β受体阻滞剂对脓毒性休克患者肺和肠道保护作用的研究OA
Study of the protective effects of β receptor blockers on the lungs and intestines in patients with septic shock
目的 观察 β 受体阻滞剂(艾司洛尔)对脓毒性休克患者肺氧合及肠道屏障功能的影响.方法 选择 2023 年 1 月至 2025 年 3 月南通大学附属南京江北医院重症监护病房(ICU)收治的 63 例脓毒性休克患者作为研究对象,4 例未完成试验,其中 2 例不能耐受最小剂量艾司洛尔,2 例研究期间放弃治疗,最终共纳入59例患者.按随机数字表法将患者分为对照组(29例)和艾司洛尔组(30例).两组患者均给予规范治疗,包括控制感染、液体复苏、抗休克、机械通气及镇痛镇静等,艾司洛尔组静脉泵入艾司洛尔,起始剂量 25 mg/h,20 min 调整 1 次剂量,以 50 mg/h 递增,直至达到目标心率 80～94 次/min,维持 72 h.比较两组患者入组前、入组后 48 h 和入组后 72 h 平均动脉压(MAP)、心率,以及入组前和入组后 72 h 肠道屏障功能指标二胺氧化酶(DAO)和 D-乳酸水平,并计算氧合指数(PaO2/FiO2),同时观察 28 d 病死率.结果 入组前两组 PaO2/FiO2、DAO、D-乳酸、心率、MAP 及入组后 48 h 和入组后 72 h MAP 比较差异均无统计学意义(均 P＞0.05).艾司洛尔组入组后 48 h PaO2/FiO2 明显高于对照组[mmHg(1 mmHg≈0.133 kPa):302.6±62.6 比 272.8±45.5,P＜0.05],入组后 72 h PaO2/FiO2 虽高于对照组,但两组比较差异无统计学意义(P＞0.05).艾司洛尔组入组后 72 h DAO、D-乳酸和入组后 48 h和 72 h心率均明显低于对照组[入组后 72 h DAO(U/L):8.9(6.9,11.5)比 11.6(9.1,15.1),入组后 72 h D-乳酸(mg/L):10.2(8.2,12.1)比 12.9(9.4,15.8),入组后 48 h心率(次/min):86.2±4.4 比96.6±10.7,入组后 72 h 心率(次/min):82.9±6.9 比 92.8±11.7,均 P＜0.05].艾司洛尔组 28 d 病死率较对照组低,但差异无统计学意义(P＞0.05).结论 艾司洛尔可以改善脓毒性休克患者肺氧合,但优势随时间推移而减弱,艾司洛尔对肠道屏障功能有保护作用,但并不能降低 28 d病死率.
Objective To observe the effect of β receptor blockers(Esmolol)on pulmonary oxygenation and intestinal barrier function in patients with septic shock.Methods A total of 63 patients with septic shock admitted to the department of intensive care unit(ICU)of Nanjing Jiangbei Hospital Affiliated to Nantong University from January 2023 to March 2025 were enrolled.Four patients failed to complete the trial,including 2 intolerant to the minimum dose of Esmolol and 2 who withdrew treatment during the study.Finally,a total of 59 patients were included.Patients were divided into a control group(29 cases)and an Esmolol group(30 cases)using the random number table method.All patients received standardized treatment,including infection control,fluid resuscitation,anti-shock therapy,mechanical ventilation,analgesia and sedation.Patients in the Esmolol group received continuous intravenous infusion of Esmolol at an initial dose of 25 mg/h.The dose was titrated by 50 mg/h every 20 minutes to achieve the target heart rate of 80-94 beats/min and maintained for 72 hours.Mean arterial pressure(MAP),heart rate and oxygenation index(PaO2/FiO2)at baseline,48 hours and 72 hours after enrollment.Intestinal barrier markers including diamine oxidase(DAO)and D-lactate at baseline and 72 hours after enrollment,and 28-day mortality were compared between the two groups.Results There were no significant intergroup differences in baseline PaO2/FiO2,DAO,D-lactate,heart rate,MAP,and MAP at 48 hours and 72 hours(all P>0.05).The PaO2/FiO2 at 48 hours was significantly higher in the Esmolol group than that in the control group[mmHg(1 mmHg≈0.133 kPa):302.6±62.6 vs.272.8±45.5,P<0.05].Although PaO2/FiO2 at 72 hours remained higher in the Esmolol group,the difference was not statistically significant(P>0.05).The 72 hours levels of DAO and D-lactate,as well as heart rate at 48 hours and 72 hours in the Esmolol group were all significantly lower than those in the control group[72 hours DAO(U/L):8.9(6.9,11.5)vs.11.6(9.1,15.1);72 hours D-lactate(mg/L):10.2(8.2,12.1)vs.12.9(9.4,15.8);48 hours heart rate(bpm):86.2±4.4 vs.96.6±10.7;72 hours heart rate(bpm):82.9±6.9 vs.92.8±11.7,all P<0.05].The 28-day mortality rate in the Esmolol group was lower than in the control group,but the difference was not statistically significant(P>0.05).Conclusions Esmolol improves early pulmonary oxygenation in patients with septic shock,whereas this beneficial effect diminishes over time.Esmolol protects intestinal barrier function but does not reduce the 28-day mortality.
刘尚香;叶正龙;邹晖;梅程清;胡志青;徐维慧;吴勇
南通大学附属南京江北医院重症监护病房,江苏 南京 210048南通大学附属南京江北医院重症监护病房,江苏 南京 210048南通大学附属南京江北医院重症监护病房,江苏 南京 210048南通大学附属南京江北医院重症监护病房,江苏 南京 210048南通大学附属南京江北医院重症监护病房,江苏 南京 210048南通大学附属南京江北医院重症监护病房,江苏 南京 210048南通大学附属南京江北医院重症监护病房,江苏 南京 210048
脓毒性休克艾司洛尔氧合指数肠道屏障功能
Septic shockEsmololOxygenation indexIntestinal barrier function
《中国中西医结合急救杂志》 2026 (4)
415-418,4
安徽省危重症呼吸疾病临床医学研究中心校级开放课题(LC202210) Anhui Provincial Clinical Medical Research Center for Critical Respiratory Diseases Open Project of the University(LC202210)
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