Gastric mucosal injury due to hemorrhagic reperfusion and efficacy of Salvia miltiorrhizae extract F and cimetidine

AIM: To observe the gastric mucosal injury caused by hemorrhagic shock and reperfusion and to compare the effect between Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) on it. METHODS: A model of hemorrhage/reperfusion injury was produced by Itoh method. Wistar rats were randomly divided into three groups: 0.9% sodium chloride treatment group (NS group), SEF treatment group (SEF group), and CI treatment group (CI group). Saline, SEF and CI were injected respectively. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesion area in the gastric mucosa. The degree of gastric mucosal lesions was categorized into grades 0, 1, 2, 3. Atom absorption method was used to measure the intracellular calcium content. Radioimmunoassay was used to measure the concentrations of prostaglandins. RESULTS: IGML (%) and grade 3 (%) were 23.18±6.82, 58.44±9.07 in NS group, 4.42±1.39, 20.32±6.95 in SEF group and 3.74±1.56, 23.12±5.09 in CI group, and the above parameters in SEF group and CI group decreased significantly (IGML: SEF vs NS, t=6.712, P=0.000<0.01; CI vs NS, t=6.943, P=0.000<0.01; grade 3: SEF vs HS, t=8.386, P=0.000; CI vs HS, t=8.411, P= 0.000), but the grade 0 and grade 1 damage in SEF group (22.05±5.96, 34.12±8.12) and CI group (18.54±4.82, 30.15±7.12) were markedly higher than those in NS group (3.01±1.01, 8.35±1.95; grade 0: SEF vs HS, t=8.434, P=0.000<0.01; CI vs NS, t=7.950, P=0.000<0.01; grade 1: SEF vs NS, t =8.422, P=0.000<0.01; CI vs NS, t=8.448, P=0.000<0.01). The intracellular calcium content (μg/mg) in SEF group (0.104±0.015) and CI group (0.102±0.010) was markedly lower than that in NS group (0.131±0.019, SEF vs NS, t=2.463, P=0.038<0.05; CI vs HS, t=3.056, P=0.017<0.05). The levels (pg/mg) of PGE_2, 6-keto-PGF_(1α) and 6-keto-PGF_(1α)/TXB_2 were 540±183, 714±124,17.38±5.93 in NS group and 581±168, 737±102, 19.04±8.03 in CI group, 760±192,1 248±158, 33.42±9.24 in SEF group, and the above parameters in SEF group markedly raised (PGE_2: SEF vs NS, t=2.282, P=0.046<0.05; SEF vs CI, t=2.265, P=0.047<0.05; 6-keto-PGF_(1α): SEF vs NS, t=6.583, P=0.000<0.000; SEF vs CI, t=6.708, P=0.000<0.01; 6-keto-PGF_(1α)/TXB_2: SEF vs NS, t=3.963, P=0.003<0.001; SEF vs Cl, t=3.243, P=0.009<0.01), whereas TXB_2 level in SEF group (45.37±7.54) was obviously lower than that in NS group (58.28±6.74, t=3.086, P=0.014<0.05) and CI group (54.32±6.89, t=2.265, P=0.047<0.05). No significant difference was shown between NS group and CI group (PGE_2: t=0.414, P=0.688>0.05; 6-keto-PGF_(1α): t=0.310, P=0.763>0.05; TXB_2: t=1.099, P=0.298>0.05; 6-keto-PGF_(1α)/TXB_2: t=0.372, P=0.718>0.05). CONCLUSION: Both SEF and CI could inhibit reperfusioninduced injury in gastric mucosa, but with different mechanisms. SEF could not only enhance the protective effect of gastric mucosa, but also abate the injury factors, while CI can only abate the injury factors.     

