异氟醚和普鲁卡因全麻对鼓膜温度的影响

选择全麻病人４４例,ＡＳＡⅠ～Ⅱ级,分为异氟醚和普鲁卡因两组。术前用药为阿托品和苯巴比妥钠。快诱导后分为异氟醚吸入和普鲁卡因静滴维持麻醉。采用线型温度感应监测鼓膜温度,检测点为维持麻醉前（Ｔ１）、手术结束时（Ｔ２）、手术后１０（Ｔ３）、２０（Ｔ４）、...     

肾实质性高血压患者血浆肾上腺髓质素测定的初步分析

探讨肾实质性高血压（ＲＰＨ）时肾上腺髓质素水平变化。方法应用放免法测定了１１例肾实质性高血压、３３例原发性高血压（ＥＨ）和２５例正常人的血浆肾上腺髓质素［ＡＤＭ（１３－５２）］、内皮素－１（ＥＴ－１）、血管紧张素Ⅱ（ＡＴⅡ）水平。结果肾实质性高血压患者ＡＤＭ（１３－５２）、ＥＴ－１较ＥＨ和正常人明显增高，ＡＴⅡ较正常人高但与ＥＨ组相似；ＡＤＭ（１３－５２）与ＥＴ－１、ＢＵＮ、平均动脉压（ＭＡＰ）有显著的正相关关系，与ＡＴⅡ无相关性。结论肾实质性高血压患者血浆ＡＤＭ（１３－５２）增高可能是继发于高血压代偿性分泌增多，并可能与肾功能减退代谢障碍、排泄减少有关     

老年动脉硬化闭塞症胰岛素抵抗与内皮素血管紧张素Ⅱ相互关系的研究

目的：探讨周围动脉粥样硬化闭塞症（ｐｅｒｉｐｈｅｒａｌａｔｈｅｒｏｓｃｌｅｒｏｓｉｓｏｂｌｉｔｅｒａｎｓ，ＰＡＳＯ）胰岛素抵抗（Ｉｎｓｕｌｉｎｒｅｓｉｓｔａｎｃｅ，ＩＲ）、内皮素（Ｅｎｄｏｔｈｅｌｉｎｓ，ＥＴ）、血管紧张素－Ⅱ（ａｎｇｉｏｔｅｎｓｉｏｎ－Ⅱ，ＡＴ－Ⅱ）之间的相互关系。方法：采用特异性葡萄糖氧化酶法和放射免疫测定法对５１例ＰＡＳＯ患者进行糖耐量实验前后血糖、胰岛素（Ｉｎｓｕｌｉｎ，ＩＮ）水平的测定，并计算其曲线下面积，同时采用放射免疫测定法检测血浆ＡＴ－Ⅱ和ＥＴ水平，并分别与ＩＮ及其曲线下面积作相关分析。结果：ＰＡＳＯ患者ＩＮ、ＥＴ、ＡＴ－Ⅱ水平分别为１４．７９ｍＵ／Ｌ、７７．６９ｎｇ／Ｌ、１１１．３３ｎｇ／Ｌ，明显高于健康对照组；同时糖负荷后１ｈＩＮ及其分泌总量明显增高；糖耐量实验前后ＩＮ水平及其曲线下面积均与ＡＴ－Ⅱ、ＥＴ呈正相关系。结论：老年ＰＡＳＯ患者存在ＩＲ现象，血管ＡＴ－Ⅱ、ＥＴ与ＩＲ之间相互影响、相互促进、共同参与ＰＡＳＯ的形成和发展。     

血透患者血浆内皮素血管紧张素Ⅱ与心肌肥厚关系

探讨血透患者血浆内皮素１（ＥＴ１）、血管紧张素Ⅱ（ＡＴⅡ）浓度改变及其与心肌肥厚的关系。方法采用放射免疫的方法。结果（１）血透４小时后ＥＴ１较血透前降低，透后７２小时再次升高。（２）血透４小时后ＡＴⅡ较血透前升高，透后７２小时仍高于透前水平。（３）维持血透３个月后左室重量（ＬＶＭ）、左室重量指数（ＬＶＭＩ）较３个月前明显升高。（４）血透患者ＢＵＮ、Ｓｃｒ、ＥＴ１、ＡＴⅡ均与ＬＶＭＩ呈正相关。结论血透患者ＬＶＨ可能与血浆ＥＴ１、ＡＴⅡ升高有关，维持血透不能持久降低其浓度。     

