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Gattinoni, Luciano
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Gattinoni, Luciano
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Gattinoni, Luciano
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Gattinoni, L.
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2016Journal Article [["dc.bibliographiccitation.artnumber","86"],["dc.bibliographiccitation.journal","CRITICAL CARE"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Quintel, Michael"],["dc.date.accessioned","2018-11-07T10:15:38Z"],["dc.date.available","2018-11-07T10:15:38Z"],["dc.date.issued","2016"],["dc.description.abstract","The Berlin definition criteria applied at positive end-expiratory pressure (PEEP) 5 cm H2O reasonably predict lung edema and recruitabilty. To maintain viable gas exchange, the mechanical ventilation becomes progressively more risky going from mild to severe acute respiratory distress syndrome (ARDS). Tidal volume, driving pressure, flow, and respiratory rate have been identified as causes of ventilation-induced lung injury. Taken together, they represent the mechanical power applied to the lung parenchyma. In an inhomogeneous lung, stress risers locally increase the applied mechanical power. Increasing lung homogeneity by PEEP and prone position decreases the harm of mechanical ventilation, particularly in severe ARDS."],["dc.identifier.doi","10.1186/s13054-016-1268-7"],["dc.identifier.isi","000373669800001"],["dc.identifier.pmid","27048605"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13487"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40846"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1364-8535"],["dc.relation.issn","1466-609X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","How ARDS should be treated"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article Discussion [["dc.bibliographiccitation.artnumber","130"],["dc.bibliographiccitation.journal","CRITICAL CARE"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2018-11-07T10:14:17Z"],["dc.date.available","2018-11-07T10:14:17Z"],["dc.date.issued","2016"],["dc.description.abstract","Partial extracorporeal CO2 removal allows a decreasing tidal volume without respiratory acidosis in patients with acute respiratory distress syndrome. This, however, may be associated with worsening hypoxemia, due to several mechanisms, such as gravitational and reabsorption atelectasis, due to a decrease in mean airway pressure and a critically low ventilation-perfusion ratio, respectively. In addition, an imbalance between alveolar and artificial lung partial pressures of nitrogen may accelerate the process. Finally, the decrease in the respiratory quotient, leading to unrecognized alveolar hypoxia and monotonous low plateau pressures preventing critical opening, may contribute to hypoxemia."],["dc.identifier.doi","10.1186/s13054-016-1310-9"],["dc.identifier.isi","000375649100001"],["dc.identifier.pmid","27170273"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13489"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40594"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1364-8535"],["dc.relation.issn","1466-609X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Ultra-protective ventilation and hypoxemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2018Journal Article [["dc.bibliographiccitation.artnumber","237"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Vasques, Francesco"],["dc.contributor.author","Duscio, Eleonora"],["dc.contributor.author","Romitti, Federica"],["dc.contributor.author","Pasticci, Iacopo"],["dc.contributor.author","Caironi, Pietro"],["dc.contributor.author","Meessen, Jennifer"],["dc.contributor.author","Latini, Roberto"],["dc.contributor.author","Cressoni, Massimo"],["dc.contributor.author","Camporota, Luigi"],["dc.contributor.author","Pesenti, Antonio"],["dc.contributor.author","Fumagalli, Roberto"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2019-03-13T16:08:29Z"],["dc.date.available","2019-03-13T16:08:29Z"],["dc.date.issued","2018"],["dc.description.abstract","A reanalysis of the ALBIOS trial suggested that patients with septic shock - defined by vasopressor-dependent hypotension in the presence of severe sepsis (Shock-2) - had a survival benefit when treated with albumin. The new septic shock definition (Shock-3) added the criterion of a lactate threshold of 2 mmol/L. We investigated how the populations defined according to Shock-2 and Shock-3 differed and whether the albumin benefit would be confirmed."],["dc.identifier.doi","10.1186/s13054-018-2169-8"],["dc.identifier.pmid","30261898"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15358"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57674"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Septic shock-3 vs 2: an analysis of the ALBIOS study"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2017Journal Article [["dc.bibliographiccitation.artnumber","46"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Intensive Care Medicine Experimental"],["dc.bibliographiccitation.volume","5"],["dc.contributor.author","Cambiaghi, Barbara"],["dc.contributor.author","Vasques, Francesco"],["dc.contributor.author","Mörer, Onnen"],["dc.contributor.author","Ritter, Christian"],["dc.contributor.author","Mauri, Tommaso"],["dc.contributor.author","Kunze-Szikszay, Nils"],["dc.contributor.author","Holke, Karin"],["dc.contributor.author","Collino, Francesca"],["dc.contributor.author","Maiolo, Giorgia"],["dc.contributor.author","Rapetti, Francesca"],["dc.contributor.author","Schulze-Kalthoff, Elias"],["dc.contributor.author","Tonetti, Tommaso"],["dc.contributor.author","Hahn, Günter"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2020-12-10T18:41:24Z"],["dc.date.available","2020-12-10T18:41:24Z"],["dc.date.issued","2017"],["dc.description.abstract","Abstract