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亚衰竭性过度拉伸损伤导致完整血管组织出现可逆性功能障碍和嘌呤能P2X7受体激活。

Subfailure Overstretch Injury Leads to Reversible Functional Impairment and Purinergic P2X7 Receptor Activation in Intact Vascular Tissue.

作者信息

Luo Weifeng, Guth Christy M, Jolayemi Olukemi, Duvall Craig L, Brophy Colleen Marie, Cheung-Flynn Joyce

机构信息

Department of Surgery, Vanderbilt University , Nashville, TN , USA.

Department of Biomedical Engineering, Vanderbilt University , Nashville, TN , USA.

出版信息

Front Bioeng Biotechnol. 2016 Sep 29;4:75. doi: 10.3389/fbioe.2016.00075. eCollection 2016.

Abstract

Vascular stretch injury is associated with blunt trauma, vascular surgical procedures, and harvest of human saphenous vein for use in vascular bypass grafting. A model of subfailure overstretch in rat abdominal aorta was developed to characterize surgical vascular stretch injury. Longitudinal stretch of rat aorta was characterized . Stretch to the haptic endpoint, where the tissues would no longer lengthen, occurred at twice the resting length. The stress produced at this length was greater than physiologic mechanical forces but well below the level of mechanical disruption. Functional responses were determined in a muscle bath, and this subfailure overstretch injury led to impaired smooth muscle function that was partially reversed by treatment with purinergic receptor (P2X7R) antagonists. These data suggest that vasomotor dysfunction caused by subfailure overstretch injury may be due to the activation of P2X7R. These studies have implications for our understanding of mechanical stretch injury of blood vessels and offer novel therapeutic opportunities.

摘要

血管拉伸损伤与钝性创伤、血管外科手术以及用于血管搭桥移植的人体大隐静脉采集有关。建立了大鼠腹主动脉亚失效过度拉伸模型以表征手术性血管拉伸损伤。对大鼠主动脉的纵向拉伸进行了表征。拉伸至触觉终点,即组织不再延长的位置,发生在静息长度的两倍处。在该长度产生的应力大于生理机械力,但远低于机械破坏水平。在肌肉浴中测定功能反应,这种亚失效过度拉伸损伤导致平滑肌功能受损,而嘌呤能受体(P2X7R)拮抗剂治疗可部分逆转这种损伤。这些数据表明,亚失效过度拉伸损伤引起的血管舒缩功能障碍可能是由于P2X7R的激活。这些研究对我们理解血管的机械拉伸损伤具有启示意义,并提供了新的治疗机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa0b/5040722/5fbdfd329d8a/fbioe-04-00075-g001.jpg

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