Expression value of endothelial glycocalyx shedding in patients with acute carbon monoxide poisoning with delayed encephalopathy
-
摘要: 目的 探讨内皮糖萼(endothelial glycocalyx,EG)脱落物在急性一氧化碳中毒迟发性脑病(delayed encephalopathy after acute carbon monoxide poisoning,DEACMP)患者的表达价值。方法 选取2020年8月—2022年11月河北医科大学哈励逊国际和平医院收治的急性重度一氧化碳中毒(acute severe carbon monoxide poisoning,ASCOP)患者132例,根据60 d后有无发生DEACMP分为预后良好组97例和预后不良组35例。分别在入院后3 d、14 d,检测内皮素-1(edothelin-1,ET-1)、一氧化氮(nitric oxide,NO)、血栓调节蛋白(thrombomodulin, TM)和多配体聚糖-1(Syndecan-l)、透明质酸(hyaluronic acid, HA)、硫酸类肝素(heparan sulfate,HS)。急性生理功能和慢性健康状况评分系统Ⅱ(acute physiology and chronic health evaluationⅡ,APACHEⅡ)评价患者病情。结果 两组患者性别、年龄、体质量、中毒至就诊时间比较,差异无统计学意义(P>0.05),昏迷时间和入院后3 d APACHE Ⅱ评分比较,预后不良组高于预后良好组,差异有统计学意义(P < 0.05)。入院后3 d、14 d,预后不良组TM、ET-1、Syndecan-l、HA、HS高于预后良好组,NO低于预后良好组,差异有统计学意义(P < 0.05)。预后良好组,入院后14 d,TM、ET-1、Syndecan-l、HA、HS低于入院后3 d,NO高于入院后3 d,差异有统计学意义(P < 0.05);预后不良组,入院后14 d,TM、ET-1、Syndecan-l、HA、HS高于入院后3 d,NO低于入院后3 d,差异有统计学意义(P < 0.01)。相关性分析:ASCOP患者EG脱落物Syndecan-l、HA、HS与APACHEⅡ评分之间呈正相关(r=0.850,P=0.001;r=0.704,P=0.007;r=0.645,P=0.017)。采用受试者工作特征曲线结果显示,EG脱落物对ASCOP患者发生DEACMP有一定预测价值,曲线下面积为0.832。结论 血管EG脱落物增加,对预测发生DEACMP的有一定的表达价值。
-
关键词:
- 急性一氧化碳中毒迟发性脑病 /
- 内皮糖萼 /
- 急性重度一氧化碳中毒
Abstract: Objective To explore the expression value of endothelial glycocalyx(EG) shedding in patients with acute carbon monoxide poisoning with delayed encephalopathy(DEACMP).Methods One hundred and thirty-two patients with acute severe carbon monoxide poisoning(ASCOP) admitted to our hospital from August 2020 to November 2022 were divided into poor prognosis group (35 cases) and good prognosis group (97 cases) according to the presence of DEACMP or not 60d after onset. Endothelin-1 (ET-1), nitric oxide (NO), thrombomodulin (TM) and multiligand glycan-1 (Syndecan-l), hyaluronic acid (HA), heparan sulfate (HS) were detected at 3 and 14 days after admission, respectively. Acute physiological function and chronic health status scoring systemⅡ (APACHEⅡ) was used to evaluate the patient's condition.Results The gender, age, body quality, and time from poisoning to visit between the two groups had no statistical differences (P>0.05). Coma duration and 3d APACHEⅡ score after admission in the poor prognosis group were higher than those in the good prognosis group and the differences were statistically significant (P < 0.05). At 3d and 14d after admission in the poor prognosis group, TM, ET-1, Syndecan-l, HA, and HS were higher than those in the good prognosis group, and NO was lower than that in the good prognosis group, with statistically significant differences (P < 0.05). In good prognosis group, at 14d after admission, TM, ET-1, Syndecan-l, HA, HS were lower than those at 3d after admission, NO was higher than that at 3d after admission, with statistically significant differences (P < 0.05). In poor prognosis group, at 14d after admission, TM, ET-1, Syndecan-l, HA, and HS were higher than those at 3d after admission, NO was lower than that at 3d after admission (P < 0.01). In correlation analysis, Syndecan-l, HA, HS and APACHEⅡ score had positive correlation in ASCOP patients(r=0.850, P=0.001; r=0.704, P=0.007; r=0.645, P=0.017). The results of the receiver operating characteristic curve(ROC) showed that the endothelial glycocalyx shedding had some predictive value for DEACMP in patients with ASCOP, and the area under the curve was 0.832.Conclusion Increased endothelial glycocalyx shedding had some expression value in predicting DEACMP. -