纳洛酮用于全麻催醒时血浆AⅡ、E、NE、ET和ANP浓度的变化

目的：通过对血管紧张素Ⅱ（ＡⅡ）、肾上腺素（Ｅ）、去甲肾上腺素（ＮＥ）、内皮素（ＥＴ）及心钠素（ＡＮＰ）浓度的动态观察，探讨纳洛酮用于全麻催醒时产生并发症的原因。方法：选择期腹部肿瘤切除手术患者３６例，随机均分为１组、Ⅱ组和Ⅲ组（生理盐水），分别于术终时静注。分别于麻醉前５分钟（Ｔ１）、注药前５分钟（Ｔ２）和注药后５分钟（Ｔ３）采取静脉血标本。用高效液相色谱法测定Ｅ和ＮＥ浓度，用放免法检测ＡⅡ Ｅ     

雷公藤多甙在大鼠肾移植模型中的实验研究

用显微外科技术建立大鼠肾移植模型（Ｗ→ＳＤ）。将大鼠分为四组：对照组仅给生理盐水，雷公藤多甙（Ｔ_Ⅱ）组给Ｔ_Ⅱ３０ｍｇ·ｋｇ~（１）·ｄ~（－１），ＣｓＡ组给ＣｓＡ１５ｍｇ·ｋｇ~（－１）·ｄ~（－１），ＣｓＡ＋Ｔ_Ⅱ组同时给ＣｓＡ１５ｍｇ·ｋｇ~（－１）·ｄ~（－１）＋Ｔ_Ⅱ３０ｍｇ·ｋｇ~（－１）·ｄ~（－１）。对照组大鼠肾移植后平均存活时间为７．３±２．２天，Ｔ_Ⅱ组平均存活时间为１８．１±３．７天，两组存活时间有显著性差异（Ｐ＜０．０５）。Ｔ_Ⅱ＋ＣｓＡ组平均存活时间为３４．６±５．２天，ＣｓＡ组为２６．１±４．６天。单纯用药的两组分别与联合用药组比较均有显著性差异（Ｐ＜０．０５）。Ｔ_Ⅱ３０ｍｇ·ｋｇ~（－１）·ｄ~（－１）对大鼠肝、肾、心脏及白细胞总数无影响，但显著抑制大鼠脾淋巴细胞的转化。Ｔ_Ⅱ也显著抑制大鼠外周血白细胞介素－２受体水平，但抑制能力不及ＣｓＡ。     

enalapril对不同肾功能高血压患者血管活性物质的作用

为转换酶抑制剂（ＡＣＥＩ）治疗高血压提供理论依据。方法２５例高血压患者按内生肌酐清除率分为肾功能正常１０例，代偿８例和氮质血症７例３组。观察ＡＣＥＩｅｎａｌａｐｒｉｌ（１０～３０ｍｇ／ｄ）４周对血管活性物质，包括血浆肾素活性（ＰＲＡ），血管紧张素Ⅱ（ＡＴⅡ），转换酶（ＡＣＥ），心钠素（ＡＮＦ），尿醛固酮（Ａｌｄｏ），缓激肽（ＢＫ）和前列腺素Ｅ２（ＰＧＥ２）的作用。结果１．服药前３组患者与正常人比，ＡＴⅡ升高，ＰＲＡ，Ａｌｄｏ无差异；氮质血症组患者ＢＫ降低，ＡＮＦ增高；２．服药后３组患者ＡＴⅡ，Ａｌｄｏ和ＡＮＦ下降，ＢＫ（除氮质血症组），ＰＧＥ２和ＰＲＡ升高；３．治疗后ＡＴⅡ与Ａｌｄｏ、ＡＴⅡ与ＡＮＦ以及ＢＫ与ＰＧＥ２分别呈正相关。结论１．肾素－血管紧张素系统（ＲＡＳ）与ＢＫ－ＰＧＳ两系统相互调节在不同肾功能高血压患者的发病中起着作用，并有着治疗意义；２．ｅｎａｌａｐｒｉｌ降低血压和保护肾脏作用可能通过抑制ＲＡＳ和激活ＢＫ－ＰＧＳ所介导     