老年阻塞性睡眠呼吸暂停低通气综合征患者咽部塌陷与病情严重程度的关系

目的　探讨老年期、非老年期阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)患者清醒和睡眠时咽部气道几何学变化与病情严重程度的关系。　方法　健康对照老年组 14名和非老年组 2 0名 ;OSAHS患者老年组 2 3名和非老年组 43名。分别行多导睡眠图 (PSG)和咽部磁共振 (MRI)扫描。　结果　 66例OSAHS患者经相关分析结果显示 :清醒静息时咽部最窄处面积 (S1)与睡眠时咽部最窄处面积 (S2 )变化一致 ;S2 越小 ,S1 S2 的差越大 (即睡眠时咽部气道塌陷越重 ) ;呼吸暂停 /低通气指数(AHI)越大 ,呼吸暂停指数 (AI)越大 ;动脉血氧饱和度低于 90 %的时间 (TSO2 <90 % )占总睡眠时间(TST)百分数 (TSO2 <90 % /TST)越大 ,最低氧饱和度 (SO2 nadir)越低。在OSAHS老年组AHI(AI+低通气指数 (HI)〕中 ,AI显著大于HI〔(2 6 8± 2 0 8)次 /h和 (15 2± 11 6)次 /h ,t =2 3 3 6,P <0 0 2 5〕。而OSAHS非老年组的最长阻塞性呼吸暂停时间 (最长OAT)显著短于最长阻塞性低通气时间 (最长OHT)〔(48 4± 2 8 6)s和 (70 2± 3 5 3 )s,t =3 146,P <0 0 0 1〕 ;其最长OAT亦显著短于OSAHS老年组〔(48 4± 2 8 6)s和 (69 8± 3 8 3 )s,t =2 3 43 ,P <0 0 2 5 )。　结论　OSAHS患者咽部气道的狭窄、塌陷程度与病情严重程度显著相关 ;     

阻塞性睡眠呼吸暂停低通气综合征患者睡眠时的呼吸中枢反应性与夜间低氧血症的关系

目的　探讨阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)患者夜间低氧血症与呼吸中枢反应性的关系。方法　应用动态脉搏容积血氧饱和度 (SpO2 )仪定量分析了 2 4例白天二氧化碳分压(PaCO2 )≥ 4 5mmHg(高CO2 组 ,1mmHg=0 133kPa)及 39例PaCO2 <4 5mmHg(等CO2 组 )的OSAHS患者夜间低氧血症的严重程度。进一步应用重复呼吸法测定了其中 15例患者 (等CO2 组 11例 ,高CO2 组 4例 )睡眠状态下呼吸中枢的低氧及高CO2 反应性。结果　 6 3例患者的睡眠呼吸暂停低通气指数 (AHI)平均为 (5 4± 2 1)次 /h ;夜间动态SaO2 监测发现高CO2 组与等CO2 组比较 ,每小时氧减饱和4 %以上的次数 (ODI4)为 (43± 2 3)次 /hvs (2 9± 18)次 /h ;SaO2 <90 %的时间占总睡眠时间的百分数(SIT90 )为 (39± 32 ) %vs(15± 18) % ,高CO2 组均较等CO2 组高 ;而睡眠时的最低SaO2 (LSaO2 )为 (5 6± 18) %vs (6 6± 16 ) % ,平均SaO2 (MSaO2 )为 (86± 12 ) %vs(93± 5 ) % ,均较等CO2 组低 (P <0 0 1) ,提示其夜间缺氧程度更重。在清醒状态下 ,高CO2 组及等CO2 组患者的高CO2 反应 (ΔP0 1/ΔPaCO2 )、低氧反应 (ΔP0 1/ΔSaO2 )、口腔阻断压 (P0 1)差异均无显著性 (P >0 1)。进入非快动眼睡眠 (NREM)及快动眼睡眠 (REM)后 ,高CO2 组     

