Djuric Marko, Nenadic Irina, Radisavljevic Nina, Todorovic Dusan, Stojanovic Maja, Dimic Nemanja, Bobos Marina, Bojic Suzana, Stevanovic Predrag, Savic Predrag, Stojakov Dejan, Palibrk Ivan, Djuric Dragan
Clinic for Anesthesiology and Intensive Care, University Clinical Hospital Center "Dr Dragisa Misovic-Dedinje", 11030 Belgrade, Serbia.
Department of Anesthesiology, Reanimatology and Intensive Care, Faculty of Medicine, University of Belgrade, 11000 Belgrade, Serbia.
Biomedicines. 2025 Sep 26;13(10):2357. doi: 10.3390/biomedicines13102357.
Endothelial dysfunction (characterized by reduced vasodilation or vasoconstriction, oxidative stress, inflammation, and pro-thrombotic condition) is a critical factor in the pathophysiology of various cardiovascular conditions, and the application of anesthetics can affect this dysfunction. Patients undergoing major surgery, especially cardiovascular surgery, are at increased risk of endothelial dysfunction. The impact of anesthetics on endothelial function can vary depending on the specific agent, dosage, duration of exposure, comorbidities, etc. Certain anesthetics, especially at higher doses, may increase the production of reactive oxygen species (ROS), leading to oxidative stress and endothelial dysfunction through reduced nitric oxid (NO) availability. Some anesthetics can modulate inflammatory responses, either by suppressing or exacerbating inflammation, or may affect the permeability of the endothelium, potentially leading to pulmonary edema and disruption of the blood-brain barrier. Anesthetics can influence endothelial glycocalyx. Understanding anesthetics effects is crucial for optimizing anesthetic management, particularly in patients with pre-existing cardiovascular issues. Therefore, the aim of this review is to critically evaluate the effects of different classes of anesthetics on endothelial function and oxidative stress. Specifically, we address how anesthetics influence NO bioavailability, endothelial glycocalyx integrity, inflammatory and oxidative pathways, and clinical outcomes in surgical patients. By summarizing current evidence, we aim to highlight mechanistic insights and identify potential perioperative strategies to minimize endothelial dysfunction.
内皮功能障碍（其特征为血管舒张或收缩功能减退、氧化应激、炎症反应和血栓前状态）是多种心血管疾病病理生理学中的关键因素，而麻醉药的应用可影响这种功能障碍。接受大手术尤其是心血管手术的患者发生内皮功能障碍的风险增加。麻醉药对内皮功能的影响可能因具体药物、剂量、暴露时间、合并症等因素而有所不同。某些麻醉药，尤其是高剂量时，可能会增加活性氧（ROS）的产生，通过降低一氧化氮（NO）的可用性导致氧化应激和内皮功能障碍。一些麻醉药可通过抑制或加剧炎症反应来调节炎症反应，或者可能影响内皮的通透性，进而可能导致肺水肿和血脑屏障破坏。麻醉药可影响内皮糖萼。了解麻醉药的作用对于优化麻醉管理至关重要，尤其是对于已有心血管问题的患者。因此，本综述的目的是批判性地评估不同类别麻醉药对内皮功能和氧化应激的影响。具体而言，我们探讨麻醉药如何影响NO的生物利用度、内皮糖萼的完整性、炎症和氧化途径以及手术患者的临床结局。通过总结现有证据，我们旨在突出机制方面的见解，并确定潜在的围手术期策略以尽量减少内皮功能障碍。
