目的 探讨并比较临床静脉输液操作中 3 种排气方法的一次性排气成功率.方法 选取 2022 年 1 月至 2022 年 3 月于萍乡市人民医院住院进行静脉输液的患者 300 例,按编号随机分成对照 1 组(n=100)、对照 2 组(n=100)和试验组(n=100).对照 1 组采用传统排气方法,对照 2 组采用 2"U"型排气法,试验组采用一次性静脉输液标准手法排气.对比 3 组的一次排气成功率、排出液体量、成功排气时间及医务人员满意度.结果 试验组排气成功率和排出药液量均显著高于其他 2 组,且对照 2 组高于对照 1 组(P＜0.05);试验组成功排气时间短于其他两组(P＜0.05),且对照 2 组时间短于对照 1 组(P＜0.05);试验组医务人员的排气满意度显著高于其他两组(P＜0.05),且对照 2 组高于对照 1 组(P＜0.05).结论 一次性静脉输液排气成功标准手法优于传统排气方法、2"U"型排气法,能够提高一次性排气成功率,缩短排气时间,减少药液浪费,从而提升工作效率,值得临床推广、应用.

The immune imbalance caused by excessive inflammatory reactions is the primary cause of sepsis. Macrophages with M1 and M2 polarization states are important immune cells that regulate the balance of the inflammatory response in sepsis. Encouraging the conversion of macrophages from the M1 to the M2 type is an important strategy for relieving sepsis. Here, we demonstrated the upregulation of vascular endothelial growth factor A (VEGFA) in a mouse model of sepsis. Then, siRNA technology was applied to inhibit the expression of VEGFA in macrophages. Flow cytometry and RT‒qPCR results showed that low expression of VEGFA inhibited LPS-induced M1 polarization of macrophages. Decreased VEGFA was also proven to lower TNF-α, IL-1β, and IL-6 secretion by LPS-induced macrophages. In addition, the effects of knocking down VEGFA on the energy metabolism pattern of macrophages were investigated by glycolysis pressure tests and mitochondrial pressure tests, and VEGFA knockdown reversed the induction of glycolysis in macrophages by LPS. The mitochondrial content and ATP content results also confirmed this finding. After the tail vein of septic mice was injected with macrophages transfected with si-VEGFA, the liver and kidney damage and the pathological conditions of the lung were alleviated. The secretion of TNF-α and IL-6 was decreased, while IL-10 was increased in their serum. Immunohistochemical staining revealed decreased expression of CD86 and increased expression of CD206 in the si-VEGFA group. This study demonstrates that decreased VEGFA inhibits glycolysis and thus inhibits LPS-induced M1 polarization of macrophages, ultimately relieving sepsis.