High tidal volume mechanical ventilation exacerbates pulmonary injury via upregulation of PAI-1 expression in rats.

IF 2.5 3区 生物学
Jun-Ming Ren, Gui-Fei Wang, Jing Bi, Zhi Wang, Wei-Wei Zhang
{"title":"High tidal volume mechanical ventilation exacerbates pulmonary injury via upregulation of PAI-1 expression in rats.","authors":"Jun-Ming Ren, Gui-Fei Wang, Jing Bi, Zhi Wang, Wei-Wei Zhang","doi":"10.1186/s41065-025-00446-z","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the impact of different mechanical ventilation strategies on pulmonary plasminogen activator inhibitor-1 (PAI-1) expression in a rat model.</p><p><strong>Methods: </strong>Seventy-two specific pathogen-free (SPF) adult male Sprague-Dawley (SD) rats were randomly assigned to four groups (n = 18): Group C (spontaneous breathing), group S (low tidal volume, VT = 6 mL/kg), group R (regular tidal volume, VT = 10 mL/kg), and group L (high tidal volume, VT = 40 mL/kg). Each group was further divided into three subgroups based on mechanical ventilation duration (2, 4, or 6 h). Following tracheotomy intubation, group C maintained spontaneous breathing, while the other groups underwent mechanical ventilation with a small animal ventilator. Lung wet-to-dry weight ratios, cell apoptosis rate, and lung injury score were recorded. PAI-1 and IL-8 levels were measured in bronchoalveolar lavage fluid (BALF), and PAI-1 mRNA expression in lung tissue was analyzed using real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>Progressive lung tissue injury was observed in Group L with increasing ventilation durations, accompanied by significant increases in PAI-1, IL-8, and PAI-1 mRNA expression, compared to group C (P < 0.05). No significant differences were identified between Group S and group C, while group R exhibited mild lung injury and minimal increases in PAI-1 expression, observed only after 6 h of ventilation. In group L, PAI-1, IL-8, and PAI-1 mRNA expression increased significantly with extended ventilation durations (P < 0.05).</p><p><strong>Conclusion: </strong>Mechanical ventilation strategies utilizing high tidal volumes were associated with substantial increases in PAI-1 expression in rat lung tissue and BALF, with these effects exacerbated by prolonged ventilation durations. These findings suggest that high tidal volume ventilation strategies may contribute to pulmonary injury by upregulating PAI-1 expression.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"129"},"PeriodicalIF":2.5000,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261637/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hereditas","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s41065-025-00446-z","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Objective: This study aimed to investigate the impact of different mechanical ventilation strategies on pulmonary plasminogen activator inhibitor-1 (PAI-1) expression in a rat model.

Methods: Seventy-two specific pathogen-free (SPF) adult male Sprague-Dawley (SD) rats were randomly assigned to four groups (n = 18): Group C (spontaneous breathing), group S (low tidal volume, VT = 6 mL/kg), group R (regular tidal volume, VT = 10 mL/kg), and group L (high tidal volume, VT = 40 mL/kg). Each group was further divided into three subgroups based on mechanical ventilation duration (2, 4, or 6 h). Following tracheotomy intubation, group C maintained spontaneous breathing, while the other groups underwent mechanical ventilation with a small animal ventilator. Lung wet-to-dry weight ratios, cell apoptosis rate, and lung injury score were recorded. PAI-1 and IL-8 levels were measured in bronchoalveolar lavage fluid (BALF), and PAI-1 mRNA expression in lung tissue was analyzed using real-time polymerase chain reaction (PCR).

Results: Progressive lung tissue injury was observed in Group L with increasing ventilation durations, accompanied by significant increases in PAI-1, IL-8, and PAI-1 mRNA expression, compared to group C (P < 0.05). No significant differences were identified between Group S and group C, while group R exhibited mild lung injury and minimal increases in PAI-1 expression, observed only after 6 h of ventilation. In group L, PAI-1, IL-8, and PAI-1 mRNA expression increased significantly with extended ventilation durations (P < 0.05).

Conclusion: Mechanical ventilation strategies utilizing high tidal volumes were associated with substantial increases in PAI-1 expression in rat lung tissue and BALF, with these effects exacerbated by prolonged ventilation durations. These findings suggest that high tidal volume ventilation strategies may contribute to pulmonary injury by upregulating PAI-1 expression.

高潮气量机械通气通过上调PAI-1表达加重大鼠肺损伤。
目的:探讨不同机械通气策略对大鼠肺纤溶酶原激活物抑制剂-1 (PAI-1)表达的影响。方法:选取72只SPF成年雄性SD大鼠,随机分为4组(n = 18): C组(自主呼吸)、S组(低潮气量,VT = 6 mL/kg)、R组(正常潮气量,VT = 10 mL/kg)、L组(高潮气量,VT = 40 mL/kg)。各组根据机械通气时间(2、4、6 h)进一步分为3个亚组。气管切开插管后,C组维持自主呼吸,其余组使用小动物呼吸机进行机械通气。记录肺干湿比、细胞凋亡率和肺损伤评分。检测支气管肺泡灌洗液(BALF)中PAI-1和IL-8的水平,实时聚合酶链反应(PCR)检测肺组织中PAI-1 mRNA的表达。结果:与C组相比,L组肺组织进行性损伤,通气时间延长,PAI-1、IL-8和PAI-1 mRNA表达显著升高(P)。结论:采用高潮气量的机械通气策略与大鼠肺组织和BALF中PAI-1表达显著升高相关,且通气时间延长加剧了这种影响。这些结果表明,高潮气量通气策略可能通过上调PAI-1表达而导致肺损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Hereditas
Hereditas Biochemistry, Genetics and Molecular Biology-Genetics
CiteScore
3.80
自引率
3.70%
发文量
0
期刊介绍: For almost a century, Hereditas has published original cutting-edge research and reviews. As the Official journal of the Mendelian Society of Lund, the journal welcomes research from across all areas of genetics and genomics. Topics of interest include human and medical genetics, animal and plant genetics, microbial genetics, agriculture and bioinformatics.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信