关键词: acute respiratory distress syndrome (ards) dopamine intensive care unit (icu) sepsis vascular endothelial growth factor receptor (vegf)

来  源:   DOI:10.7759/cureus.64102   PDF(Pubmed)

Abstract:
BACKGROUND: Sepsis is a dysregulated host immune response stemming from a systemic inflammatory response to microbial invasion, encompassing bacteria, viruses, and other pathogens. The vascular endothelial growth factor (VEGF) was initially identified for its potent induction of endothelial permeability. Studies have proposed a therapeutic role of dopamine in mitigating VEGF-induced permeability, shedding light on its potential in acute respiratory distress syndrome (ARDS) management.
OBJECTIVE: To determine the effect of dopamine as an inhibitor of VEGF and to prevent the progression of sepsis to acute lung injury (ALI) and ARDS.
METHODS: A total of 154 critical care unit patients with a diagnosis of sepsis were randomized into two groups: Group I (control group) and Group II (Study group). Both received standard treatment, as per ICU protocol. In addition, the study group (Group II) received a dopamine infusion of 2 micrograms/kg/min. Baseline routine investigation, procalcitonin, and chest X-ray were done. Day one and day seven blood samples were stored for analysis of VEGF levels. Murray\'s score and sequential organ failure assessment (SOFA) score (organ dysfunction) were calculated from day one to day seven.
RESULTS: VEGF levels on day seven were significantly lower in the study group compared to the control group (p<0.05). The PaO2/FiO2 ratio at day seven was significantly increased in the study group than in the control group, indicating an improvement in oxygenation status in the study group. There was a mean ICU stay of 9.3 days in the study group versus 11.6 days in the control group (p<0.05). The SOFA score showed a significant improvement in the study group from day five onwards, indicating a therapeutic effect of dopamine on organ dysfunction in sepsis.
CONCLUSIONS: Dopamine reduces VEGF and lung injury mediated by increased endothelial permeability.
摘要:
背景:脓毒症是一种失调的宿主免疫反应,源于对微生物入侵的全身性炎症反应,包括细菌,病毒,和其他病原体。血管内皮生长因子(VEGF)最初被鉴定为其对内皮通透性的有效诱导。研究提出了多巴胺在减轻VEGF诱导的通透性中的治疗作用,阐明其在急性呼吸窘迫综合征(ARDS)管理中的潜力。
目的:确定多巴胺作为VEGF抑制剂的作用,并预防脓毒症发展为急性肺损伤(ALI)和ARDS。
方法:将154例诊断为脓毒症的重症监护病房患者随机分为两组:I组(对照组)和II组(研究组)。两人都接受了标准治疗,按照ICU协议。此外,研究组(第二组)接受2微克/千克/分钟的多巴胺输注.基线常规调查,降钙素原,做了胸部X光检查.第1天和第7天储存血样用于VEGF水平分析。从第1天到第7天计算Murray评分和序贯器官衰竭评估(SOFA)评分(器官功能障碍)。
结果:第7天,研究组的VEGF水平明显低于对照组(p<0.05)。研究组第7天PaO2/FiO2比值明显高于对照组,表明研究组的氧合状态有所改善。研究组的平均ICU停留时间为9.3天,对照组为11.6天(p<0.05)。SOFA评分显示研究组从第5天开始有显著改善,表明多巴胺对脓毒症器官功能障碍的治疗作用。
结论:多巴胺减少了血管内皮通透性增加介导的VEGF和肺损伤。
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