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非侵入性正压通气对心肌梗死所致心力衰竭大鼠模型的作用及机制。

Effects and Mechanism of Noninvasive Positive-Pressure Ventilation in a Rat Model of Heart Failure Due to Myocardial Infarction.

机构信息

Tianjin Cardiovascular Diseases Institute, Tianjin Chest Hospital, Tianjin, China (mainland).

Department of Cardiology, Tianjin Chest Hospital, Tianjin, China (mainland).

出版信息

Med Sci Monit. 2021 Feb 20;27:e928476. doi: 10.12659/MSM.928476.

DOI:10.12659/MSM.928476
PMID:33609350
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7903847/
Abstract

BACKGROUND Impaired heart function induced by myocardial infarction is a leading cause of chronic heart failure (HF). This study aimed to investigate the effects and mechanism of noninvasive positive-pressure ventilation (NIPPV) in a rat model of HF due to myocardial infarction. MATERIAL AND METHODS To explore the therapeutic effect and mechanism of NIPPV on acute myocardial infarction-induced HF, we established a rat model of HF by ligating the anterior descending branch of the left coronary artery and confirmed by ultrasonic cardiography and brain natriuretic peptide 45 detection. RESULTS The levels of heat-shock protein (HSP)-70 increased and matrix metalloproteinase (MMP)-2, MMP-9, and tumor necrosis factor (TNF)-alpha decreased in the group that received NIPPV treatment compared with the control group. In addition, the histopathologic results showed less severe inflammatory infiltration and a smaller area of myocardial fibrosis in the NIPPV treatment group. CONCLUSIONS In a rat model of HF due to myocardial infarction, NIPPV resulted in increased levels of HSP70 and reduced expression of MMP2, MMP9, and TNF-alpha and reduced myocardial neutrophil infiltration and fibrosis. Taken together, we showed that NIPPV is an effective treatment for HF induced by myocardial infarction by inhibiting the release of inflammatory factors and preventing microvascular embolism.

摘要

背景

心肌梗死后心脏功能受损是慢性心力衰竭(HF)的主要原因。本研究旨在探讨无创正压通气(NIPPV)在心肌梗死后 HF 大鼠模型中的作用及其机制。

材料与方法

为了探讨 NIPPV 对急性心肌梗死诱导的 HF 的治疗作用及其机制,我们通过结扎左冠状动脉前降支建立了 HF 大鼠模型,并通过超声心动图和脑钠肽 45 检测进行了确认。

结果

与对照组相比,接受 NIPPV 治疗的组中热休克蛋白(HSP)-70 水平升高,基质金属蛋白酶(MMP)-2、MMP-9 和肿瘤坏死因子(TNF)-α水平降低。此外,组织病理学结果显示,NIPPV 治疗组的炎症浸润程度较轻,心肌纤维化面积较小。

结论

在心肌梗死后 HF 大鼠模型中,NIPPV 通过抑制炎症因子的释放和防止微血管栓塞,导致 HSP70 水平升高,MMP2、MMP9 和 TNF-α表达降低,心肌中性粒细胞浸润和纤维化减少。综上所述,我们表明 NIPPV 通过抑制炎症因子的释放和防止微血管栓塞,是一种有效的治疗心肌梗死后心力衰竭的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec2e/7903847/9e6b5e293b9e/medscimonit-27-e928476-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec2e/7903847/4ccf3e55e0da/medscimonit-27-e928476-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec2e/7903847/4ccf3e55e0da/medscimonit-27-e928476-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ec2e/7903847/220467f13f12/medscimonit-27-e928476-g002.jpg
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Exogenous ubiquitin reduces inflammatory response and preserves myocardial function 3 days post-ischemia-reperfusion injury.
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