一氧化碳中毒机制和临床治疗进展
Research Advances in the Mechanism and Clinical Management of Carbon Monoxide Poisoning

一氧化碳(CO)中毒通过与血红蛋白结合形成碳氧血红蛋白(CO-Hb)抑制氧气运输，导致组织缺氧，进而引发心脏、脑等器官的功能损伤。当前治疗方法包括常压氧和高压氧(HBO)，尽管能够缩短CO半衰期，但治疗效果有限，且面临治疗时效性差、设备可得性等问题。近年来，血红蛋白一氧化碳清除剂作为新型治疗策略获得关注。这些清除剂通过优化血红蛋白与CO的结合特性，能够加速CO的清除，改善中毒症状。在小鼠模型中，工程化血红蛋白(如Ngb-H64Q-CCC)能够有效提高生存率并改善生理功能，显示出较好的治疗潜力。然而，血红蛋白清除剂的临床应用仍面临大规模生产、安全性等挑战，需进一步研究和优化。
Carbon monoxide (CO) poisoning inhibits oxygen transport by binding to hemoglobin to form carboxyhemoglobin (CO-Hb), leading to tissue hypoxia, which in turn causes functional damage to the heart, brain, and other organs. Current treatments include normobaric oxygen and hyperbaric oxygen (HBO), which have limited therapeutic effects despite their ability to shorten the half-life of CO and face problems such as poor timeliness of treatment and availability of equipment. In recent years, hemoglobin CO scavengers have gained attention as a novel therapeutic strategy. These scavengers are able to accelerate CO clearance and improve poisoning symptoms by optimizing the binding properties of hemoglobin to CO. In mouse models, engineered hemoglobins (e.g., Ngb-H64Q-CCC) are effective in increasing survival and improving physiological functions, showing good therapeutic potential. However, the clinical application of hemoglobin scavengers still faces challenges such as large-scale production and safety, and requires further research and optimization.