阻塞型睡眠呼吸暂停综合征与胰岛素抵抗的关系

目的　探讨阻塞型睡眠呼吸暂停综合征 (OSAS)低氧与胰岛素抵抗之间的关系及持续正压通气 (CPAP)治疗OSAS对胰岛素抵抗的影响。方法　分析 6 1例OSAS患者CPAP治疗前后及 16例未治疗OSAS患者多导睡眠监测各项指标与空腹血糖、胰岛素和餐后 2h血糖、胰岛素的关系 ,另选择 5 6例不符合SAS诊断者为对照组。结果　OSAS组治疗前呼吸紊乱指数 ( 36 .4±18.2 )次 /h ,最低氧饱和度 ( 74.5± 6 .2 ) % ,餐后血糖 ( 10 .6± 2 .4)mmol/L ,餐后胰岛素 ( 6 9.7±2 7.7)uIU/ml,胰岛素敏感性 ( 0 .8± 0 .2 )。CPAP治疗第 10天复查上述各项指标结果分别为 ( 3.3± 3.4)次 /h、( 86 .5± 1.3) %、( 7.2± 0 .6 )mmol/L、( 39.7± 10 .2 ) μIU/ml、1.2± 0 .2。P值分别 <0 .0 1、<0 .0 1、<0 .0 5、<0 .0 1、<0 .0 1。结论　OSAS组治疗前血浆胰岛素和血糖比对照组高 ,治疗后OSAS组比未治疗组低。表明OSAS低氧可产生胰岛素抵抗。     

扩张性心肌病并心力衰竭患者双室同步起搏治疗对心率变异性的影响

观察双室同步起搏对扩张性心肌病并心力衰竭 (简称心衰 )患者心功能及心率变异性 (HRV)的影响。选择1 5例扩张性心肌病并顽固心衰患者 ,置入双室起搏器 ,观察心功能、HRV及血浆丙二醛、一氧化氮、内皮素 1、血管紧张素 Ⅱ的变化。结果 :心功能NYHA分级从术前 3.32± 0 .31级提高为 2 .1 8± 0 .33级 ,左室射血分数由 0 .2 9± 0 .0 3增至 0 .36± 0 .0 3(P <0 .0 5 ) ;2 4h正常RR间期均值标准差、相邻RR间期差值均方根、相邻RR间期差值 >5 0ms占正常RR间期数的百分比、总功率、低频及高频波段功率分别由 73± 8.1ms、4 1± 8.0ms2 、5 .3%± 1 .5 %、1 0 2 4± 4 1 3ms2 、1 1 5± 35ms2 及 4 8± 1 5ms2 增至 1 0 7± 1 3ms、70± 1 1ms2 、1 1 .3%± 3.4 %、1 92 1± 4 84ms2 、1 94± 35ms2 及 91± 2 9ms2 (P均 <0 .0 1 ) ;血浆丙二醛、内皮素 1分别由 4 31± 37nmol/L、83.1± 2 1ng/L降至 32 3± 2 9nmol/L、6 7.3± 1 6ng/L ,一氧化氮由 38.1± 7.6 μmol/L增至 5 1 .3± 9.2 μmol/L(P均 <0 .0 1 ) ,血管紧张素 Ⅱ无变化 (P >0 .0 5 )。结论 :同步起搏改善扩张性心肌病心衰患者心功能及HRV。     

STOP-Bang问卷及Epworth嗜睡评分预测OSAHS及与睡眠相关性研究

目的探讨STOP-Bang问卷(SBQ)和Epworth嗜睡评分(ESS)在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)诊断和评估睡眠质量中的价值。方法以51名鼾症患者为研究对象,行整夜多导睡眠监测前接受SBQ和ESS评估。结果 (1)单纯鼾症组与OSAHS组SBQ、ESS,非快动眼睡眠(Ⅰ期、Ⅱ期、Ⅲ+Ⅳ期)及快动眼睡眠(REM)、觉醒次数和微觉醒指数比较差异显著(P0.05)。(2)SBQ≥3分筛查OSAHS灵敏度、特异度分别为89.50%、30.80%;ESS≥9分筛查OSAHS灵敏度、特异度分别为78.90%、69.20%;SBQ≥3与ESS≥9筛查OSAHS的差异有统计学意义(χ~2=7.513,P=0.006)。(3)SBQ与呼吸暂停/低通气指数(AHI)、Ⅱ期睡眠、觉醒次数、微觉醒指数正相关(P0.05),与Ⅲ+Ⅳ期睡眠(%)和REM睡眠(%)负相关(P0.05)。ESS与AHI、Ⅰ期睡眠、Ⅱ期睡眠、觉醒次数、微觉醒指数正相关(P0.05),与Ⅲ+Ⅳ期睡眠(%)和REM睡眠(%)负相关(P0.05)。结论 SBQ与ESS均能预测OSAHS、评估OSAHS睡眠质量,两者联合使用优于单一量表。     

