男性急性颈髓损伤病人的水钠代谢紊乱及相关激素变化

目的 研究男性急性完全性颈髓损伤患继发的水钠代谢紊乱及有关的内分泌变化，探讨颈髓损伤继发低钠血症的发生机制。方法 男性颈髓损伤组（简称男性CSCI组）19例，男性对照组14例，研究其水钠代谢变化，放免检测血浆肾素活性（PRA）、抗利尿激素（ADH）浓度及血清睾丸酮浓度。结果 与对照组比较，男性CSCI组血钠浓度降低，此外还有多尿、尿钠排出增多以及液体入量低于尿量等变化（P＜0.05)；CSCI组PRA、血浆ADH及血清睾丸酮浓度均低于对照组。结论 男性颈髓损伤患其伤后血清睾丸酮浓度下降，可能其继发性的低钠血症有一定的促发作用。     

急性颈髓损伤病人的水钠代谢变化及尿PGE2变化

目的研究急性完全性颈髓损伤病人继发的水钠代谢紊乱及尿中前列腺素PGE2排出量的相应变化,探讨颈髓损伤病人继发水钠代谢紊乱的发生机制.方法完全性颈髓损伤(CSCI)病人28例,对照18例.检测血压、心率、血电解质、尿量、液体入量以及尿电解质排出量的变化,放免检测尿前列腺素PGE2的变化.结果 CSCI组血Na+值低于对照组(P＜0.01),92.9%可出现低钠血症.CSCI组尿量(P＜0.01)及24 h尿Na+排出量(P＜0.05)均高于对照组;血压、心率均低于对照组(P＜0.01);24 h尿PGE2排出总量高于对照组(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.     

急性颈髓损伤继发低钠血症及循环系统变化的临床研究

目的研究急性颈髓损伤(CSCI)继发低钠血症与急性CSCI后出现的循环系统异常情况两者之间的关系,并探讨急性CSCI继发低钠血症的发生机制.方法回顾性分析126例急性CSCI患者的临床资料,比较低钠血症组与正常血钠组血压(BP)、心率(HR)变化,及轻、重度低钠血症患者的BP、HR、中心静脉压(CVP)变化情况.结果低钠血症组的BP、HR均低于正常血钠组,差异有显著意义(P<0.01).严重低钠血症组的BP、HR、CVP均低于轻度低钠血症组,有显著性差异(P<0.05).结论急性CSCI继发低钠血症与急性CSCI时抑制了体内的交感神经系统相关,持续监测急性CSCI患者的BP、HR、CVP等循环系统指标可以预测CSCI后是否会发生低钠血症及其严重程度,对于急性CSCI患者的病情判断或预后估计有一定的临床意义.     

急性颈髓损伤患者的水钠代谢变化及其机制

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.     

急性颈髓损伤患者的水钠代谢变化及其机制

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PGE2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&;#177;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&;#177;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PGE2的变化。结果：CSCI组血Na^+浓度[(132．70&;#177;3．20)mmol／L]低于对照组(t=2．01，P&;lt;O．01)，低钠血症发生率为92．9％；CSCI组尿量(3610&;#177;761)mL／d，Na^+排出量(473．7&;#177;169．4)mmol／d均高于对照组(分别为t=2．01，P&;lt;O．01；t=2．08，P&;lt;O．05)；血压、心率均低于对照组(t=2．01，2．01，P&;lt;O．01)；24h尿PGE2排出量高于对照组(t=2．04，P&;lt;O．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。     

颈髓损伤后水电解质紊乱30例临床分析

目的:探讨颈髓损伤后电解质紊乱的临床特点及诊断治疗。方法:回顾30例颈髓损伤患者(完全性损伤15例,不完全性损伤15例)血压、心率、血清钠、血清钾、血浆渗透压、尿量及24h尿钠排出量等资料。结果:23例患者于伤后2～8d出现低钠血症,其中完全性损伤15例全部出现,发生率100%,1例患者并发抗利尿激素分泌异常综合征。根据血钠水平,经采用控制每日水量、补钠治疗10～21d后,23例均治愈,血钠平均恢复至138(135～142)mmol/L,血浆渗透压、尿钠均正常。结论:低钠血症是颈髓损伤后极为常见的并发症,但并发抗利尿激素分泌异常综合征十分少见;机体内抗利尿激素不适当分泌,导致的稀释性低钠血症可能是颈髓损伤继发低钠血症的发生机制之一。严格控制入液量及补钠为主要治疗方法。     

颈髓损伤后水电解质紊乱的临床诊断治疗

目的 探讨颈髓损伤后电解质紊乱的临床特点及诊断治疗.方法 回顾30例颈髓损伤患者（完全性损伤15例，不完全性损伤15例）血压、心率，血清钠、钾、血浆渗透压、尿量及24ｈ尿钠排出量等资料：23例患者于伤后2－8天出现低钠血症，其中完全性损伤15例全部出现，发生率100％，1例患者并发抗利尿激素分泌异常综合征 结果 根据血钠水平,经采用控制每日水量、补钠治疗5－14天后，23例均治愈,血钠平均恢复至138(135－142)mmol/l,血浆渗透压、尿钠均正常.结论 低钠血症是颈髓损伤后极为常见的并发症，但并发抗利尿激素分泌异常综合征十分少见；机体内抗利尿激素不适当分泌，导致的稀释性低钠血症可能是颈髓损伤继发低钠血症的发生机制之一。严格控制入液量及补钠为主要治疗方法.     

