Impact of low pulmonary vascular pressure on ventilator-induced lung injury
OBJECTIVETo study the impact of low pulmonary vascular pressure on ventilator-induced lung injury. DESIGNRandomized prospective animal study. SUBJECTSIsolated perfused rabbit heart-lung preparation. SETTINGSAnimal research laboratory in a university hospital. INTERVENTIONSTwenty isolated sets of nor...
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| Veröffentlicht in: | Critical care medicine 2002-10, Vol.30 (10), p.2183-2190 |
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| creator | Broccard, Alain F Vannay, Christine Feihl, François Schaller, Marie-Denise |
| description | OBJECTIVETo study the impact of low pulmonary vascular pressure on ventilator-induced lung injury.
DESIGNRandomized prospective animal study.
SUBJECTSIsolated perfused rabbit heart-lung preparation.
SETTINGSAnimal research laboratory in a university hospital.
INTERVENTIONSTwenty isolated sets of normal lungs were perfused (constant flow, 0.3 L/min; left atrial pressure, 6 mm Hg), ventilated for 20 min (pressure control ventilation, 15 cm H2O; baseline period), and then randomized into three groups. Group A (control, n = 7) was perfused and ventilated as previously described during three consecutive 20-min periods. In group B (high airway pressure/normal left atrial pressure, n = 7), pressure control ventilation was 20, 25, and 30 cm H2O during each period. Group C (high airway pressure/low left atrial pressure, n = 6) was ventilated as group B but, in contrast to groups A and B, left atrial pressure was reduced to 1 mm Hg.
MEASUREMENTS AND MAIN RESULTSThe rate of edema formation (WGR, weight gain per minute normalized for initial lung weight) and the ultrafiltration coefficient (Kf) were measured during and after each period and their changes from baseline [ΔWGR (edema formation index) and ΔKf (vascular permeability index)] calculated to compare groups. The incidence and timing of vascular failure were compared. Vascular failure was considered to be present if all the following conditions were metpulmonary hypertension, accelerated weight gain, and occurrence of fluid leak from the lungs. At the end of the study, ΔWGR (g·g·min) was higher in group C (0.54 ± 0.17) than in groups B (0.08 ± 0.04) and A (0.00 ± 0.01;p < .05), as well as in group B compared with A (p < .05). Similar differences between groups (p < .05) were found for ΔKf (g·min·cm H2O·100 g)C, 7.24 ± 2.36; B, 1.40 ± 0.49; A, 0.01 ± 0.03. Vascular failure was not observed in groups A and B but occurred in all but one preparation in group C (p < .05; C vs. A and B).
CONCLUSIONReducing left atrial pressure results in more severe ventilator-induced lung injury. These results suggest that lung blood volume modulates cyclic tidal lung stress. |
| doi_str_mv | 10.1097/00003246-200210000-00002 |
| format | Article |
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DESIGNRandomized prospective animal study.
SUBJECTSIsolated perfused rabbit heart-lung preparation.
SETTINGSAnimal research laboratory in a university hospital.
INTERVENTIONSTwenty isolated sets of normal lungs were perfused (constant flow, 0.3 L/min; left atrial pressure, 6 mm Hg), ventilated for 20 min (pressure control ventilation, 15 cm H2O; baseline period), and then randomized into three groups. Group A (control, n = 7) was perfused and ventilated as previously described during three consecutive 20-min periods. In group B (high airway pressure/normal left atrial pressure, n = 7), pressure control ventilation was 20, 25, and 30 cm H2O during each period. Group C (high airway pressure/low left atrial pressure, n = 6) was ventilated as group B but, in contrast to groups A and B, left atrial pressure was reduced to 1 mm Hg.