阻塞性睡眠呼吸暂停综合征患者血小板活化的研究

目的　探讨阻寒性睡眠呼吸暂停综合征患者体内血小板的活化状态。方法　用流式细胞仪检测 30例OSAS患者和 30例正常对照者外周血小板的α颗粒膜糖蛋白 - 14 0 (CD6 2P)、血小板质膜表面糖蛋白GpⅡb/GPⅢa复合物(CD4 1/CD6 1)的表达。结果　中、重度OSAS患者的CD6 2p和CD4 1/CD6 1表达阳性率 [( 7 77±12 0 5) %、( 3 4 5± 9 4 9) % ]和平均荧光强度 [( 5 4 9± 6 94 ) %、( 4 56± 10 0 2 ) % ]均明显高于正常对照组 [( 4 32± 5 6 9) %、( 0 4 2± 0 18) %、( 3 98±5 18) %和 ( 2 4 4± 0 4 9) % ]P <0 0 0 5。结论　中、重度OSAS患者存在明显的血小板活化 ,这可能是OSAS患者发生心脑血管并发症的机制之一。     

睡眠呼吸暂停综合征患者氧亲和力的变化

目的 :了解睡眠呼吸暂停综合征 (SAS)患者P50 (即血红蛋白氧饱和度 5 0 %时相应的氧分压 )是否有改变 ,探讨P50 与夜间血氧饱和度的相关性以及P50 可否预测SAS患者的病情严重程度。方法 :随机选择SAS患者 5 6例 ,其平均睡眠呼吸暂停 低通气指数 (AHI)为 (3 7 5 1± 2 0 2 1)次 h ,平均夜间血氧饱和度为 86 5 2 %± 1 91% ,清醒时的血氧饱和度为 95 2 0 %± 1 40 % ,并选择正常人 42例作为对照组进行P50 水平的测试。 11例患者经持续气道正压通气 (CPAP)治疗后重复进行测试。结果 :1 SAS患者日间P50 值为 (2 9 2 7± 1 3 1)mmHg(1mmHg=0 13 3kPa) ,对照组为 (2 7 63± 1 0 1)mmHg,二者存在显著性差异 (P <0 0 5 ) ;2 SAS患者P50 与夜间平均血氧饱和度呈明显负相关 (r=- 0 962 1,P <0 0 5 ) ;3 11例SAS患者经CPAP治疗 3个月后 ,P50 水平显著下降至 (2 7 2 7± 0 63 )mmHg,与正常对照组相比无显著性差异。结论 :1 SAS患者的氧离曲线右移 ,这可能是对组织低氧的一个保护性机制 ,以延迟肺动脉高压的形成 ,红细胞的增多及其它器官系统并发症的发生。 2 P50 能够反映SAS患者夜间低氧的严重程度 ,因而可以作为一个常规指标进行检测     

急性下壁心肌梗死胸前导联ST段压低与冠状动脉病变的关系及临床意义探讨

目的 :探讨急性下壁心肌梗死胸前导联ST段压低与冠状动脉病变的关系及临床意义。方法 :回顾分析 2 0 0 0年 7月至 2 0 0 2年 5月住院的首次急性下壁心肌梗死患者 6 0例。按胸前导联ST段压低范围将患者分为 4组 :无胸前导联ST段压低组 (Ⅰ组 ,n =2 2 ) ;胸前导联V1～ 3ST段压低组 (Ⅱ组 ,n =12 ) ;胸前导联V4～ 6 ST段压低组 (Ⅲ组 ,n =12 ) ;胸前导联V1～ 6 ST段压低组 (Ⅳ组 ,n =14 )。分析内容包括冠心病危险因素、心电图、心肌酶谱、心脏彩超、冠状动脉造影以及心肌梗死的并发症。结果 :左前降支 (LAD)病变发生率在Ⅰ与Ⅲ、Ⅳ各组分别为 4 7 1%、6 0 %、72 7% (P >0 0 5 ) ,而在Ⅱ组仅为 9 1% ,与Ⅰ组比较 ,Ⅱ组的LAD病变发生率低 (P <0 0 5 ) ,但Ⅰ组LAD病变程度较轻 ,>90 %狭窄者仅占 12 5 % ,而Ⅲ、Ⅳ组分别占 83 3%、87 5 % (P <0 0 5 ) ;回旋支 (LCX)病变在Ⅰ、Ⅱ、Ⅲ、Ⅳ组分别占 17 6 %、4 5 5 %、6 0 %、6 3 6 % ,与Ⅰ组比较 ,Ⅲ、Ⅳ各组的LCX病变发生率较高 (P <0 0 5 ) ,且Ⅳ组多支病变比例较高 (P <0 0 5 ) ;左室射血分数 (LVEF)在Ⅰ、Ⅱ、Ⅲ、Ⅳ组分别为 0 6 3± 0 0 5、0 6 2± 0 0 6、0 5 5± 0 10、0 5 1± 0 13,与Ⅰ组相比 ,Ⅳ组的LVEF较低 (P <0 0 5 ) ;低血压状?     

