<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>4(12)</volume><submitter>Bassi TG</submitter><pubmed_abstract>In a porcine healthy lung model, temporary transvenous diaphragm neurostimulation (TTDN) for 50 hours mitigated hippocampal apoptosis and inflammation associated with mechanical ventilation (MV).&lt;h4>Hypothesis&lt;/h4>Explore whether TTDN in combination with MV for 12 hours mitigates hippocampal apoptosis and inflammation in an acute respiratory distress syndrome (ARDS) preclinical model.&lt;h4>Methods and models&lt;/h4>Compare hippocampal apoptosis, inflammatory markers, and serum markers of neurologic injury between never ventilated subjects and three groups of mechanically ventilated subjects with injured lungs: MV only (LI-MV), MV plus TTDN every other breath, and MV plus TTDN every breath. MV settings in volume control were tidal volume 8 mL/kg and positive end-expiratory pressure 5 cm H&lt;sub>2&lt;/sub>O. Lung injury, equivalent to moderate ARDS, was achieved by infusing oleic acid into the pulmonary artery.&lt;h4>Results&lt;/h4>Hippocampal apoptosis, microglia, and reactive-astrocyte percentages were similar between the TTDN-every-breath and never ventilated groups. The LI-MV group had a higher percentage of these measures than all other groups (&lt;i>p&lt;/i> &lt; 0.05). Transpulmonary driving pressure at study end was lower in the TTDN-every-breath group than in the LI-MV group; systemic inflammation and lung injury scores were not significantly different. The TTDN-every-breath group had considerably lower serum concentration of homovanillic acid (cerebral dopamine production surrogate) at study end than the LI-MV group (&lt;i>p&lt;/i> &lt; 0.05). Heart rate variability declined in the LI-MV group and increased in both TTDN groups (&lt;i>p&lt;/i> &lt; 0.05).&lt;h4>Interpretations and conclusions&lt;/h4>In a moderate-ARDS porcine model, MV is associated with hippocampal apoptosis and inflammation, and TTDN mitigates that hippocampal apoptosis and inflammation.</pubmed_abstract><journal>Critical care explorations</journal><pagination>e0820</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9788975</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Diaphragm Neurostimulation Mitigates Ventilation-Associated Brain Injury in a Preclinical Acute Respiratory Distress Syndrome Model.</pubmed_title><pmcid>PMC9788975</pmcid><pubmed_authors>Bassi TG</pubmed_authors><pubmed_authors>Rohrs EC</pubmed_authors><pubmed_authors>Gani MM</pubmed_authors><pubmed_authors>Reynolds SC</pubmed_authors><pubmed_authors>Wittmann MJ</pubmed_authors><pubmed_authors>Nicholas MM</pubmed_authors><pubmed_authors>Fernandez MKC</pubmed_authors><pubmed_authors>Evans MD</pubmed_authors><pubmed_authors>Ornowska MM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Diaphragm Neurostimulation Mitigates Ventilation-Associated Brain Injury in a Preclinical Acute Respiratory Distress Syndrome Model.</name><description>In a porcine healthy lung model, temporary transvenous diaphragm neurostimulation (TTDN) for 50 hours mitigated hippocampal apoptosis and inflammation associated with mechanical ventilation (MV).&lt;h4>Hypothesis&lt;/h4>Explore whether TTDN in combination with MV for 12 hours mitigates hippocampal apoptosis and inflammation in an acute respiratory distress syndrome (ARDS) preclinical model.&lt;h4>Methods and models&lt;/h4>Compare hippocampal apoptosis, inflammatory markers, and serum markers of neurologic injury between never ventilated subjects and three groups of mechanically ventilated subjects with injured lungs: MV only (LI-MV), MV plus TTDN every other breath, and MV plus TTDN every breath. MV settings in volume control were tidal volume 8 mL/kg and positive end-expiratory pressure 5 cm H&lt;sub>2&lt;/sub>O. Lung injury, equivalent to moderate ARDS, was achieved by infusing oleic acid into the pulmonary artery.&lt;h4>Results&lt;/h4>Hippocampal apoptosis, microglia, and reactive-astrocyte percentages were similar between the TTDN-every-breath and never ventilated groups. The LI-MV group had a higher percentage of these measures than all other groups (&lt;i>p&lt;/i> &lt; 0.05). Transpulmonary driving pressure at study end was lower in the TTDN-every-breath group than in the LI-MV group; systemic inflammation and lung injury scores were not significantly different. The TTDN-every-breath group had considerably lower serum concentration of homovanillic acid (cerebral dopamine production surrogate) at study end than the LI-MV group (&lt;i>p&lt;/i> &lt; 0.05). Heart rate variability declined in the LI-MV group and increased in both TTDN groups (&lt;i>p&lt;/i> &lt; 0.05).&lt;h4>Interpretations and conclusions&lt;/h4>In a moderate-ARDS porcine model, MV is associated with hippocampal apoptosis and inflammation, and TTDN mitigates that hippocampal apoptosis and inflammation.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-04T21:04:33.34Z</modification><creation>2025-04-04T21:04:33.34Z</creation></dates><accession>S-EPMC9788975</accession><cross_references><pubmed>36601565</pubmed><doi>10.1097/CCE.0000000000000820</doi></cross_references></HashMap>