表 1 预后良好组和预后不良组临床资料的比较
X±S 项目 预后良好组(97例) 预后不良组(35例) 检验值 P 女性/例(%) 49(50.51) 13(37.14) 1.847 0.123 年龄/岁 66.67±6.32 70.25±6.85 0.976 0.350 体重/kg 70.44±5.15 67.25±6.27 1.267 0.231 中毒至就诊时间/h 13.76±4.48 15.21±5.83 1.330 0.211 昏迷时间/h 17.42±3.56 26.36±4.52 5.696 0.001 APACHE Ⅱ评分(入院后3 d)/分 16.89±4.33 23.51±6.27 6.268 0.001 表 2 预后良好组和预后不良组内皮功能的比较
X±S 项目 预后良好组(97例) 预后不良组(35例) t P TM/(μg/L) 入院后3 d 14.82±3.50 17.15±4.75 6.713 0.001 入院后14 d 9.52±2.471) 22.34±5.291) 15.428 0.001 ET-1/(ng/L) 入院后3 d 36.24±6.30 41.28±8.57 5.410 0.001 入院后14 d 30.73±7.841) 55.39±9.131) 18.681 0.001 NO/(μmol/ L) 入院后3 d 53.77±6.12 45.43±8.381) 5.970 0.001 入院后14 d 61.65±7.341) 40.05±9.621) 16.273 0.001 与入院后3 d比较,1)P < 0.05。 表 3 预后良好组和预后不良组EG脱落物的比较
X±S 项目 预后良好组(97例) 预后不良组(35例) t P Syndecan-l/(μg/L) 入院后3 d 21.53±4.54 28.28±6.16 5.175 0.001 入院后14 d 16.69±5.781) 47.58±11.451) 29.624 0.001 HA/(μg/L) 入院后3 d 19.32±3.02 24.54±4.361) 0.015 0.001 入院后14 d 13.58±12.161) 40.23±11.841) 23.017 0.001 HS/(μg/L) 入院后3 d 25.37±6.42 31.13±8.061) 4.548 0.001 入院后14 d 20.50±7.391) 44.72±9.211) 24.809 0.001 与入院后3 d比较,1)P < 0.05。 -
[1] 李晨, 梁梦琳, 张兴国. 急性一氧化碳中毒迟发性脑病发病机制研究进展[J]. 中华劳动卫生职业病杂志, 2022, 40(7): 543-546. https://www.cnki.com.cn/Article/CJFDTOTAL-SZZZ202301031.htm
[2] Zhang JJ, Bi WK, Cheng YM, et al. Early predictors of brain injury in patients with acute carbon monoxidepoisoning and the neuroprotection of mild hypothermia[J]. Am J Emerg Med, 2022, 61: 18-28. doi: 10.1016/j.ajem.2022.08.016
[3] Mu C, Chen J, Guo T, et al. Potential markers for predicting delayed encephalopathy in patients with acute carbon monoxide poisoning[J]. J Clin Neurosci, 2022, 95: 129-133. doi: 10.1016/j.jocn.2021.11.022
[4] Ando T, Uzawa K, Yoshikawa T, et al. The effect of tetrastarch on the endothelial glycocalyx layer in early hemorrhagic shock using fluorescence intravital microscopy: a mouse model[J]. J Anesth, 2023, 37(1): 104-118. doi: 10.1007/s00540-022-03138-4
[5] Hofmann N, Zipperle J, Brettner F, et al. Effect of Coagulation Factor Concentrates on Markers of Endothelial CellDamage in Experimental Hemorrhagic Shock[J]. Shock, 2019, 52(5): 497-505. doi: 10.1097/SHK.0000000000001286
[6] 李晨, 王敏, 梁梦琳, 等. 表观扩散系数联合C-反应蛋白对一氧化碳中毒迟发性脑病的相关性分析[J]. 中华急诊医学杂志, 2023, 32(3): 327-331.
[7] 冯顺易, 李勇. 中重度急性一氧化碳中毒迟发性脑病的危险因素分析[J]. 临床急诊杂志, 2021, 22(12): 824-827. https://lcjz.whuhzzs.com/article/doi/10.13201/j.issn.1009-5918.2021.12.008
[8] Nañagas KA, Penfound SJ, Kao LW. Carbon Monoxide Toxicity[J]. Emerg Med Clin North Am, 2022, 40(2): 283-312. doi: 10.1016/j.emc.2022.01.005
[9] Weaver LK. Carbon monoxide poisoning[J]. Undersea Hyperb Med, 2020, 47(1): 151-169.
