血栓弹力图在OSAHS并发慢性心力衰竭患者中的应用价值

目的 通过血栓弹力图评估阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnea hypopnea syndrome,OSAHS）并发慢性心力衰竭（CHF）患者的血凝状态,探讨血栓弹力图在OSAHS并发CHF患者中的应用价值。 方法 选择确诊为OSAHS并发CHF患者60例,按照2015年我国《阻塞性睡眠呼吸暂停低通气综合征诊治指南（基层版）》诊断标准中的睡眠呼吸指数（AHI）,将OSAHS并发CHF患者分为轻度组（20例,AHI 5~15次/h）、中度组（20例,AHI 16~30次/h）和重度组（20例,AHI>30次/h）。另随机选取同一时段我院健康体检者20例作为正常对照组,所有入组患者均记录一般情况,包括年龄、身高、体质量、性别、高血压病、吸烟史、饮酒史、腰围、睡眠监测结果、血栓弹力图结果（R值、MA值）。 结果 ①随着OSAHS并发CHF患者体质量指数（body mass index,BMI）的升高,AHI相应增大,差异有统计学意义（P<0.05）。②OSAHS并发CHF患者各组与正常对照组比较,R值明显减小,差异有统计学意义（P<0.05）。OSAHS并发CHF患者各组间R值比较,差异有统计学意义（P<0.05）。③OSAHS并发CHF患者各组与正常对照组比较,MA值明显增大,差异有统计学意义（P<0.05,P<0.01）。OSAHS并发CHF患者各组间MA值比较,差异有统计学意义（P<0.05,P<0.01）。 结论 OSAHS并发CHF患者病情越重R值越小、MA值相应增大。     

高血压并发阻塞性睡眠呼吸暂停低通气综合征老年患者血脂水平

目的研究老年高血压合并阻塞性睡眠呼吸暂停综合征的血脂水平。方法 2008年9月至2010年12月我院收治老年高血压患者210例,根据呼吸暂停低通气指数(AHI)监测分为单纯高血压对照组44例,高血压合并轻度OSAHS组60例和高血压合并中重度OSAHS组106例,监测各组血压,比较各组患者的血脂水平差异。结果相对于单纯高血压患者,并发阻塞性睡眠呼吸暂停低通气综合征的患者,呼吸暂停低通气指数(AHI)高,血浆总胆固醇(TC)、甘油三酯(TG)和低密度脂蛋白胆固醇(LDL-C)水平均增高,高密度脂蛋白胆固醇(HDL-C)水平降低,有统计学意义(P<0.05)。结论老年高血压病人合并有OSAHS者,血脂水平受到明显影响。早期诊断和进行相应治疗对于预防心脑血管并发症、改善患者预后具有重要意义。     

OSAHS患者血浆hsCRP水平的研究

目的探讨阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者血浆超敏C反应蛋白（hsCRP）的水平。方法选取经多导睡眠图（PSG）确诊且未经治疗并排除其他疾病的OSAHS患者55例为实验组，19例PSG监测正常者为对照组，分别测定两组患者血浆hsCRP浓度。结果OSAHS组患者血浆hsCRP水平明显高于对照组（P〈0．05），而且中重度患者血浆hsCRP水平高于轻度患者（P〈0．05），血浆hsCRP水平与AHI、BMI及睡眠中最低血氧饱和度（LSp02）有较好的相关性（P均〈0．05）。结论OSAHS患者血浆hsCRP水平明显升高，其与OSAHS严重程度相关而独立于肥胖。     