MEASUREMENTS AND MAIN RESULTSThe rate of edema formation (WGR, weight gain per minute normalized for initial lung weight) and the ultrafiltration coefficient (Kf) were measured during and after each period and their changes from baseline [ΔWGR (edema formation index) and ΔKf (vascular permeability index)] calculated to compare groups. The incidence and timing of vascular failure were compared. Vascular failure was considered to be present if all the following conditions were metpulmonary hypertension, accelerated weight gain, and occurrence of fluid leak from the lungs. At the end of the study, ΔWGR (g·g·min) was higher in group C (0.54 ± 0.17) than in groups B (0.08 ± 0.04) and A (0.00 ± 0.01;p < .05), as well as in group B compared with A (p < .05). Similar differences between groups (p < .05) were found for ΔKf (g·min·cm H2O·100 g)C, 7.24 ± 2.36; B, 1.40 ± 0.49; A, 0.01 ± 0.03. Vascular failure was not observed in groups A and B but occurred in all but one preparation in group C (p < .05; C vs. A and B).
CONCLUSIONReducing left atrial pressure results in more severe ventilator-induced lung injury. These results suggest that lung blood volume modulates cyclic tidal lung stress.</description><identifier>ISSN: 0090-3493</identifier><identifier>EISSN: 1530-0293</identifier><identifier>DOI: 10.1097/00003246-200210000-00002</identifier><identifier>PMID: 12394942</identifier><identifier>CODEN: CCMDC7</identifier><language>eng</language><publisher>Hagerstown, MD: by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</publisher><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Atrial Function, Left - physiology ; Biological and medical sciences ; Blood Pressure ; Capillary Permeability ; Emergency and intensive respiratory care ; Hemodynamics ; Hypertension, Pulmonary - etiology ; Hypertension, Pulmonary - physiopathology ; In Vitro Techniques ; Intensive care medicine ; Medical sciences ; Pressure ; Pulmonary Circulation ; Pulmonary Edema - etiology ; Pulmonary Edema - physiopathology ; Rabbits ; Respiration, Artificial - adverse effects ; Respiration, Artificial - methods ; Respiratory Distress Syndrome, Adult - etiology ; Respiratory Distress Syndrome, Adult - physiopathology ; Respiratory Distress Syndrome, Adult - therapy ; Respiratory Mechanics ; Weight Gain</subject><ispartof>Critical care medicine, 2002-10, Vol.30 (10), p.2183-2190</ispartof><rights>2002 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4522-2a5b486156268fc9401566d1ebd59e3c4e7d8772d0829bb915189bb539a2dce53</citedby><cites>FETCH-LOGICAL-c4522-2a5b486156268fc9401566d1ebd59e3c4e7d8772d0829bb915189bb539a2dce53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14353844$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12394942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Broccard, Alain F</creatorcontrib><creatorcontrib>Vannay, Christine</creatorcontrib><creatorcontrib>Feihl, François</creatorcontrib><creatorcontrib>Schaller, Marie-Denise</creatorcontrib><title>Impact of low pulmonary vascular pressure on ventilator-induced lung injury</title><title>Critical care medicine</title><addtitle>Crit Care Med</addtitle><description>OBJECTIVETo study the impact of low pulmonary vascular pressure on ventilator-induced lung injury.
DESIGNRandomized prospective animal study.
SUBJECTSIsolated perfused rabbit heart-lung preparation.
SETTINGSAnimal research laboratory in a university hospital.
INTERVENTIONSTwenty isolated sets of normal lungs were perfused (constant flow, 0.3 L/min; left atrial pressure, 6 mm Hg), ventilated for 20 min (pressure control ventilation, 15 cm H2O; baseline period), and then randomized into three groups. Group A (control, n = 7) was perfused and ventilated as previously described during three consecutive 20-min periods. In group B (high airway pressure/normal left atrial pressure, n = 7), pressure control ventilation was 20, 25, and 30 cm H2O during each period. Group C (high airway pressure/low left atrial pressure, n = 6) was ventilated as group B but, in contrast to groups A and B, left atrial pressure was reduced to 1 mm Hg.
