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碘对比剂致肾组织损伤的病理生理学。

Pathophysiology of renal tissue damage by iodinated contrast media.

机构信息

Institute of Vegetative Physiology, Charité Medical University, Berlin, Germany.

出版信息

Clin Exp Pharmacol Physiol. 2011 May;38(5):292-9. doi: 10.1111/j.1440-1681.2011.05503.x.

Abstract
  1. The present review focuses on the cytotoxic effects of iodinated contrast media (CM) that are shared by all types of CM. 2. Although the clinical nephrotoxicity of CM has been progressively improved, all currently available CM still possess a level of cytotoxicity, which is probably caused by iodine. 3. The toxicity caused by specific CM properties, such as osmolarity, viscosity and ionic strength, can be differentiated from the cytotoxicity common to all CM in studies using cell culture, isolated blood vessels and isolated tubules. 4. The cytotoxicity induced by CM leads to apoptosis and cell death of endothelial and tubular cells and may be initiated by cell membrane damage, together with oxidative stress. 5. Cell damage may be aggravated by factors such as tissue hypoperfusion and hypoxia, properties of individual CM, such as ionic strength, high osmolarity and/or viscosity, and clinically unfavourable conditions. 6. Clinically detectable renal failure may result from the summation of all these factors.
摘要
  1. 本综述重点介绍了所有类型的碘造影剂(CM)共有的细胞毒性作用。

  2. 尽管 CM 的临床肾毒性已逐步得到改善,但目前所有可用的 CM 仍具有一定程度的细胞毒性,这可能是由碘引起的。

  3. 通过细胞培养、离体血管和离体小管研究,可以将 CM 的特性(如渗透压、粘度和离子强度)引起的毒性与所有 CM 共有的细胞毒性区分开来。

  4. CM 诱导的细胞毒性导致内皮细胞和肾小管细胞凋亡和死亡,可能由细胞膜损伤以及氧化应激引发。

  5. 细胞损伤可能会加重组织灌注不足和缺氧等因素、CM 的个体特性(如离子强度、高渗透压和/或粘度)以及临床不利条件的影响。

  6. 临床上可检测到的肾衰竭可能是由所有这些因素共同作用的结果。

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