男性高血压合并阻塞性睡眠暂停综合征患者动脉弹性与血浆肾素-血管紧张素-醛固酮活性改变的研究

目的:了解合并阻塞性睡眠呼吸暂停综合征的中年男性高血压病患者,动脉弹性改变和血浆肾素-血管紧张素-醛固酮活性改变,探讨两者的相互关系,从而对合并睡眠暂停的高血压病患者的针对性治疗提供理论依据。方法:选择中年男性高血压病住院患者276例,进行多导睡眠监测,根据睡眠呼吸暂停低通气指数(AHI)分为原发性高血压(EH)组(n=101)和原发性高血压合并阻塞性睡眠呼吸暂停综合征(EH+OSAS)组(n=175),两组分别测定晨起卧位肾素活性、血管紧张素Ⅱ(AngⅡ)、血浆醛固酮(Ald)、肱-踝动脉脉搏波传导速度(BaPWV),以及24h动态血压监测,观察两组患者血压、心率、肾素-血管紧张素-醛固酮活性及BaPWV的变化。结果:1EH+OSAS组患者血浆肾素活性[EH+OSAS:1.44(0.51,3.27)比EH:1.83(0.32,4.56)μg/L]和血管紧张素Ⅱ[EH+OSAS:54.99(45.07,71.61)比EH:58.89(50.16,65.52)ng/L]均低于EH组(P0.05),差异有统计学意义;EH+OSAS组患者血浆醛固酮[EH+OSAS:0.115(0.096,0.147)比EH:0.106(0.094,0.140)μg/L]高于EH组,差异有统计学意义(P0.05)。2EH+OSAS组患者左右BaPWV均高于EH组[左BaPWV:EH+OSAS:1 520(1 341,1 667)比EH:1 426(1 284,1 614)cm/s,P0.05;右BaPWV:EH+OSAS:1 537(1 375,1 690)比EH:1 479(1 304,1 621)cm/s,P0.05]。3患者睡眠呼吸暂停低通气指数(AHI)与血浆醛固酮浓度及左右BaPWV呈显著正相关。4患者左右BaPWV与醛固酮浓度呈显著正相关,与睡眠监测中最低血氧饱和度和平均血氧饱和度呈显著负相关。结论:1合并阻塞性睡眠呼吸暂停的男性高血压病患者的血浆醛固酮浓度明显升高,其血浆肾素、血管紧张素Ⅱ及醛固酮浓度较单纯高血压组具有明显差异性。2合并阻塞性睡眠呼吸暂停的男性高血压病患者的动脉弹性损害比单纯高血压组更加严重,可能与血浆醛固酮的升高有关。     

糖尿病并高血压患者血浆PRA、AngⅡ、ALD变化的临床意义

目的探讨糖尿病（DM）并高血压（HP）患者血浆肾素活性（PRA）、血管紧张素Ⅱ（AngⅡ）、醛固酮（ALD）变化的临床意义。方法选择DM患者320例,其中DM并HP160例（观察组）,单纯DM160例（对照组）。检测两组在普通饮食和低钠饮食下立位、卧位时的血浆PRA、AngⅡ、ALD。结果与对照组比较,观察组在普通饮食下卧位时的血浆PRA、AngⅡ、ALD明显升高（P均〈0．05）;低钠饮食下两组PRA比较无统计学差异（P〉0．05）,观察组卧位时的ALD及立位时的AagⅡ均明显高于对照组（P〈0．01或〈0．05）。结论DM并HP患者血浆PRA、AngⅡ、ALD明显升高,其可作为预测HP的风险或治疗DM并HP的靶点。     

阻塞性睡眠呼吸暂停低通气综合征血浆尾加压素Ⅱ检测及其意义

目的探讨不同程度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆尾加压素Ⅱ(UⅡ)水平的变化,分析其在OSAHS发生发展中的作用。方法将2005年4月至2005年12月于温州医学院附属第一人民医院睡眠中心行多导睡眠(PSG)监测的鼾症患者60例分为单纯鼾症组和轻、中、重度OSAHS组,每组各15例。选取15名健康体检者为正常对照组。检测各组UⅡ水平,进行相关性分析。结果UⅡ水平正常对照组(1.14±0.65)ng/L、单纯鼾症组(1.37±0.42)ng/L、轻度OSAHS组(10.44±4.12)ng/L、中度OSAHS组(38.55±15.8)ng/L、重度OSAHS组(94.78±19.63)ng/L,单纯鼾症组与轻、中、重度OSAHS组两两比较,组间差异均有显著性意义(P<0.01)。结论UⅡ可能是参与OSAHS发生、发展的重要因素。     

血管内皮生长因子、血清皮质醇、尿儿茶酚胺在阻塞性睡眠呼吸暂停低通气综合征中的意义探讨

目的 检测阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)患者血管内皮生长因子(vascular endothelial growth factor,VEGF)、血清皮质醇及夜间尿儿茶酚胺(UCA)的浓度,初步探讨其在OSAHS并发心脑血管疾病中的意义.方法 65例OSAHS合并心脑血管病患者、70例单纯OSAHS患者、74例正常对照组,检测血浆VEGF、血清皮质醇和夜间UCA浓度.结果 血浆VEGF、血清皮质醇及夜间UCA在OSAHS患者高于正常人,OSAHS合并心脑血管病患者更高,差异均有统计学意义(P<0.05).结论 OSAHS患者血浆VEGF、血清皮质醇和夜间UCA浓度均较正常对照组升高;合并心脑血管病的OSAHS患者比单纯OSAHS患者血浆VEGF、血清皮质醇和夜间UCA浓度升高更显著;血浆VEGF、血清皮质醇及夜间UCA浓度升高在OSAHS患者并发心脑血管疾病中可能起着重要作用.     