慢性肾功能衰竭患者血浆心钠素和肾素,血管紧张素II.醛固酮变化…

本文用ＲＩＡ法测定了３０例健康人、ＣＲＦ２４例非透析病人和１４例血透病人的血浆ＡＮＰ，ＰＲＡ，ＡＴⅡ，ＡＬＤ水平。结果表明ＣＲＦ病人ＡＮＰ，ＰＲＡ，ＡＴⅡ，ＡＬＤ明显高于对照组（Ｐ＜０．０５～０．０１），其中高血压组ＡＮｐ明显高于非高血压（Ｐ＜０．０５），血透后ＡＮＰ明显下降（Ｐ＜０．０１），ＡＮＰ和Ｓｃｒ，ＭＡＰ呈正相关，ＡＮＰ，ＡＴⅡ均和Ａ呈负相关，结合文献初步探讨了ＣＲＦ时，ＡＮＰ和ＰＡＳ的     

动脉硬化闭塞症与血管内皮细胞活性因子关系的研究

目的　探讨动脉硬化闭塞症（ＡＳＯ） 与内皮素１（ＥＴ１） 、一氧化氮（ＮＯ） 等血管内皮细胞活性因子的相互关系。方法　选择９６ 例ＡＳＯ 患者，采用密度梯度法检测循环内皮细胞计数（ＣＥＣ），采用放射免疫测定法检测血浆ＥＴ１ 、血栓素Ｂ２（ＴＸＢ２）、６酮前列腺素Ｆ１α（６ＫＰＧＦ１α） ，降钙素基因相关肽（ＣＧＲＰ） 、血管紧张素Ⅱ（ＡＴⅡ）、肿瘤坏死因子（ＴＮＦ），采用酶联免疫检测细胞间粘附分子１（ＩＣＡＭ１）、Ｐ选择素（ＰＳ）。采用Ｇｒｉｓｓ 法检测血浆ＮＯ水平。结果　所有患者均存在高ＥＴ１、ＴＸＢ２ 、ＡＴⅡ、粘附分子、ＣＥＣ血症，存在低ＮＯ、ＣＧＲＰ、６ＫＰＧＦ１α血症，且以Ⅲ期病人最明显。结论　ＡＳＯ 的发生发展同血管内皮细胞活性因子密切相关，ＥＴ１、ＮＯ 等血管活性因子的检测有助于ＡＳＯ发病机制的探讨和病情严重程度的判别。     

硬膜外阻滞和N_2O-O_2-安氟醚吸入麻醉对围术期老年男性R-A-A系统的影响

２０例择期行前列腺摘除或膀胱肿瘤部分切除病人，随机分为两组，每组１０例，分别行硬膜外麻醉（双管法）和氧化亚氮－氧气－安氟醚（ＧＯＥ）吸入麻醉，测定麻醉和手术过程中血浆肾素活性，血管紧张素Ⅱ（ＡⅡ）和醛固酮（Ａｌｄ）浓度的变化，并进行比较。结果：硬膜外组病人的三者浓度在麻醉和手术过程中无明显变化，而ＧＯＥ组麻醉和手术使ＲＡＡ浓度显著升高，两组差异高度显著。结论：双管法硬膜外阻滞可消除盆腔手术病人手术引起的肾素、血管紧张素和醛固酮反应，而ＧＯＥ吸入麻醉却无这方面作用。     

颅脑手术围术期肾素血管紧张素醛固酮和皮质醇的变化

目的与方法：对２３例颅脑手术病人行气管内全麻分别在术前、开颅、病灶切除时和术毕观察围术期血浆肾素、血管紧张素、醛固酮和皮质醇的变化。结果：与术前值比较，皮质醇在开颅时升高，在病灶切除时和术毕降低；肾素、醛固醇在开颅时变化不大，在病灶切除时和术毕时升高；血管紧张素各期变化不大。结论：颅脑手术中应激反应仍较活跃，但肾素、血管紧张素、醛固酮和皮质醇围术期改变与其他部位有所不同。     

Effects of angiotensin converting enzyme inhibition on sodium excretion in patients with hypoxaemic chronic obstructive pulmonary disease.