血管紧张素Ⅱ对内皮依赖性血管舒张功能的影响

目的 :探讨血浆中血管紧张素Ⅱ (AngⅡ )水平与肱动脉内皮依赖性舒张功能的关系。 方法 :测定冠心病 (CHD)组 30例、原发性高血压 (EH)组 2 8例、EH并发CHD(EH加CHD)组 39例和正常对照组 2 0例的血脂、AngⅡ、vWF、内皮素 1(ET 1)、一氧化氮 (NO)水平以及反应性充血时和含服硝酸甘油后肱动脉内径的变化。结果 :EH组、CHD组和EH加CHD组血流介导的肱动脉舒张 (FMD)和硝酸甘油所致的肱动脉舒张均低于对照组 [分别为 (7.32± 4 .36 )、(5 .6 2± 3.0 9)和 (3.72± 3.0 6 ) %∶(14 .2 1± 7.71) %以及 (17.82± 6 .0 0 )、(12 .6 1±4 .2 9)和 (9.5 2± 4 .85 ) %∶(19.33± 9.6 2 ) % ,均P <0 .0 5 ]。多因素线性逐步回归分析显示 :在CHD组和EH加CHD组与血清高密度脂蛋白胆固醇 (HDL C)水平呈正相关 [分别为 (r =0 .317,P <0 .0 1)和 (r =0 .2 98,P <0 .0 1) ],EH加CHD组与血浆AngⅡ水平呈负相关 (r =- 0 .4 71,P <0 .0 1) ;剔除HDL C影响因素后仍呈负相关 (r =- 0 .2 84 ,P >0 .0 1) ,硝酸甘油所致的肱动脉舒张与上述各因素无关。根据FMD程度将 4组受试者合并后再分为A、B两组 ,A组FMD≤ 5 % ,B组FMD >5 % ,结果显示 ,A组的AngⅡ和ET 1明显高于B组 [分别为(10 1.4 5± 13.4 2 )∶(35 .6 4± 9.6 2 )ng/L和     

阻塞性睡眠呼吸暂停综合征的睡眠结构改变

目的研究阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）病情严重程度及持续气道内正压（ＣＰＡＰ）治疗对睡眠结构的影响。方法通过分析多导睡眠图，分析了３１例非ＯＳＡＳ者和１４７例ＯＳＡＳ患者的睡眠结构及ＣＰＡＰ治疗对１１例ＯＳＡＳ患者睡眠结构的影响。结果与对照组相比ＯＳＡＳ组的睡眠结构存在如下异常：（１）睡眠期转换次数（ＯＳＡＳ组：１２０±７１，对照组：９２±６０，Ｐ＝０．０１０６）、快波睡眠次数（ＯＳＡＳ组：８８±５４，对照组：６５±４５，Ｐ＝０．００７５）、醒觉次数（ＯＳＡＳ组：２７±２８，对照组：１９±１８，Ｐ＝０．０１７）差异有显著性；（２）慢波睡眠次数（ＯＳＡＳ组：５±９，对照组：８±８，Ｐ＝０．００３５）、占总睡眠时间的比例（ＯＳＡＳ组：５％±８％，对照组：８％±９％，Ｐ＝０．００６２）及慢波睡眠的缺乏率（ＯＳＡＳ组：４８％，对照组：２６％，Ｐ＜０．０５）亦明显不同；（３）睡眠呼吸紊乱指数低于２５的ＯＳＡＳ者与对照组比较睡眠各参数相差不大；（４）ＣＰＡＰ治疗能使上述参数得到不同程度的改善。结论ＯＳＡＳ主要引起睡眠的破碎、深睡减少及浅睡增加，且与病情的严重程度有一定关系。ＣＰＡＰ治疗能够改善这些紊乱。     