阻塞性睡眠呼吸暂停低通气综合征患者血浆神经肽Y水平与睡前及晨起血压的相关性

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆神经肽Y(NPY)浓度与患者睡前及晨起血压水平的相关性.方法 分组:肥胖OSAHS患者32例(OSAHS组)、非OSAHS肥胖者26例(单纯肥胖组)和体质量正常的健康成人27名(正常对照组).其中OSAHS组和单纯肥胖组接受多导睡眠仪(PSG)监测.血浆NPY的浓度采用酶联免疫吸附试验(ELISA)法测定.结果 OSAHS组血浆NPY浓度显著高于单纯肥胖组(P＜0.05)及正常对照组(P＜0.01).OSAHS患者睡前舒张压、晨起收缩压及舒张压比单纯肥胖组明显升高,差异有统计学意义.相关分析显示,OSAH S组血浆NPY浓度与患者睡前舒张压、晨起收缩压及舒张压呈正相关(P值分别为0.049、0.017、0.006).结论 OSAHS组NPY水平升高,NPY对OSAHS患者血压尤其晨起血压升高起到一定促进作用.     

阻塞性睡眠呼吸暂停综合征合并高血压患者的睡眠分析

目的 分析阻塞性睡眠呼吸暂停综合征(OSAHS)合并高血压患者的睡眠.方法 将我院收治的OSAHS合并高血压患者作为研究1组,OSAHS血压正常患者作为研究2组,并以单纯鼾症患者作为对照组,应用多导睡眠监测仪对三组患者进行睡眠监测.结果①研究1组、研究2组觉醒时间较对照组明显增多,研究1组浅睡眠较研究2组、对照组明显增多;中度睡眠研究2组、对照组明显减少(P<0.05).② 研究1组呼吸暂停低通气指数、呼吸暂停指数明显高于研究2组(P<0.05).③研究1组呼吸暂停时间占睡眠时间百分比较研究2组升高(P<0.05).④ 研究1组最低血氧饱和度明显高于研究2组(P<0.05).结论 OSAHS合并高血压患者呼吸紊乱较血氧正常患者重,睡眠质量相对较差.     

血浆同型半胱氨酸在阻塞性睡眠呼吸暂停低通气综合征并心血管疾病中的意义探讨

目的 初步探讨同型半胱氨酸(HCY)在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)并心血管疾病(CVD)中的意义.方法 单纯鼾症组15例、单纯OSAHS组42例及OSAHS合并CVD组37例.行睡眠呼吸监测,检测血浆HCY、血脂.OSAHS组30例、OSAHS+CVD组24例进行nCPAP治疗,3个月后比较两组治疗前后睡眠呼吸紊乱、HCY水平变化.结果 ①单纯鼾症组、OSAHS组、OSAHS+CVD组HCY值渐升高,P<0.05.各组间TC、TG、VLDL水平不同,但两两比较差异不全有意义.②相关分析显示AHI及RIT与HCY关系最密切,相关系数r分别为0.899、0.835.③经nCPAP治疗后,OSAHS组、OSAHS+CVD组睡眠呼吸紊乱得到改善,血浆HCY浓度较治疗前下降,P<0.05.结论 OSAHS患者HCY水平升高,HCY可能进一步参与心血管疾病的发生发展过程.nCPAP治疗可降低HCY水平.     