BACKGROUND--Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop cor pulmonale with sodium and water retention. The sodium retention has been explained as a result of increased plasma levels of aldosterone. If this was true angiotensin converting enzyme (ACE) inhibition would be expected to lower plasma levels of aldosterone and improve the renal excretion of sodium. METHODS--Six patients with stable hypoxaemic COPD (PaO2 < 8.0 kPa) and a history of an oedematous exacerbation received an intravenous hypertonic saline load (6 ml/kg body weight of 2.7% saline over one hour) before and while taking 4 mg/day perindopril, an ACE inhibitor, for one month. Aldosterone, antidiuretic hormone (ADH), plasma and urine electrolyte levels, osmolality, and volume were measured over four hours. The repeatability of the saline load test was assessed in six patients with a similar severity of hypoxaemic COPD. For comparison the saline load test was also performed in six patients with mild COPD. RESULTS--The hypertonic saline load test results were repeatable. Perindopril reduced the mean (SD) plasma level of aldosterone from 142 (88) pg/ml to 54 (24) pg/ml at 0 minutes before the saline infusion, and from 64 (35) pg/ml to 30 (17) pg/ml after the infusion without improving the urinary volume or sodium excretion. Before starting treatment with perindopril 43.7 (6.9) mmol (20%) of the sodium load was excreted compared with 49.6 (7.9) mmol (22% of load) when taking perindopril. Patients with mild COPD excreted more sodium (77.6 (21.4) mmol (38.7% of load)) despite having similar plasma aldosterone levels to those in the patients receiving perindopril. CONCLUSIONS--Patients with stable hypoxaemic COPD have an impaired ability to excrete sodium which is not improved by the administration of an ACE inhibitor. ACE inhibition lowered the plasma level of aldosterone without improving sodium excretion. This suggests that the inability of patients with hypoxaemic COPD to excrete sodium is not caused by their increased plasma levels of aldosterone.     

Role of aldosterone in the sodium retention of patients with nephrotic syndrome

The role of aldosterone in the abnormal sodium retention in patients with nephrotic syndrome has been debated. In fact, studies using a converting enzyme inhibitor to lower plasma aldosterone have rejected such a role. We therefore studied 5 nephrotic patients and 6 control subjects by using the more specific aldosterone antagonist, spironolactone. After withdrawal of diuretics 5 days prior to the study, the nephrotic patients and control subjects were placed on a high-sodium diet (285 +/- 6 mEq/day) for 8 days. After 4 days, spironolactone 200 mg p.o., b.i.d., was given for the remaining 4 days. Plasma renin activity and plasma aldosterone levels were similar in both nephrotic patients and control subjects before the study, after sodium loading and after spironolactone had been given. After 4 days of high sodium intake control subjects were in sodium balance, but the nephrotic patients were in a positive sodium balance (approx. 80 mEq/day; p less than 0.01). On days 3 and 4 of spironolactone, the nephrotic patients exhibited an increase in urinary sodium excretion (205 +/- 20 vs. 312 +/- 13 mEq/day; p less than 0.005) but not the control subjects (279 +/- 16 vs. 286 +/- 13 mEq/day; NS). It is therefore concluded that aldosterone is a significant contributor to the sodium retention in patients with nephrotic syndrome.     