MEASUREMENTS AND MAIN RESULTSThe rate of edema formation (WGR, weight gain per minute normalized for initial lung weight) and the ultrafiltration coefficient (Kf) were measured during and after each period and their changes from baseline [ΔWGR (edema formation index) and ΔKf (vascular permeability index)] calculated to compare groups. The incidence and timing of vascular failure were compared. Vascular failure was considered to be present if all the following conditions were metpulmonary hypertension, accelerated weight gain, and occurrence of fluid leak from the lungs. At the end of the study, ΔWGR (g·g·min) was higher in group C (0.54 ± 0.17) than in groups B (0.08 ± 0.04) and A (0.00 ± 0.01;p < .05), as well as in group B compared with A (p < .05). Similar differences between groups (p < .05) were found for ΔKf (g·min·cm H2O·100 g)C, 7.24 ± 2.36; B, 1.40 ± 0.49; A, 0.01 ± 0.03. Vascular failure was not observed in groups A and B but occurred in all but one preparation in group C (p < .05; C vs. A and B).
CONCLUSIONReducing left atrial pressure results in more severe ventilator-induced lung injury. These results suggest that lung blood volume modulates cyclic tidal lung stress.</description><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Atrial Function, Left - physiology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Capillary Permeability</subject><subject>Emergency and intensive respiratory care</subject><subject>Hemodynamics</subject><subject>Hypertension, Pulmonary - etiology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Intensive care medicine</subject><subject>Medical sciences</subject><subject>Pressure</subject><subject>Pulmonary Circulation</subject><subject>Pulmonary Edema - etiology</subject><subject>Pulmonary Edema - physiopathology</subject><subject>Rabbits</subject><subject>Respiration, Artificial - adverse effects</subject><subject>Respiration, Artificial - methods</subject><subject>Respiratory Distress Syndrome, Adult - etiology</subject><subject>Respiratory Distress Syndrome, Adult - physiopathology</subject><subject>Respiratory Distress Syndrome, Adult - therapy</subject><subject>Respiratory Mechanics</subject><subject>Weight Gain</subject><issn>0090-3493</issn><issn>1530-0293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUtv3CAQgFGVqtlu-xciLsnNLU_bHKsoaVdZqZf2jDAed51g44DJav992Ee6p3BgGPTNAB8IYUq-UaKq7yQPzkRZMEIY3WfFfmIf0IJKnhOm-AVaEKJIwYXil-hzjI-EUCEr_gldUsaVUIIt0MNqmIydse-w81s8JTf40YQdfjHRJmcCngLEmAJgP-IXGOfemdmHoh_bZKHFLo3_cD8-prD7gj52xkX4eopL9Pf-7s_tr2L9--fq9se6sEIyVjAjG1GXVJasrDurBMnLsqXQtFIBtwKqtq4q1pKaqaZRVNI6R8mVYa0FyZfo5th3Cv45QZz10EcLzpkRfIq6YtlBJUQG6yNog48xQKen0A_5dZoSvRep30Tq_yIPWyyXXp3OSM0A7bnwZC4D1ycgizKuC2a0fTxzgkteH-4gjtzWuxlCfHJpC0FvwLh5o9_7SP4KyfKJ-A</recordid><startdate>200210</startdate><enddate>200210</enddate><creator>Broccard, Alain F</creator><creator>Vannay, Christine</creator><creator>Feihl, François</creator><creator>Schaller, Marie-Denise</creator><general>by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>200210</creationdate><title>Impact of low pulmonary vascular pressure on ventilator-induced lung injury</title><author>Broccard, Alain F ; Vannay, Christine ; Feihl, François ; Schaller, Marie-Denise</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4522-2a5b486156268fc9401566d1ebd59e3c4e7d8772d0829bb915189bb539a2dce53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Atrial Function, Left - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Capillary Permeability</topic><topic>Emergency and intensive respiratory care</topic><topic>Hemodynamics</topic><topic>Hypertension, Pulmonary - etiology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Intensive care medicine</topic><topic>Medical sciences</topic><topic>Pressure</topic><topic>Pulmonary Circulation</topic><topic>Pulmonary Edema - etiology</topic><topic>Pulmonary Edema - physiopathology</topic><topic>Rabbits</topic><topic>Respiration, Artificial - adverse effects</topic><topic>Respiration, Artificial - methods</topic><topic>Respiratory Distress Syndrome, Adult - etiology</topic><topic>Respiratory Distress Syndrome, Adult - physiopathology</topic><topic>Respiratory Distress Syndrome, Adult - therapy</topic><topic>Respiratory Mechanics</topic><topic>Weight Gain</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Broccard, Alain F</creatorcontrib><creatorcontrib>Vannay, Christine</creatorcontrib><creatorcontrib>Feihl, François</creatorcontrib><creatorcontrib>Schaller, Marie-Denise</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Critical care medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Broccard, Alain F</au><au>Vannay, Christine</au><au>Feihl, François</au><au>Schaller, Marie-Denise</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of low pulmonary vascular pressure on ventilator-induced lung injury</atitle><jtitle>Critical care medicine</jtitle><addtitle>Crit Care Med</addtitle><date>2002-10</date><risdate>2002</risdate><volume>30</volume><issue>10</issue><spage>2183</spage><epage>2190</epage><pages>2183-2190</pages><issn>0090-3493</issn><eissn>1530-0293</eissn><coden>CCMDC7</coden><abstract>OBJECTIVETo study the impact of low pulmonary vascular pressure on ventilator-induced lung injury.