Background Severe hypoperfusion can cause lung damage. We studied the effects of regional perfusion block in normal lungs and in the lungs that had been conditioned by lavage with 500 ml saline and high V T (20 ml kg−1) ventilation. Methods Nineteen pigs (61.2 ± 2.5 kg) were randomized to five groups: controls (n = 3), the right lower lobe block alone (n = 3), lavage and high V T (n = 4), lung lavage, and high V T plus perfusion block of the right (n = 5) or left (n = 4) lower lobe. Gas exchange, respiratory mechanics, and hemodynamics were measured hourly. After an 8-h observation period, CT scans were obtained at 0 and 15 cmH2O airway pressure. Results Perfusion block did not damage healthy lungs. In conditioned lungs, the left perfusion block caused more edema in the contralateral lung (777 ± 62 g right lung vs 484 ± 204 g left; p < 0.05) than the right perfusion block did (581 ± 103 g right lung vs 484 ± 204 g left; p n.s.). The gas/tissue ratio, however, was similar (0.5 ± 0.3 and 0.8 ± 0.5; p n.s.). The lobes with perfusion block were not affected (gas/tissue ratio right 1.6 ± 0.9; left 1.7 ± 0.5, respectively). Pulmonary artery pressure, PaO2/FiO2, dead space, and lung mechanics were more markedly affected in animals with left perfusion block, while the gas/tissue ratios were similar in the non-occluded lobes. Conclusions The right and left perfusion blocks caused the same “intensity” of edema in conditioned lungs. The total amount of edema in the two lungs differed because of differences in lung size. If capillary permeability is altered, increased blood flow may induce or increase edema."],["dc.identifier.doi","10.1186/s40635-017-0161-2"],["dc.identifier.eissn","2197-425X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77572"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Effects of regional perfusion block in healthy and injured lungs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2019Journal Article [["dc.bibliographiccitation.artnumber","203"],["dc.bibliographiccitation.issue","Suppl 1"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Gattinoni, L."],["dc.contributor.author","Vassalli, F."],["dc.contributor.author","Romitti, F."],["dc.contributor.author","Vasques, F."],["dc.contributor.author","Pasticci, I."],["dc.contributor.author","Duscio, E."],["dc.contributor.author","Quintel, M."],["dc.date.accessioned","2019-07-09T11:51:48Z"],["dc.date.available","2019-07-09T11:51:48Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s13054-019-2437-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16195"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60013"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","BioMed Central"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Extracorporeal gas exchange: when to start and how to end?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Intensive Care"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Marini, John J."],["dc.contributor.author","Chiumello, Davide"],["dc.contributor.author","Busana, Mattia"],["dc.contributor.author","Camporota, Luigi"],["dc.date.accessioned","2021-04-14T08:31:18Z"],["dc.date.available","2021-04-14T08:31:18Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s13613-020-00756-7"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17607"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83554"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2110-5820"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","COVID-19: scientific reasoning, pragmatism and emotional bias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2021-11-01Journal Article Research Paper [["dc.bibliographiccitation.artnumber","55"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Intensive Care Medicine Experimental"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Marini, John J."],["dc.contributor.author","Crooke, Philip S."],["dc.contributor.author","Tawfik, Pierre"],["dc.contributor.author","Chatburn, Robert L."],["dc.contributor.author","Dries, David J."],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2021-11-25T11:25:12Z"],["dc.date.accessioned","2022-08-18T12:41:27Z"],["dc.date.available","2021-11-25T11:25:12Z"],["dc.date.available","2022-08-18T12:41:27Z"],["dc.date.issued","2021-11-01"],["dc.date.updated","2022-07-29T12:18:45Z"],["dc.description.abstract","Abstract\r\n \r\n Background\r\n High rates of inflation energy delivery coupled with transpulmonary tidal pressures of sufficient magnitude may augment the risk of damage to vulnerable, stress-focused units within a mechanically heterogeneous lung. Apart from flow amplitude, the clinician-selected flow waveform, a relatively neglected dimension of inflation power, may distribute inflation energy of each inflation cycle non-uniformly among alveoli with different mechanical properties over the domains of time and space. In this initial step in modeling intracycle power distribution, our primary objective was to develop a mathematical model of global intracycle inflation power that uses clinician-measurable inputs to allow comparisons of instantaneous ICP profiles among the flow modes commonly encountered in clinical practice: constant, linearly decelerating, exponentially decelerating (pressure control), and spontaneous (sinusoidal).