5) underwent unilateral endobronchial instillation of hydrochloric Acid. The PBF distribution was compared between injured and uninjured sides and with that of untreated control animals (n = 6). Changes in lung density after injury were measured using computed tomography (CT). Regional PBF distribution was determined quantitatively in vivo 2 hours after Acid instillation by measuring the concentration of [^68Ga]-radiolabeled microspheres using positron emission tomography. Results CT scans revealed increased lung density in areas of Acid Aspiration. Lung injury was accompanied by impaired gas exchange. Acid Aspiration decreased the arterial pressure of oxygen from 157 mmHg [139;165] to 74 mmHg [67;86] at 20 minutes and tended toward restoration to 109 mmHg [69;114] at 110 minutes ( P
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reduced pulmonary blood flow in regions of injury 2 hours after Acid Aspiration in rats
BMC Anesthesiology, 2015Co-Authors: Torsten Richter, Ralf Bergmann, Guido Musch, Jens Pietzsch, Thea KochAbstract:Background: Aspiration-induced lung injury can decrease gas exchange and increase mortality. Acute lung injury following Acid Aspiration is characterized by elevated pulmonary blood flow (PBF) in damaged lung areas in the early inflammation stage. Knowledge of PBF patterns after Acid Aspiration is important for targeting intravenous treatments. We examined PBF in an experimental model at a later stage (2 hours after injury). Methods: Anesthetized Wistar-Unilever rats (n = 5) underwent unilateral endobronchial instillation of hydrochloric Acid. The PBF distribution was compared between injured and uninjured sides and with that of untreated control animals (n = 6). Changes in lung density after injury were measured using computed tomography (CT). Regional PBF distribution was determined quantitatively in vivo 2 hours after Acid instillation by measuring the concentration of [ 68 Ga]-radiolabeled microspheres using positron emission tomography. Results: CT scans revealed increased lung density in areas of Acid Aspiration. Lung injury was accompanied by impaired gas exchange. Acid Aspiration decreased the arterial pressure of oxygen from 157 mmHg [139;165] to 74 mmHg [67;86] at 20 minutes and tended toward restoration to 109 mmHg [69;114] at 110 minutes (P < 0.001). The PBF ratio of the middle region of the injured versus uninjured lungs of the Aspiration group (0.86 [0.7;0.9], median [25%;75%]) was significantly lower than the PBF ratio in the left versus right lung of the control group (1.02 [1.0;1.05]; P = 0.016). Conclusions: The PBF pattern 2 hours after Aspiration-induced lung injury showed a redistribution of PBF away from injured regions that was likely responsible for the partial recovery from hypoxemia over time. Treatments given intravenously 2 hours after Acid-induced lung injury may not preferentially reach the injured lung regions, contrary to what occurs during the first hour of inflammation.