The Effects of Saralasin, an Angiotensin II Antagonist on Blood Pressure and the Renin-Angiotensin-Aldosterone System in Normal and Hypertensive Subjects

Summary: The effects of saralasin, an angiotensin II antagonist, on blood pressure and the renin-angiotensin-aldosterone system in recumbent normal and hypertensive subjects.
Blood pressure reduction with saralasin infusion was seen only in hypertensive patients with abnormally elevated basal plasma renin and angiotensin II levels, and after sodium depletion the reduction in blood pressure was more marked. In normal subjects, and in hypertensives with plasma renin and angiotensin II levels within the normal range, there was no marked fall in blood pressure across saralasin infusion regardless of the sodium status of the individual.
Plasma aldosterone concentration fell during saralasin infusion in those subjects with high baseline renin and angiotensin II levels. This fall occurred in the sodium replete and deplete states. In the normal subjects, and those hypertensives with normal plasma renin levels, there was no fall in aldosterone in the sodium replete state. However, after sodium depletion the expected rise in aldosterone was abolished during saralasin infusion, the plasma aldosterone falling to within the normal sodium replete range, rising again after the saralasin infusion was stopped.
This study supports the concept of a direct role for renin and angiotensin II in the maintenance of hypertension in those subjects with elevated basal plasma renin. Plasma aldosterone would appear to be controlled, at least in part, by the prevailing plasma angiotensin II level in those subjects with elevated basal levels of angiotensin II; that is in high renin hypertensives, and in normal subjects and normal renin hypertensives who are sodium deplete.     

Enhanced aldosterone response to angiotensin II in human hypertension.

Adrenal and vascular responsiveness to graded doses of angiotensin II (A II) were recorded for seven normal subjects and 12 patients with essential hypertension while in balance on an intake of 200 mEq sodium/100 mEq potassium. Patients with essential hypertension had been previously studied and known to have normal responses of plasma renin activity to sodium restriction and upright posture. A II was administered for 30 minutes at rates of 0.1, 0.3, 1, and 3 ng/kg per minute and plasma aldosterone responses were assessed 20 and 30 minutes later; blood pressure was monitored at intervals of 1 minute during infusion of A II at each rate. A significant increment in plasma aldosterone occurred at an infusion rate of 0.3 ng/kg per minute in patients with hypertension. This change was not seen until the infusion rate reached 1.0 ng/kg per minute in the normotensive control subjects. Even at an A II infusion rate of 1 ng/kg per minute, the increment in plasma aldosterone levels in normotensive subjects (4.2 +/- 0.6 ng/dl) was significantly less (P less than 0.001) than that in patients with essential hypertension (19 +/- 3 ng/dl). In both groups, a significant rise in mean arterial blood pressure occurred at an A II dose of 0.3 ng/kg per minute, but the pressor response of the hypertensive group was significantly greater at the highest infusion rate (3 ng/kg per minute) (P less than 0.05). Thus, enhanced adrenal and pressor responsiveness to infused A II was observed in the hypertensive subjects, suggesting a change in A II receptor affinity.     

醛固酮合酶基因多态性与高血压患者血压及RAAS激素水平的相关性研究

目的探讨醛固酮合酶(CYP11B2)基因-344C/T多态性与高血压患者血压及肾素-血管紧张素-醛固酮系统(RAAS)激素水平的相关性。方法用放射免疫法检测171例原发性高血压患者(92例男性,79女性)RAAS激素水平,包括血浆肾素活性(PRA)、血浆血管紧张素II(AT-II)和醛固酮(ALD)水平。用聚合酶链反应(PCR)和限制性酶切方法检测所有患者的CYP11B2基因-344C/T多态性,按CC、CT和TT三种基因型分组。分析其与高血压患者血压及RAAS激素水平的相关性。结果 CYP11B2基因-344C/T多态性与高血压患者血压及血浆PRA和AT-II水平无关,但与血浆ALD水平相关,TT和CT基因型者的血浆ALD水平要高于CC基因型者,其差异有统计学意义(0.66±0.36or0.61±0.35versus0.42±0.23nmol/L,P=0.036)。结论本研究显示,高血压患者的CYP11B2基因-344C/T多态性与血浆ALD水平相关,提示该多态性可能参与了高血压患者血浆ALD水平的调节。     