Distal nephron sodium-potassium exchange in children with nephrotic syndrome

While recent literature data suggest that a primary impairment in sodium excretion is the basic abnormality in the pathogenesis of edema formation in the nephrotic syndrome, there is ample evidence that functional hypovolemia contributes to stimulation of renal sodium and fluid retention. Vasoactive hormones such as renin and aldosterone are involved in this process. Discrimination between both mechanisms would be possible by assessment of aldosterone bioactivity and will have therapeutical consequences by indicating the need for administration of i.v. albumin or diuretics. In this paper, several indices of aldosterone bioactivity were assessed in 85 patients with minimal lesion nephrotic syndrome (118 measurements were performed in patients while in remission and 210 following relapses), and in 41 nephrotic patients with different types of nephropathy and were related to plasma renin and aldosterone levels. A better correlation was found between log aldosterone and U(K+)/U(Na+) + U(K+) ratio than with other parameters measuring renal potassium handling such as transtubular potassium gradient, fractional excretion of potassium and urine K+/urine Na+ or urine K+ creatinine ratios. In patients with renal sodium retention (FE(Na)% less than 0.5), an U(K+)/U(Na+) + U(K+) ratio higher than 0.60 identifies patients with increased aldosterone levels and indicates functional hypovolemia. This index may therefore be used to assess which patients will benefit from i.v. albumin administration.     

Epidural Analgesia Inhibits the Renin and Aldosterone Response to Surgery

Renin activity and aldosterone concentration in plasma and excretion of sodium and potassium in urine were measured during a period of 24 hours in 12 patients undergoing hysterectomy under general anaesthesia or epidural analgesia. Analgesia extended from T4 to S5 and was effective throughout the study. The normal stress-induced increase in plasma renin activity and aldosterone was inhibited by epidural analgesia. Urinary excretion of potassium was significantly lower in the epidural group, but sodium and water retention showed no difference between groups. It is concluded that neurogenic stimuli from the surgical area are important release mechanisms of the renin-aldosterone response to surgery. The results suggest that post-operative sodium retention is caused by factors other than the mineralocorticoid system.     

Sodium retention in nephrotic syndrome is due to an intrarenal defect: evidence from steroid-induced remission

There is increasing evidence that the sodium retention of nephrotic syndrome is directly due to an intrarenal mechanism and not to a low blood volume stimulating the renin-angiotensin-aldosterone system. However the mechanism of the natriuresis that occurs during remission is not known. Patients with nephrotic syndrome were therefore studied during steroid-induced remission. At the onset of natriuresis, blood volume and plasma albumin were low and did not change. Plasma renin activity and plasma aldosterone were initially high and both fell during the natriuresis. At the end of the natriuresis when patients had lost their oedema, plasma renin activity and plasma aldosterone rose to high levels, plasma albumin and blood volume remained low, and yet the patients were no longer retaining sodium and were in sodium balance. These observations suggest that the natriuresis of remission is due to the correction of an intrarenal mechanism causing the sodium retention. This study raises two major unanswered questions. Firstly, when the presumed intrarenal mechanism is corrected, what tells the kidney to excrete large amounts of sodium when the blood volume remains low? Secondly, why do the patients come back into sodium balance when the blood volume is low, and plasma renin activity and plasma aldosterone are elevated?     

Lack of effect of captopril on the sodium retention of the nephrotic syndrome

The mechanism of sodium retention in the nephrotic syndrome remains controversial, though the classic pathophysiological explanation is stimulation of the renin-angiotensin-aldosterone system. Recent evidence has shown that many patients with the nephrotic syndrome have a normal or low plasma renin activity suggesting that there might be an intrarenal cause for their sodium retention. We gave captopril, an oral angiotensin-converting enzyme inhibitor, during 10 separate episodes of sodium retention in nephrotic syndrome. There was evidence of stimulation of the renin system in 7 of these episodes. Despite a marked fall in plasma aldosterone, all patients continued to retain sodium and water and gain weight. This demonstrates that the sodium retention of nephrotic syndrome is not due to stimulation of the renin-angiotensin-aldosterone system, but must be due to some other mechanism, which is probably intrarenal.     