阻塞性睡眠呼吸暂停综合征患者睡眠状态下呼吸中枢控制功 …

目的 探讨阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）患者上气道阻塞与睡眠状态下呼吸中枢控制功能的低下是否有关，方法 通过经鼻气管插管建立鼻咽通气道测定了１６例重度ＯＳＡＳ患者在清楚状态，非快动眼（ＮＲＥＭ）Ｉ＋Ⅱ睡眠期，Ⅲ＋Ⅳ睡眠期，快速眼（ＲＥＭ）睡眠期的口腔阻断压（Ｐ０．１）低氧反应指标（△Ｐ０．１／△ＳａＯ２，△ＶＥ／△ＳａＯ２）及高二氧化碳反应指标（△Ｐ０．１／△ＳａＯ２，△ＶＥ／△ＳａＯ２）。     

Short-term effects of oral theophylline in addition to CPAP in mild to moderate OSAS

Theophylline is effective in the treatment of central apneas and periodic breathing. In obstructive sleep apnea syndrome (OSAS), results of pharmacological monotherapy with theophylline are inconsistent. The present study investigates whether additional theophylline in patients with OSAS and continuous positive airway pressure (CPAP) therapy might improve ventilation, lower effective CPAP pressure levels or affect sleep architecture. Patients with mild to moderate OSAS (mean apnea index [AI] 12.8+/-11.7) and CPAP therapy (Autoset system; n=16, all male) received either 900 mg of oral sustained-release theophylline (T) or placebo (P) on two separate nights, 3 days apart, using a randomized double-blind crossover study design. There was no change in AI (T: 0.7+/-1.4 vs. P: 0.7+/-0.6/h; P=0.3) or apnea-hypopnea index (AHI; T: 4.3+/-3.3 vs. P: 4.5+/-3.7/h; P=0.84) when theophylline was added to CPAP therapy. We observed no difference in mean CPAP pressure (T: 6.9+/-2.1 vs. P: 6.7+/-1.9 cm H2O; P=0.7) or 95% pressure percentiles (T: 9.7+/-2.7 vs. P: 9.3+/-2.1cm H2O; P=0.3) when nights with theophylline were compared to placebo nights. Theophylline reduced significantly total sleep time (T: 290.6+/-58.9 vs. P: 338.0+/-40.1 min; P=0.02) and thus sleep efficiency (SE; T: 70.5+/-14.9%, P: 82.0+/-70.5%; P=0.005). Rapid eye movement and slow wave sleep were not affected. Oral theophylline did not show any additional effects on ventilation parameters or pressures in patients with mild to moderate OSAS once CPAP therapy has been successfully installed. SE was reduced with theophylline with unchanged sleep architecture. The role of oral theophylline may be in patients with predominately central apneas not eligible for ventilation therapy or severe cases.     

Assessment of continuous positive airway pressure treatment in obstructive sleep apnea syndrome using 24-hour urinary catecholamines