Failure of renin suppression by angiotensin II in hypertension

Angiotensin II was infused at rates varying from 0.1 to 10 ng/kg per minute into 49 subjects with hypertension and 26 normotensive subjects and changes in blood pressure, plasma angiotensin II, and plasma renin activity (PRA) were determined after 20 and 30 minutes at each dose. Similar dose-related increases in angiotensin II and blood pressure occurred with a threshold of 1 ng/kg per minute in the normotensive and hypertensive subjects. Whereas angiotensin II induced a significant, dose-related decrement in renin activity in the normotensive subjects, with a threshold of 1.0 ng/kg per minute, no significant change in renin activity occurred in either the normal-renin or high-renin hypertensive subjects. In a separate study, nine normotensive and six hypertensive sodium-restricted subjects were given a converting enzyme inhibitor, SQ 20881, 30 microgram/kg. Despite a significantly greater fall in blood pressure (P less than 0.006) and angiotensin II concentration (P less than 0.045) in the hypertensive subjects, they did not have a greater rise in plasma renin activity. We conclude that angiotensin II reduces renin release in normal man at infusion rates that yield plasma angiotensin II levels within the physiological range but has a strikingly reduced influence on renin release in hypertension. In high-renin hypertension due to renal artery stenosis or nephrosclerosis, renin release is presumed to be relatively autonomous because of a dominant, intrarenal mechanism. The mechanism in normal-renin essential hypertension is not clear, but the abnormality could well be related to the pathogenesis of the hypertension.     

血管紧张素转换酶抑制剂对阻塞性睡眠呼吸暂停低通气综合征合并高血压患者睡眠呼吸障碍干预效应的研究

目的 研究血管紧张素转换酶抑制剂(ACEI)对于阻塞性睡眠呼吸暂停低通气综合征(OSAHS)合并高血压患者睡眠呼吸障碍的干预效应.方法 63例经多导睡眠图证实的OSAHS患者被纳入本研究(男54例,女9例),平均年龄(53±12)岁,按照其病情和服药情况分为3组,OSAHS无高血压组(A组)21例,OSAHS合并高血压...     

Beta-adrenergic receptor blockade as a therapeutic approach for suppressing the renin-angiotensin-aldosterone system in normotensive and hypertensive subjects.

Although beta-adrenergic-blocking drugs suppress the renin system (RAAS), plasma angiotensin II (Ang II) responses during beta-blockade have not been defined. This study quantifies the effects of beta-blockade on the RAAS and examines its impact on prorenin processing by measuring changes in the ratio of plasma renin activity (PRA) to total renin. In normotensive (N = 14) and hypertensive (N = 16) subjects, blood pressure (BP), heart rate, PRA, plasma prorenin, plasma total renin (prorenin + PRA), ratio of PRA to total renin (%PRA), plasma Ang II, and urinary aldosterone were measured before and after 1 week of beta-blockade. Plasma renin activity, Ang II, and urinary aldosterone levels were similar for normotensive and hypertensive subjects. Plasma renin activity correlated with Ang II. Total renin, which is proportional to (pro)renin gene expression, was lower in hypertensive subjects and was inversely related to BP. Beta-blockade decreased BP and heart rate in both groups, with medium- and high-renin hypertensive subjects responding more frequently than those with low renin. Beta-blockade consistently suppressed PRA, Ang II, and aldosterone. Total renin was unchanged, thus, %PRA fell. These results indicate that beta-blockers suppress plasma angiotensin II levels, in parallel with the marked reductions in PRA and urinary aldosterone levels in normotensive and hypertensive subjects. The suppression of Ang II levels was comparable to that produced during angiotensin converting enzyme (ACE) inhibition. However, by reducing prorenin processing to renin, beta-blockers do not stimulate renin secretion, unlike ACE inhibitors and Ang II receptor antagonists. This unique action of beta-blockers has important implications for the treatment of cardiovascular disease.     

Nisoldipine--effects on the renin-angiotensin-aldosterone system and catecholamines. Studies in normotensive and hypertensive subjects

We have studied the effects of nisoldipine, a new calcium channel antagonist, on the renin-angiotensin-aldosterone system and on plasma catecholamines in 10 healthy volunteers and in 29 patients with primary essential hypertension. Of these 29 patients, thirteen had normal renin hypertension (NRH), and sixteen had low renin hypertension (LRH). Eight healthy volunteers received placebo. Short-term (24 h) effects were measured in all subjects and long-term (up to 6 months) effects of 10-40 mg nisoldipine daily were monitored in the 29 hypertensive patients. Plasma renin activity (PRA) increased slightly, although this rise was not statistically significant, 1 h after the first dose of nisoldipine in both normotensive subjects and hypertensive patients. After 2 h PRA had returned to the pre-treatment level. No change in PRA was observed after administration of placebo. Plasma angiotensin II (AII) levels showed considerable variation after nisoldipine administration. Plasma aldosterone levels decreased despite the increase in PRA and AII concentrations. However, no concomitant reduction in urinary aldosterone excretion was observed. Plasma noradrenaline levels increased slightly 2-4 h after administration of nisoldipine, and decreased again thereafter, but no changes in plasma adrenaline levels were seen. Nisoldipine had no long-term effects on the renin-angiotensin-aldosterone system or on serum catecholamine levels.     