Suppression of surgical hyperaldosteronism by potassium canrenoate during gynecologic surgery under sevoflurane anesthesia

BACKGROUND: Surgical hyperaldosteronism leads to sodium and water retention during surgery and often causes postoperative edema. This study investigated the effect of potassium canrenoate (PC) on pituitary adrenocortical function in lower abdominal surgery under sevoflurane anesthesia. METHODS: Twenty patients were randomized to receive 400 mg of PC (the PC group, n=10) or saline (the control group, n=10) intravenously. The following parameters were determined: plasma aldosterone, adrenocorticotropic hormone (ACTH), plasma renin activity (PRA), serum sodium and potassium, urinary sodium and potassium, and urine output. RESULTS: The aldosterone and ACTH levels showed significant increases in the control group during surgery. Plasma ACTH also increased significantly in the PC group, but plasma aldosterone levels were unchanged during surgery. The urine Na/K ratio of the PC group was significantly higher than that of the control group. CONCLUSION: The present study suggested that PC suppresses the increase of plasma aldosterone caused by surgical stress. That may prevent sodium retention and potassium excretion during surgery.     

Effect of high-dose aldosterone infusions on renal electrolyte excretion in patients with renal insufficiency

We investigated the effect of aldosterone infusion (0.5 mg/h for 6 h) on electrolyte excretion in 11 patients with severe renal insufficiency (creatinine clearance 6-20 ml/min), with normal or elevated serum potassium levels and a wide range of plasma aldosterone levels, and compared the data with those obtained in 7 healthy subjects. The studies were done under conditions of fixed sodium and potassium intake. In the normal subjects, aldosterone infusion caused a significant rise in potassium excretion and a significant fall in sodium and chloride excretion (p less than 0.01). In 1 patient with a high plasma aldosterone, virtually no response occurred to the aldosterone infusion. In the others, the increase in potassium excretion and reduction in chloride excretion were not different from the changes observed in the normals, but the fall in sodium excretion was less due to a higher urinary sodium before infusion in the normals (p less than 0.05). Fractional electrolyte excretions as well as the changes in fractional excretion by aldosterone were larger in the patients (p less than 0.05). Apparently, the renal tubules of patients with chronic renal failure are still responsive to maximal stimulation with aldosterone, in spite of their basically elevated fractional electrolyte output. These findings suggest that, with some exceptions, the hyperkalemia in patients with chronic renal failure is in part due to relative hypoaldosteronism.     

Hormonal, renal, and autonomic nerve factors involved in the excretion of sodium and water during dynamic salt and water loading in hypoxaemic chronic obstructive pulmonary disease.

BACKGROUND--Some patients with hypoxaemic chronic obstructive pulmonary disease (COPD) develop sodium and water retention and a subclinical autonomic neuropathy. The possibility that these might be associated has been investigated. METHODS--The ability of 24 patients with COPD to excrete a 6 ml/kg 2.7% intravenous saline or 15 ml/kg oral water load was studied and changes in plasma electrolyte levels, osmolality, plasma aldosterone and vasopressin levels, urinary volume and sodium content, glomerular filtration rate, renal blood flow, and cardiovascular autonomic nerve function were measured. Patients were divided into groups of eight: those in group A (controls) had mild COPD with a Pa02 of > 9 kPa and no oedema, patients in group B were more hypoxaemic but had never been oedematous, whilst those in group C were hypoxaemic and mildly oedematous at the time of the study. RESULTS--Patients in groups B and C excreted less sodium and water during saline loading and a lesser proportion of the water load. Patients in group C had a reduction in renal blood flow and glomerular filtration rate and all had a subclinical autonomic neuropathy, which was also found in three patients in group B. Their plasma aldosterone level was raised but did suppress appropriately on saline loading. Vasopressin levels were abnormally raised for the osmolality in patients in group C and in those with autonomic dysfunction throughout the water load and at 240 minutes after the salt load. Sodium and urine excretion was highly correlated with autonomic dysfunction, aldosterone levels at time zero, and renal blood flow. The 11 patients with autonomic dysfunction were more likely to be oedematous, more hypoxaemic, excreted much less urine and sodium, had lower glomerular filtration rate and renal blood flow, and higher aldosterone and vasopressin levels than the remaining patients. CONCLUSIONS--In patients with COPD the inability to excrete sodium and water is multifactorial. This is the first study to show that autonomic dysfunction is at least associated and might play an important part in the impaired sodium and water homeostasis seen in patients with severe COPD.