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is related to diurnal sympathetic hyperactivity and increased blood pressure, both factors that are likely to lead to the development of cardiovascular disease. HYPOTHESIS: The study investigated whether 24-h urinary catecholamines would reflect the effect of obstructive sleep apnea on autonomic activity. METHODS: Standard polysomnography was performed in 17 patients with OSAS (age 53.7 +/- 13.5 years, mean +/- standard deviation). The number of apnea/hypopnea episodes per hour of sleep (apnea/hypopnea index [AHI]); number of oxygen desaturation episodes per hour (desaturation index [DSI]); arousals per hour (arousal index); lowest oxygen saturation (lowest SpO2); and percentages of stages 1, 2, 3/4, and rapid eye movement sleep (% stage 1, -2, and -3/4, and % REM, respectively) were measured. Overnight continuous positive airway pressure (CPAP) titration was performed the night after the baseline sleep measurements had been taken. Twenty-four-hour urinary adrenaline and noradrenaline were also examined. RESULTS: During the CPAP treatment, both 24-h urinary adrenaline and noradrenaline were significantly lower compared with natural sleep. Continuous positive airway pressure significantly decreased the AHI, DSI, % stage 1, and arousal index and significantly increased the lowest SpO2. There were no significant differences in % stage 2, % stage 3/4, and % REM between before and during CPAP treatment. Multiple analysis of covariance tests revealed that lowest SpO2 was the most important factor for increasing 24-h urinary noradrenaline levels (F = 4.75, p = 0.048). CONCLUSIONS: One night CPAP treatment could improve autonomic dysfunction. The assessment of 24-h urinary noradrenaline would provide important information for evaluating the effect of CPAP treatment.     

Genioglossus activity during sleep in normal control subjects and children with obstructive sleep apnea

Children with obstructive sleep apnea syndrome (OSAS) have more collapsible airways compared with normal subjects, yet sustain stable breathing during wakefulness and part of sleep. This indicates successful neuromuscular compensation. Using a custom intraoral surface electrode to record pharyngeal dilator muscle activity (the genioglossus [EMGgg] normalized to the wakeful baseline), we performed overnight polysomnograms in three groups of children: (1) patients with OSAS without continuous positive airway pressure (CPAP) (n = 13); (2) patients with OSAS with CPAP (n = 5); and (3) control subjects without CPAP (n = 13). Our objective was to evaluate the EMGgg as a function of sleep state and during disordered breathing, compared with stable sleep and wakefulness. In control subjects, the EMGgg decreased from wakefulness to Stage 2 (mean +/- SD, 65 +/- 6%), and further during REM (51 +/- 9%) (p < 0.05). In patients with OSAS, the EMGgg for apneic breaths during REM (37 +/- 9%) was lower than during stable breathing (83 +/- 17%) (p < 0.05) and wakefulness (p < 0.05). CPAP lowered the EMGgg in patients with OSAS during all sleep states. These data indicate that (1) EMGgg compensatory mechanisms remain active during sleep in patients with severe OSAS; (2) EMGgg reductions are temporally associated with sleep apnea events; and (3) REM sleep is associated with the lowest and most variable EMGgg.     

Sleep in critically ill patients requiring mechanical ventilation

STUDY OBJECTIVES: To objectively measure sleep in critically ill patients requiring mechanical ventilation and to define selection criteria for future studies of sleep continuity in this population. DESIGN: Prospective cohort analysis. SETTING: University teaching hospital medical-surgical ICU. PATIENTS: Twenty critically ill (APACHE II [acute physiology and chronic health evaluation II] acute physiology score [APS], 10 +/- 5), mechanically ventilated adults (male 12, female 8, age 62 +/- 15 years) with mild to moderate acute lung injury (lung injury score, 1.8 +/- 0.9) 10 +/- 7 days after admission to the ICU. MEASUREMENTS AND RESULTS: Patients were divided into three groups based on 24-h polysomnography (PSG) findings. No patient demonstrated normal sleep. In the "disrupted sleep" group (n = 8), electrophysiologic sleep was identified and was distributed throughout the day (6:00 AM to 10:00 PM; 4.0 +/- 2.9 h) and night (10:00 PM to 6:00 AM; 3.0 +/- 1.9 h) with equivalent proportions of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Nocturnal sleep efficiency was severely reduced (38 +/- 24%) with an increased proportion of stage 1 NREM sleep (40 +/- 28% total sleep time [TST]) and a reduced proportion of REM sleep (10 +/- 14% TST). Severe sleep fragmentation was reflected by a high frequency of arousals (20 +/- 17/h) and awakenings (22 +/- 25/h). Electrophysiologic sleep was not identifiable in the PSG recordings of the remaining patients. These were classified either as "atypical sleep" (n = 5), characterized by transitions from stage 1 NREM to slow wave sleep with a virtual absence of stage 2 NREM and reduced stage REM sleep, or "coma" (n = 7), characterized by > 50% delta or theta EEG activity with (n = 5) and without (n = 2) evidence of EEG activation either spontaneously or in response to deep painful stimuli. The combined atypical sleep and coma groups had a higher APS (13 +/- 4 vs 6 +/- 4) and higher doses of sedative medications than the disrupted sleep group. CONCLUSION: Sleep, as it is conventionally measured, was identified only in a subgroup of critically ill patients requiring mechanical ventilation and was severely disrupted. We have proposed specific criteria to select patients for future studies to evaluate potential causes of sleep disruption in this population.     