老年原发性高血压患者动态血压参数与部分体液因素的相关性研究

目的观察老年原发性高血压患者动态血压参数与血浆肾素、血管紧张素Ⅱ及醛固酮的相关性及其临床意义。方法将162例患者分为A纽82例（〉60岁）,B组80例（〈60岁）,采用放射免疫法检测162例原发性高血压患者的血浆肾素、血管紧张素Ⅱ及醛固酮水平,同时测定24h动态血压,进行相关分析。结果（1）老年高血压具有是脉压增大,波动性大,晨峰高血压现象及并发症多的特点;（2）A组血浆肾素、血管紧张素Ⅱ及醛固酮水平明显高于B组;（3）血浆肾素、血管紧张素Ⅱ及醛固酮与老年高血压的特点,特别是脉压增大、波动性大、晨峰高血压现象有关。结论老年原发性高血压患者血浆肾素和血管紧张素Ⅱ浓度升高,提示血浆肾素、血管紧张素一醛固酮系统对老年原发性高血压心血管系统有影响,导致老年原发性高血压患者血压特征性的变化,血浆肾素、血管紧张素Ⅱ和醛固酮的测定可作为老年原发性高血压患者病情监测及治疗指标之一。     

The metabolic clearance of aldosterone decreases similarly during infusion of angiotensin II in patients with essential hypertension and in normal subjects.

To determine if the abnormally large increases in levels of plasma aldosterone which occur during infusion of angiotensin II in some patients with essential hypertension are due to abnormal decreases in the metabolic clearance of aldosterone, we measured clearances of aldosterone before and during infusion of angiotensin II in 12 patients with essential hypertension and in 10 normal subjects. The metabolic clearance of aldosterone in the patients and that in the normal subjects were the same before angiotensin II was infused and the clearances decreased similarly during infusion of angiotensin II. In agreement with our previous observations, the plasma aldosterone responses to angiotensin II were greater than normal in most of the patients with low renin essential hypertension. Thus, the brisk increases in levels of plasma aldosterone during infusion of angiotensin II in patients with essential hypertension reflect abnormally large increases in the secretion of aldosterone. These results add further support to the idea that adrenal sensitivity to angiotensin II is increased in some patients with essential hypertension.     

阻塞性睡眠呼吸暂停低通气综合征呼出气冷凝液8-异前列烷的昼夜变化及其意义

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea-hypopnea syndrome,OSAHS)患者呼出气冷凝液(exhaled breath condensate,EBC)8-异前列烷(8-isoprostane,8-isoPG)的昼夜变化及其意义.方法 采用德国JAEGER公司的呼出气收集器.收集40例OSAHS患者和30名正常对照者睡眠监测前后的EBC,同时采集睡眠监测后的血清,采用酶联免疫技术测定EBC及血清中8-isoPG的含量,并与睡眠监测指标进行相关性分析.结果 OSAHS组EBC中8-isoPG睡眠监测前为(13.08±1.42)ng/L、睡眠临测后为(14.93±1.39)ng/L(P<0.01).正常对照组EBC中8-isoPG睡眠监测前为(11.06±0.72)ng/L、睡眠监测后为(10.97±0.70)ng/L(P>0.05).OSAHS组睡眠监测后EBC及血清中8-isoPG比正常对照组升高,P<0.01.OSAHS患者睡眠监测后EBC 8-isoPG与血清8-isoPG呈正相关(r=0.685,P<0.01),与AHI呈正相关(r=0.650,P<0.05),与睡眠中最低血氧饱和度、基础血氧饱和度和平均血氧饱和度呈负相关(r=-0.406,-0.439,-0.454,P值均<0.05).结论 OSAHS患者存在夜间氧化应激反应增强,OSAHS患者早晨EBC中8-isoPG可以作为评价患者氧化应激状态和估计病情严重程度的较好指标.