<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>44</viewCount><searchCount>0</searchCount></scores><additional><omics_type>Unknown</omics_type><volume>13(5)</volume><submitter>Briot R</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>We assessed the in vivo effects of terbutaline, a beta2-agonist assumed to reduce microvascular permeability in acute lung injury.&lt;h4>Methods&lt;/h4>We used a recently developed broncho-alveolar lavage (BAL) technique to repeatedly measure (every 15 min. for 4 hours) the time-course of capillary-alveolar leakage of a macromolecule (fluorescein-labeled dextran) in 19 oleic acid (OA) lung injured dogs. BAL was performed in a closed lung sampling site, using a bronchoscope fitted with an inflatable cuff. Fluorescein-labeled Dextran (FITC-D70) was continuously infused and its concentration measured in plasma and BAL fluid. A two-compartment model (blood and alveoli) was used to calculate KAB, the transport rate coefficient of FITC-D70 from blood to alveoli. KAB was estimated every 15 minutes over 4 hours. Terbutaline intra-venous perfusion was started 90 min. after the onset of the injury and then continuously infused until the end of the experiment.&lt;h4>Results&lt;/h4>In the non-treated injured group, the capillary-alveolar leakage of FITC-D70 reached a peak within 30 minutes after the OA injury. Thereafter the FITC-D70 leakage decreased gradually until the end of the experiment. Terbutaline infusion, started 90 min after injury, interrupted the recovery with an aggravation in FITC-D70 leakage.&lt;h4>Conclusions&lt;/h4>As cardiac index increased with terbutaline infusion, we speculate that terbutaline recruits leaky capillaries and increases FITC-D70 leakage after OA injury. These findings suggest that therapies inducing an increase in cardiac output and a decrease in pulmonary vascular resistances have the potential to heighten the early increase in protein transport from plasma to alveoli within the acutely injured lung.</pubmed_abstract><journal>Critical care (London, England)</journal><pagination>R166</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2784397</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Increased cardiac index due to terbutaline treatment aggravates capillary-alveolar macromolecular leakage in oleic acid lung injury in dogs.</pubmed_title><pmcid>PMC2784397</pmcid><pubmed_authors>Anglade D</pubmed_authors><pubmed_authors>Grimbert F</pubmed_authors><pubmed_authors>Martiel JL</pubmed_authors><pubmed_authors>Bayat S</pubmed_authors><pubmed_authors>Briot R</pubmed_authors><view_count>44</view_count></additional><is_claimable>false</is_claimable><name>Increased cardiac index due to terbutaline treatment aggravates capillary-alveolar macromolecular leakage in oleic acid lung injury in dogs.</name><description>&lt;h4>Introduction&lt;/h4>We assessed the in vivo effects of terbutaline, a beta2-agonist assumed to reduce microvascular permeability in acute lung injury.&lt;h4>Methods&lt;/h4>We used a recently developed broncho-alveolar lavage (BAL) technique to repeatedly measure (every 15 min. for 4 hours) the time-course of capillary-alveolar leakage of a macromolecule (fluorescein-labeled dextran) in 19 oleic acid (OA) lung injured dogs. BAL was performed in a closed lung sampling site, using a bronchoscope fitted with an inflatable cuff. Fluorescein-labeled Dextran (FITC-D70) was continuously infused and its concentration measured in plasma and BAL fluid. A two-compartment model (blood and alveoli) was used to calculate KAB, the transport rate coefficient of FITC-D70 from blood to alveoli. KAB was estimated every 15 minutes over 4 hours. Terbutaline intra-venous perfusion was started 90 min. after the onset of the injury and then continuously infused until the end of the experiment.&lt;h4>Results&lt;/h4>In the non-treated injured group, the capillary-alveolar leakage of FITC-D70 reached a peak within 30 minutes after the OA injury. Thereafter the FITC-D70 leakage decreased gradually until the end of the experiment. Terbutaline infusion, started 90 min after injury, interrupted the recovery with an aggravation in FITC-D70 leakage.&lt;h4>Conclusions&lt;/h4>As cardiac index increased with terbutaline infusion, we speculate that terbutaline recruits leaky capillaries and increases FITC-D70 leakage after OA injury. These findings suggest that therapies inducing an increase in cardiac output and a decrease in pulmonary vascular resistances have the potential to heighten the early increase in protein transport from plasma to alveoli within the acutely injured lung.</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009</publication><modification>2021-02-21T04:06:30Z</modification><creation>2019-03-27T00:26:54Z</creation></dates><accession>S-EPMC2784397</accession><cross_references><pubmed>19845949</pubmed><doi>10.1186/cc8137</doi></cross_references></HashMap>