Agarwal Shivam, Srivastava Vinod K, Arshad Zia, Sharma Pallavi, Prakash Ravi
Anesthesiology and Critical Care, King George's Medical University, Lucknow, IND.
Cureus. 2024 Jul 8;16(7):e64102. doi: 10.7759/cureus.64102. eCollection 2024 Jul.
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.
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.
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.
VEGF levels on day seven were significantly lower in the study group compared to the control group (p<0.05). The PaO/FiO 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.
Dopamine reduces VEGF and lung injury mediated by increased endothelial permeability.
脓毒症是一种宿主免疫反应失调，源于对微生物入侵（包括细菌、病毒和其他病原体）的全身炎症反应。血管内皮生长因子（VEGF）最初因其对内皮通透性的强力诱导作用而被发现。研究提出多巴胺在减轻VEGF诱导的通透性方面具有治疗作用，这为其在急性呼吸窘迫综合征（ARDS）管理中的潜力提供了线索。
确定多巴胺作为VEGF抑制剂的作用，并预防脓毒症进展为急性肺损伤（ALI）和ARDS。
总共154名诊断为脓毒症的重症监护病房患者被随机分为两组：第一组（对照组）和第二组（研究组）。两组均按照重症监护病房方案接受标准治疗。此外，研究组（第二组）接受2微克/千克/分钟的多巴胺输注。进行了基线常规检查、降钙素原检测和胸部X光检查。第一天和第七天的血样被储存起来用于分析VEGF水平。从第一天到第七天计算默里评分和序贯器官衰竭评估（SOFA）评分（器官功能障碍）。
与对照组相比，研究组第七天的VEGF水平显著降低（p<0.05）。研究组第七天的PaO/FiO比值比对照组显著升高，表明研究组的氧合状态有所改善。研究组的平均重症监护病房住院时间为9.3天，而对照组为11.6天（p<0.05）。从第五天起，研究组的SOFA评分有显著改善，表明多巴胺对脓毒症器官功能障碍有治疗作用。
多巴胺可降低由内皮通透性增加介导的VEGF和肺损伤。