[10] Nguyen AB, Iqbal O, Block RC, et al. Prevention and treatment of atherothrombosis: Potential impact of nanotechnology[J]. Vascul Pharmacol, 2022, 148(11): 107127.
[11] Coceani F, Kelsey L. Endothelin-1 release from the lamb ductus arteriosus: are carbon monoxide and nitric oxide regulatory agents?[J]. Life Sci, 2000, 66(26): 2613-2623. doi: 10.1016/S0024-3205(00)00595-6
[12] Bhattacharjee D, Mondal S, Saha A, et al. Effect of vasodilator and immunosuppressive therapy on the endothelialdysfunction in patients with systemic sclerosis[J]. Clin Experim Med, 2023, 23(3): 905-915.
[13] 唐名扬, 冯健, 欧登科, 等. 蓝光对小鼠血压及血管内皮功能影响的研究[J]. 中国循环杂志, 2021, 36(7): 712-717. https://www.cnki.com.cn/Article/CJFDTOTAL-ZGXH202107014.htm
[14] Abdul Y, Karakaya E, Chandran R. et al. Endothelin A receptors contribute to senescence of brain microvascularendothelial cells[J]. Canadian J Physiol Pharmacol, 2022, 100(12): 1087-1096. doi: 10.1139/cjpp-2022-0071
[15] Huang X, Hu H, Sun T, et al. Plasma Endothelial Glycocalyx Components as a Potential Biomarker for Predicting the Development of Disseminated Intravascular Coagulation in Patients With Sepsis[J]. J Intensive Care Med, 2021, 36(11): 1286-1295. doi: 10.1177/0885066620949131
[16] Foote CA, Soares RN, Ramirez-Perez FI, et al. Endothelial Glycocalyx[J]. Compr Physiol, 2022, 12(4): 3781-3811.
[17] Baby S, Reljic T, Villalba N, et al. Endothelial glycocalyx-associated molecules as potential serological markers for sepsis-associated encephalopathy: A systematic review and meta-analysis[J]. PLoS One, 2023, 18(2): e0281941.
[18] Hobbs KJ, Johnson PJ, Wiedmeyer CE, et al. Plasma syndecan-1 concentration as a biomarker for endothelial glycocalyx degradation in septic adult horses[J]. Equine Vet J, 2023, 55(3): 456-462.
[19] Zheng X, Machin DR. Patching up a degraded endothelial glycocalyx in sepsis[J]. Am J Physiol Heart Circ Physiol, 2023, 325(4): H673-H674.
[20] Lipowsky HH, Gao L, Lescanic A. Shedding of the endothelial glycocalyx in arterioles, capillaries, and venules and its effect on capillary hemodynamics during inflammation[J]. Am J Physiol Heart Circ Physiol, 2011, 301(6): H2235-H2245.
[21] Anand T, Reyes AA, Sjoquist MC, et al. Resuscitating the Endothelial Glycocalyx in Trauma and Hemorrhagic Shock[J]. Ann Surg Open, 2023, 4(3): e298.
[22] Delgadillo LF, Lomakina EB, Kuebel J, et al. Changes in endothelial glycocalyx layer protective ability after inflammatorystimulus[J]. Am J Physiol Cell Physiol, 2021, 320(2): C216-C224.
[23] Patterson EK, Cepinskas G, Fraser DD. Endothelial Glycocalyx Degradation in Critical Illness and Injury[J]. Front Med(Lausanne), 2022, 9: 898592..
[24] 林源希, 李真玉. 糖萼在脓毒症血管内皮损伤中的变化及其修复策略研究进展[J]. 解放军医学杂志, 2022, 47(10): 1049-1056. https://www.cnki.com.cn/Article/CJFDTOTAL-JFJY202210010.htm
[25] 马海波, 杨迎春, 刘晶晶, 等. 右美托咪定对脑缺血再灌注损伤小鼠糖萼的影响[J]. 中国医药导报, 2020, 17(13): 8-12, 26. https://www.cnki.com.cn/Article/CJFDTOTAL-YYCY202013004.htm
[26] Lee JS, Kim TY, Bae KS, et al. Usefulness of a modified poisoning severity score for predicting prognosis in acute carbon monoxide poisoning[J]. Am J Emerg Med, 2022, 51: 156-162.