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作 者:江卫东
机构地区:[1]河南濮阳市中原油田第四医院外科
出 处:《医学综述》2009年第10期1577-1579,共3页Medical Recapitulate
摘 要:目的探讨急性颅脑损伤患者低钠血症的病理机制及治疗。方法对98例急性颅脑损伤患者(ABI组)血心钠肽(ANP)、脑钠肽(BNP)、内源性类洋地黄物质(EDLS)、抗利尿激素(ADH)及血尿钠浓度、血尿渗透压作同步测定。并与44例同期健康体检者(对照组)对照。结果98例ABI患者中有41例出现低钠血症,且多集中出现在重伤(78.2%)或特重伤病员中(85.0%)。结论中枢性低钠血症与下丘脑一垂体轴功能受损致EDLS、ADH分泌增加相关,血ANP、BNP浓度降低未直接影响到血钠浓度。静脉给予外源性促甲状腺素释放激素(TRH)可以对抗ABI患者ADH分泌增加所引起的稀释性低钠血症。Objective The aim is to explored the pathological mechanism and treatment of hyo- natremia in the patients with acute brain injury. Methods The blood center natriuretic peptide (ANP), brain natriuretic peptide( BNP), Endogenous digitalis substance (EDLS), antidiuretic hormone (ADH) ,and hematuria sodium concentration, hematuria osmotic pressure in 98 patients with acute brain injury(ABI)were simultaneous determined. Results 41 cases of 98 patients with ABI were hy- ponatremia and are more concentrated in a special heavy casualty or serious injuries. Conclusion Central hyponatremia and the hypothalamus-damage to the pituitary axis EDLS are related to the addi- tion of ADH secretion,blood ANP, BNP concentrations did not directly affect the lower serum sodium concentration. Exogenous intravenous Thyrotropin-releasing hormone (TRH)can be used to confront pa- tients with ABI ADH secretion caused by the increase in the dilution of hyponatremia.
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