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羟基自由基诱导的犬和兔心房与心室心肌损伤的效应。

Effects of hydroxyl radical induced-injury in atrial versus ventricular myocardium of dog and rabbit.

机构信息

Department of Physiology and Cell Biology, College of Medicine, The Ohio State University Columbus, OH, USA.

出版信息

Front Physiol. 2010 Sep 30;1:25. doi: 10.3389/fphys.2010.00025. eCollection 2010.

DOI:10.3389/fphys.2010.00025
PMID:21423367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3059949/
Abstract

UNLABELLED

Despite the widespread use of ventricular tissue in the investigation involving hydroxyl radical Aim: (OH*) injury, one of the most potent mediators in ischemia-reperfusion injury, little is known about the impact on atrial myocardium. In this study we thus compared the OH*-induced injury response between atrial and right ventricular muscles from both rabbits and dogs under identical experimental conditions.

METHODS

Small, contracting ventricular and atrial rabbit and dog trabeculae were directly exposed to OH*, and contractile properties were examined and quantified.

RESULTS

A brief OH* exposure led to transient rigor like contracture with marked elevation of diastolic tension and depression of developed force. Although the injury response showed similarities between atrial and ventricular myocardium, there were significant differences as well. In rabbit atrial muscles, the development of the contracture and its peak was much faster as compared to ventricular muscles. Also, at the peak of contracture, both rabbit and dog atrial muscles show a lesser degree of contractile dysfunction.

CONCLUSION

These results indicate that both atrial and ventricular muscles develop a rigor-like contracture after acute OH*-induced injury, and atrial muscles showed a lesser degree of contractile dysfunction. Comparison of dog versus rabbit tissue shows that the response was similar in magnitude, but slower to develop in dog tissue.

摘要

目的

尽管羟基自由基(OH*)损伤是缺血再灌注损伤中最有效的介质之一,但在涉及到 OH损伤的研究中,人们对心房心肌的影响知之甚少。因此,在相同的实验条件下,本研究比较了兔和犬的心房和右心室肌肉的 OH诱导损伤反应。

方法

直接将收缩的兔和犬心室和心房小梁暴露于 OH*中,并检查和量化收缩性能。

结果

短暂的 OH*暴露导致短暂的僵硬性收缩,伴有明显的舒张张力升高和收缩力下降。尽管心房和心室心肌的损伤反应具有相似性,但也存在显著差异。与心室肌肉相比,兔心房肌肉的收缩和收缩峰值更快。此外,在收缩峰值时,兔和犬的心房肌肉显示出较小程度的收缩功能障碍。

结论

这些结果表明,急性 OH*诱导损伤后,心房和心室肌肉均会发生僵硬性收缩,并且心房肌肉显示出较小程度的收缩功能障碍。犬与兔组织的比较表明,反应的幅度相似,但在犬组织中发展较慢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/e8740718615d/fphys-01-00025-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/403d09c15838/fphys-01-00025-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/8325b553655d/fphys-01-00025-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/4a77451e2a6c/fphys-01-00025-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/48dcba7b7729/fphys-01-00025-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/e8740718615d/fphys-01-00025-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/403d09c15838/fphys-01-00025-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/8325b553655d/fphys-01-00025-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/4a77451e2a6c/fphys-01-00025-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/48dcba7b7729/fphys-01-00025-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/124b/3059949/e8740718615d/fphys-01-00025-g005.jpg

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