\r\n \r\n \r\n Methods\r\n We first tested the predictions of our mathematical model of passive inflation with the actual physical performance of a mechanical ventilator–lung system that simulated ventilation to three types of patients: normal, severe ARDS, and severe airflow obstruction. After verification, model predictions were then generated for 5000 ‘virtual ARDS patients’. Holding constant the tidal volume and inflation time between modes, the validated model then varied the flow profile and quantitated the resulting intensity and timing of potentially damaging ‘elastic’ energy and intracycle power (pressure–flow product) developed in response to random combinations of machine settings and severity levels for ARDS.\r\n \r\n \r\n Results\r\n Our modeling indicates that while the varied flow patterns ultimately deliver similar total amounts of alveolar energy during each breath, they differ profoundly regarding the potentially damaging pattern with which that energy distributes over time during inflation. Pressure control imposed relatively high maximal intracycle power.\r\n \r\n \r\n Conclusions\r\n Flow amplitude and waveform may be relatively neglected and modifiable determinants of VILI risk when ventilating ARDS."],["dc.identifier.citation","Intensive Care Medicine Experimental. 2021 Nov 01;9(1):55"],["dc.identifier.doi","10.1186/s40635-021-00420-9"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/93554"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112993"],["dc.language.iso","en"],["dc.publisher","Springer International Publishing"],["dc.rights","CC BY 4.0"],["dc.rights.holder","The Author(s)"],["dc.subject","Mechanical ventilation"],["dc.subject","Mathematical model"],["dc.subject","Ventilator-induced lung injury"],["dc.subject","VILI"],["dc.subject","Power"],["dc.subject","Intracycle power"],["dc.subject","Energetics"],["dc.subject","Modes of ventilation"],["dc.title","Intracycle power and ventilation mode as potential contributors to ventilator-induced lung injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2019Journal Article [["dc.bibliographiccitation.firstpage","954"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","American Journal of Respiratory and Critical Care Medicine"],["dc.bibliographiccitation.lastpage","956"],["dc.bibliographiccitation.volume","200"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Busana, Mattia"],["dc.contributor.author","Gattinoni, Luciano"],["dc.date.accessioned","2020-12-10T18:38:17Z"],["dc.date.available","2020-12-10T18:38:17Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1164/rccm.201906-1164ED"],["dc.identifier.eissn","1535-4970"],["dc.identifier.issn","1073-449X"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16632"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77258"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Breathing and Ventilation during Extracorporeal Membrane Oxygenation: How to Find the Balance between Rest and Load"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI2021Journal Article [["dc.bibliographiccitation.firstpage","431"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Pharmaceutics"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Otto, Matthias"],["dc.contributor.author","Krebs, Jörg"],["dc.contributor.author","Welker, Peter"],["dc.contributor.author","Holm, René"],["dc.contributor.author","Thiel, Manfred"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Quintel, Michael"],["dc.contributor.author","Tsagogiorgas, Charalambos"],["dc.date.accessioned","2021-06-01T09:42:40Z"],["dc.date.available","2021-06-01T09:42:40Z"],["dc.date.issued","2021"],["dc.description.abstract","Aerosol therapy in patients suffering from acute respiratory distress syndrome (ARDS) has so far failed in improving patients’ outcomes. This might be because dependent lung areas cannot be reached by conventional aerosols. Due to their physicochemical properties, semifluorinated alkanes (SFAs) could address this problem. After induction of ARDS, 26 pigs were randomized into three groups: (1) control (Sham), (2) perfluorohexyloctane (F6H8), and (3) F6H8-ibuprofen. Using a nebulization catheter, (2) received 1 mL/kg F6H8 while (3) received 1 mL/kg F6H8 with 6 mg/mL ibuprofen. Ibuprofen plasma and lung tissue concentration, bronchoalveolar lavage (BAL) fluid concentration of TNF-α, IL-8, and IL-6, and lung mechanics were measured. The ibuprofen concentration was equally distributed to the dependent parts of the right lungs. Pharmacokinetic data demonstrated systemic absorption of ibuprofen proofing a transport across the alveolo-capillary membrane. A significantly lower TNF-α concentration was observed in (2) and (3) when compared to the control group (1). There were no significant differences in IL-8 and IL-6 concentrations and lung mechanics. F6H8 aerosol seemed to be a suitable carrier for pulmonary drug delivery to dependent ARDS lung regions without having negative effects on lung mechanics."],["dc.description.sponsorship","Novaliq GmbH, Germany"],["dc.identifier.doi","10.3390/pharmaceutics13030431"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85319"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","MDPI"],["dc.relation.eissn","1999-4923"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Inhalationally Administered Semifluorinated Alkanes (SFAs) as Drug Carriers in an Experimental Model of Acute Respiratory Distress Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2020Journal Article [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Gattinoni, Luciano"],["dc.contributor.author","Chiumello, Davide"],["dc.contributor.author","Rossi, Sandra"],["dc.date.accessioned","2020-12-10T18:39:04Z"],["dc.date.available","2020-12-10T18:39:04Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1186/s13054-020-02880-z"],["dc.identifier.eissn","1364-8535"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17227"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77531"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","COVID-19 pneumonia: ARDS or not?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI