|摘要||背景:大多数急性颈髓损伤患者可继发严重的水钠代谢紊乱,但其发生机制还不清楚.目的:研究急性完全性颈髓损伤患者继发的水钠代谢紊乱及尿中前列腺素PGE 2排出量的相应变化,探讨颈髓损伤患者继发水钠代谢紊乱的发生机制.设计:以诊断为依据的病例对照研究.地点、对象和方法:实验在北京大学第三医院骨科完成,研究对象为完全性颈髓损伤(CSCI)组患者28例,其中男19例,女9例;年龄(37.14±9.39)岁;对照组为同期骨科住院的非脊髓损伤和急性创伤患者18例,男13例,女5例,年龄(38.11±11.89)岁.检测两组水钠代谢和尿前列腺素PGE2的变化.主要观察指标:两组血压心率、血电解质、尿量、液体入量以及尿电解质排出量的变化,尿前列腺素PGE 2的变化.结果:CSCI组血Na+浓度[(132.70±3.20)mmol/L]低于对照组(t=2.01,P＜0.01),低钠血症发生率为92.9%;CSCI组尿量(3610±761)mL/d,Na+排出量(473.7±169.4)mmol/d均高于对照组(分别为t=2.01,P＜0.01;t=2.08,P＜0.05);血压、心率均低于对照组(t=2.01,2.01,P＜0.01);24 h尿PGE 2排出量高于对照组(t=2.04,P＜0.01).结论:颈髓损伤后交感神经系统抑制,血压降低,肾血流量减少,肾皮质缺血缺氧,继而刺激肾脏前列腺素合成增多,产生利钠利尿作用,可能是颈髓损伤继发低钠血症的发生机制之一.
BACKGROUND: Although secondary severe water-electrolyte imbalance was a common complication after acute cervical spinal cord injury(GSCI), its mechanism remains unknown.OBJECTIVE: To investigate the water-sodium imbalance and the corresponding changes of urinary prostaglandin E2(PGE2) in patients with acute complete GSCI and analyze its possible mechanism.DESIGN: A diagnosis-based case-control trial was conducted.SETTING, PARTICIPANTS and METHODS: The trial was completed in the Department of Orthopaedics, Peking University Third Hospital. Twenty-eight acute complete GSGI patients, including 19 males and 9 females, were included as the trial group(CSCI group) . Eighteen cases, including 13 males and 5 females, were included in the control group. Their average ages were (37. 14 +9.39) years and (38. 11 + 11.89) years, respectively. The changes of water-sodium metabolism and the PGE2 were detected.MAIN OUTCOME MEASURES: The changes of blood pressure, heart rate, blood electrolytes concentrations, volume of urine and fluid intake, and electrolytes excretion in urine were measured. The changes of PGE2 in urine were also detected.RESULTS: Hyponatremia occurred in 26 cases(92.9% ) in CSCI group. The average concentration of serum sodium in CSCI group [(132.70 ±3.20) mmol/L] was significantly lower than that in control group(t=2.01, P ＜0.01) .The urine volume[ (3 610±761) mL/day]and sodium excretion in 24 hours urine[ (473.7± 169.4) mmol/day] were significantly larger than those in control group( t = 2.01, P ＜ 0.01 and t =2.08, P ＜ 0. 05, respectively). Meanwhile, the blood pressure and heart rate in CSCI group were both significantly lower than those in control group (comparison of systolic pressure: t = 2.01, P ＜ 0.01; comparison of diasfolic pressure: t = 2.01, P ＜ 0. 01; comparison of heart rate: t = 2.01, P ＜0.01 ), and the total amount of PGE2 in 24 hours urine in CSCI group was significantly higher than that in control group( t = 2.04, P ＜ 0.01 ).CONCLUSION: Acute CSCI may result in inhibition of sympathetic system,low blood pressure, decreased renal blood flow and renal cortical ischemia and anoxia, and further in increased synthesis of prostaglandin, which has the effects of polyuria and natriuresis. It is suggested that these might be one of the mechanisms of secondary hyponatremia after CSCI.|