护理干预对颈髓损伤后低钠血症的影响

目的探讨护理干预对颈髓损伤后低钠血症的影响。方法 60例颈髓损伤伴低血钠患者分成对照组(n=30)和护理干预组(n=30)。对照组未给予相关低钠血症的护理干预,护理干预组由责任护士给予相关低钠血症的护理干预。对1个月后两组的血清钠值及病程进行分析。结果 1个月后护理干预组血钠值明显高于对照组(P<0.01),并且护理干预组病程较对照组明显缩短(P<0.01),病情反复病例较对照组少(P<0.05)。结论护理干预有利于改善颈髓损伤患者的低钠血症。     

急性颈髓损伤病人血压和心率的变化及护理

目的探讨急性颈髓损伤病人血压、心率变化及护理。方法CSCI组48例,对照组30例,监测血压及心率变化。结果CSCI组血压及心率均明显低于对照组(P<0.01)。结论颈髓损伤后交感神经系统抑制,血压降低,心率减慢;对低血压及心动过缓的病人及时发现,合理治疗及护理,可维持心脏功能,减轻和预防颈髓的继发性损害,有利于病人的康复。     

急性颈髓损伤患者循环功能改变分析

目的：为急性颈髓损伤（CSCI）患者有针对性的监护提供依据。方法：将42例CSCI患者以颈4平面为界分为颈4以下组（含颈4）25例,颈4以上组17例,以30例非CSCI患者为对照组。对各组的血压、心率和心电图的变化进行分析。结果：CSCI患者收缩压、舒张压及心率均明显低于对照组,心电图异常发生率明显高于对照组 颈4以上组收缩压、舒张压和心率均明显低于颈4以下组,均有统计学意义。结论：对CSCI尤其颈4以上者应密切监测循环功能。     

窒息新生儿低钠血症与心钠素、抗利尿激素水平关系的研究

目的 :探讨血浆心钠素 (ANP)与抗利尿激素 (ADH)在窒息新生儿合并低钠血症中所起的作用及其临床意义。方法 :应用放射免疫分析法对 4 0例窒息新生儿血浆ANP、ADH水平变化进行动态观察 ,并与 2 0例正常足月儿进行对照 ,同时观察补液量对血清钠变化的影响。结果 :①新生儿窒息急性期血浆ANP、ADH水平明显增高 ,窒息程度越重 ,血浆ANP、ADH水平越高 ,血清钠水平越低 (P <0 0 1)。②限水组生后一周血清钠水平已恢复正常 ,未限水组血清钠明显低于正常。结论 :ANP、ADH可影响窒息新生儿水盐代谢 ,引起以稀释性低钠血症为主的稀释性和失钠性低钠血症。治疗应严格控制液体量 <3 0～ 50ml·kg- 1/d ,适当补钠 ,必要时可用速尿利尿     

ADH levels during salt depletion in dogs

Abstract. Two groups of trained dogs were subjected to sodium chloride depletion and plasma ADH concentration, renin activity, plasma sodium, plasma osmolality, blood volume, hematocrit and body weight were measured. In one group of animals, sodium depletion was created by restricting intake to 5 mEq/24 h. Despite a statistically significant decrease in body weight and blood volume and a corresponding increase in plasma renin activity, plasma ADH concentration was not seen to change significantly from control values. Similar findings were seen in a second group of dogs which were given a diuretic in addition to dietary sodium restriction. In these animals the decrease in blood volume and rise in plasma renin activity were proportionately greater. Plasma ADH concentration was not observed to change significantly in this group of animals either. Both groups of animals developed significant hyponatremia during the experiment. It is concluded that in these dogs, the secretion of ADH was not suppressed and consequently hyponatremia developed. It is suggested that endogenous angiotensin was responsible for the continued secretion of ADH at control levels.     