DESIGNRandomized prospective animal study.
SUBJECTSIsolated perfused rabbit heart-lung preparation.
SETTINGSAnimal research laboratory in a university hospital.
INTERVENTIONSTwenty isolated sets of normal lungs were perfused (constant flow, 0.3 L/min; left atrial pressure, 6 mm Hg), ventilated for 20 min (pressure control ventilation, 15 cm H2O; baseline period), and then randomized into three groups. Group A (control, n = 7) was perfused and ventilated as previously described during three consecutive 20-min periods. In group B (high airway pressure/normal left atrial pressure, n = 7), pressure control ventilation was 20, 25, and 30 cm H2O during each period. Group C (high airway pressure/low left atrial pressure, n = 6) was ventilated as group B but, in contrast to groups A and B, left atrial pressure was reduced to 1 mm Hg.
MEASUREMENTS AND MAIN RESULTSThe rate of edema formation (WGR, weight gain per minute normalized for initial lung weight) and the ultrafiltration coefficient (Kf) were measured during and after each period and their changes from baseline [ΔWGR (edema formation index) and ΔKf (vascular permeability index)] calculated to compare groups. The incidence and timing of vascular failure were compared. Vascular failure was considered to be present if all the following conditions were metpulmonary hypertension, accelerated weight gain, and occurrence of fluid leak from the lungs. At the end of the study, ΔWGR (g·g·min) was higher in group C (0.54 ± 0.17) than in groups B (0.08 ± 0.04) and A (0.00 ± 0.01;p < .05), as well as in group B compared with A (p < .05). Similar differences between groups (p < .05) were found for ΔKf (g·min·cm H2O·100 g)C, 7.24 ± 2.36; B, 1.40 ± 0.49; A, 0.01 ± 0.03. Vascular failure was not observed in groups A and B but occurred in all but one preparation in group C (p < .05; C vs. A and B).
CONCLUSIONReducing left atrial pressure results in more severe ventilator-induced lung injury. These results suggest that lung blood volume modulates cyclic tidal lung stress.</abstract><cop>Hagerstown, MD</cop><pub>by the Society of Critical Care Medicine and Lippincott Williams & Wilkins</pub><pmid>12394942</pmid><doi>10.1097/00003246-200210000-00002</doi><tpages>8</tpages></addata></record> |
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| subjects | Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Atrial Function, Left - physiology Biological and medical sciences Blood Pressure Capillary Permeability Emergency and intensive respiratory care Hemodynamics Hypertension, Pulmonary - etiology Hypertension, Pulmonary - physiopathology In Vitro Techniques Intensive care medicine Medical sciences Pressure Pulmonary Circulation Pulmonary Edema - etiology Pulmonary Edema - physiopathology Rabbits Respiration, Artificial - adverse effects Respiration, Artificial - methods Respiratory Distress Syndrome, Adult - etiology Respiratory Distress Syndrome, Adult - physiopathology Respiratory Distress Syndrome, Adult - therapy Respiratory Mechanics Weight Gain |
| title | Impact of low pulmonary vascular pressure on ventilator-induced lung injury |
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