Quantification and predictors of plasma volume expansion from mannitol treatment

Objective: To determine the effects of acute hypertonic mannitol infusion on intravascular volume expansion and to identify potential predictors of hypervolemia. Design: Measurements of plasma volume and volume regulatory hormones were performed in healthy volunteers before and over 90 min after acute infusion of 20 % mannitol solution in a therapeutic dose of 0.5 g/kg body weight, equalling an average infusion volume of 180 ml. Setting: Clinical research unit in an 800-bed teaching hospital in the eastern part of Switzerland. Participants: Eight normal male volunteers. Measurements and results: Baseline plasma volume was determined by the indocyanine green dye dilution technique. Serial plasma protein measurements were performed after mannitol infusion to calculate intravascular volume changes. Mannitol administration resulted in a plasma expansion that persisted for more than 90 min and peaked at 112 % of the baseline plasma volume 15 min after infusion. Concomitantly, an increase in systolic blood pressure and a fall in plasma sodium concentration occurred. Pharmacokinetic analyses of mannitol distribution and elimination revealed a close relation between plasma volume expansion and mannitol serum concentrations. While renin activity and aldosterone concentrations were suppressed proportionally to the intravascular volume increase, antidiuretic hormone was increased despite notable volume expansion and hyponatremia. Similarly, a rise in atrial natriuretic peptide was detected. Conclusions: Therapeutic doses of hypertonic mannitol cause substantial plasma volume expansion, resulting in increased blood pressure. Plasma volume expansion is related to mannitol serum concentrations and mannitol clearance determines the time required to restore normovolemia. ADH and ANP are potentially aggravating factors of mannitol-induced hyponatremia. Received: 27 January 1997 Accepted: 18 August 1997     

老年男性COPD患者血清性激素水平的动态变化

目的探讨慢性阻塞性肺疾病（COPD）患者血清性激素水平的动态变化,为临床治疗提供依据。方法应用化学发光法检测60例老年男性COPD患者急性加重期与稳定期血清性激素水平。选择同期健康对照组50例。结果COPD急性加重期血清睾酮水平明显低于另外两组（P〈0．01）,而稳定期睾酮水平亦低于对照组（P〈0．05）;加重期雌二醇水平低于对照组（P〈0．05）,但稳定期与其他两组相比雌二醇水平无显著差异。结论老年男性COPD患者不论急性加重期或稳定期,血清睾酮水平均低下。在常规治疗的前提下,适当的补充男性激素有助于改善男性COPD的生活质量和并可能会延缓COPD的进展。     

等张运动和抗阻运动对肾脏相关激素的影响

目的探讨等张运动和抗阻运动对肾脏相关激素的影响，为肾脏疾病的临床康复治疗提供参考依据。方法8例健康男性以相同的靶心率(40％HRmax)和运动时间(20min)交替进行等张运动和抗阻运动，观察运动前、后血浆肾素活性(PRA)、醛固酮(ALDO)和抗利尿激素(ADH)的应激变化。结果血浆PRA、ADH和ALDO在等张运动和抗阻运动后均显著增高，抗阻运动后血浆ADH和PRA水平与等张运动后比较，有增高趋势。结论运动引起血浆PRA、ADH和ALDO增加是机体在应激状态下维持水、电解质平衡的一种适应性反应；抗阻运动后血浆ADH和PRA呈现增高的趋势提示影响肾脏相关激素变化的因素与运动的强度有关。     

Haemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans

Summary. Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6° head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (P<0·05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P<0·05). PV was increased by 6·3% (P<0·05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P<0·05) from 90 ±5 ml pre-HDT to 105 ±4 ml during HDT and returned to 88 ±5 ml in seated recovery. Plasma ADH was reduced by 28% (P<0·05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P<0·05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.     

肝硬化腹水低钠血症的临床研究

目的研究肝硬化腹水低钠血症合理有效的治疗方法．址补钠还是限钠。方法将146例肝硬化腹水低钠血症患者随机分成补钠和限钠治疗两组,观察比较两组的血钠、尿钠、PRA、AⅡ、ALD、利尿效果、腹水消退、肾功能损害情况和肝性脑病、HRS发生率和死亡率。结果与限钠组相比,补钠组血钠、尿钠升高,PRA、AⅡ、ALD活性下降,尿量增多明显,腹水消退较快,肾功损害、肝性脑病、HRS发生率和死亡率均较低。结论治疗肝硬化腹水低钠血症应适量补钠。     

慢性心力衰竭患者血钠水平对血浆肾素活性、醛固酮和N末端前脑钠肽水平的影响

目的探讨慢性心力衰竭（心衰）患者血钠水平对血浆。肾素活性（PRA）、醛固酮（ALD）和N末端前脑钠肽（NT．proBNP）水平的影响。方法91例慢性心衰患者,根据治疗前血钠水平分正常血钠组和低血钠组,均在人院第二天清晨卧位采血测定PRA、ALD和NT．proBNP水平,常规治疗心衰及低钠血症一周后以同样的方法采血复查血钠、PRA、ALD和NT-proBNP水平,对上述指标进行统计分析。结果入院时低血钠组PRA、ALD和NT-proBNP比正常血钠组高,差异有统计学意义（P〈0．05l低血钠组患者常规治疗心衰及低钠血症一周后,PRA、ALD和NT-proBNP水平较入院时降低．差异有统计学意义（P〈O．05）正常血钠组常规治疗心衰一周后PRA、ALD和NT．proBNP水平较入院时降低,差异有统计学意义（P〈0．05）;而两组患者治疗前后PRA、ALD和NT．proBNP水平下降值有明显差异（p〈O．05）,低血钠组下降史明显。结论低钠血症可能促进慢性心衰患者PRA、ALD和NT-proBNP分泌增加,心衰伴低钠血症患者的神经内分泌水平激活更明显。低钠血症经治疗血钠水平恢复正常后,神经内分泌激素水平明显降低。