Daytime sleepiness and EEG spectral analysis in apneic patients before and after treatment with continuous positive airway pressure

BACKGROUND: Obstructive sleep apnea syndrome (OSAS) is characterized by recurrent apneas during sleep, resulting in repetitive hypoxemic episodes and interruptions of the normal sleep pattern. A previous study showed EEG slowing (ie, a higher ratio of delta + theta frequencies to alpha + beta frequencies on EEG) during rapid eye movement (REM) sleep and wakefulness in untreated OSAS patients. STUDY AND OBJECTIVES: To determine whether EEG slowing is reversible with continuous positive air pressure (CPAP) treatment and to verify whether the persistence of excessive daytime sleepiness (EDS) is correlated with residual slowing of the EEG. PATIENTS: Ten healthy subjects (9 men and 1 woman) and 14 patients with moderate-to-severe OSAS (13 men and 1 woman) were studied before and after 6 months of treatment with CPAP. RESULTS: Untreated OSAS patients showed EEG slowing in frontal and central cortical regions during both wakefulness and during REM sleep compared to healthy control subjects. This EEG slowing was found to be independent of time spent with arterial oxygen saturation < 90%, severity of OSAS, or mean sleep latency as determined by the multiple sleep latency test. CPAP treatment was found to correct the EEG slowing for both REM sleep and wakefulness. Daytime sleepiness also greatly improved with treatment, but some degree of somnolence remained. CONCLUSION: CPAP treatment was found to correct the EEG slowing that was observed in untreated OSAS patients. Persistent EDS may be related to persistent obesity after CPAP treatment.     

Effect of ethanol on the efficacy of nasal continuous positive airway pressure as a treatment for obstructive sleep apnea

The effect of ethanol ingestion on the efficacy of nasal continuous positive airway pressure (nasal CPAP) as a treatment for the obstructive sleep apnea (OSA) syndrome was studied in ten obese male subjects undergoing this therapy. On the first night of polysomnography, the lowest level of CPAP that maintained airway patency was determined (critical level). On the second (control) night (C), subjects slept the entire night on this level of CPAP. On the third night (E), subjects ingested either 1.5 ml/kg (part A, N = 6) or 2.0 ml/kg (part B, N = 4) of 50 percent ethanol (100 proof vodka) over one half-hour starting 1 h before bedtime. A serum ethanol level was obtained at bedtime (part A: 63.7 +/- 17.3 mg/dl; part B: 108.6 +/- 20.6 mg/dl), and subjects were monitored on the critical level of CPAP. Comparison of nights C and E for parts A + B showed no difference in total sleep time (TST) or the amount of different sleep stages as an absolute time or a percentage of TST except that there was more stage 2 (as a percent of TST) on E nights. The apnea + hypopnea index and C and E nights did not differ and was quite low (3.6 +/- 3.7/h vs 1.9 +/- 2.7/h). Similarly, ethanol ingestion did not increase the number of desaturations to at or below 90 and 85 percent, or lower the mean arterial oxygen saturation in NREM or REM sleep. Analysis of parts A and B separately also showed no differences with respect to the apnea + hypopnea index or the number of desaturations on control and ethanol nights. We conclude that acute moderate ethanol ingestion does not decrease the efficacy of an optimum level of nasal CPAP.     

In vivo platelet activation is increased during sleep in patients with obstructive sleep apnea syndrome

BACKGROUND: Patients with obstructive sleep apnea syndrome (OSAS) have an increased risk of cardiovascular events including myocardial infarction and stroke. OBJECTIVE: To determine whether in vivo platelet activation and the generation of procoagulant platelet-derived microparticles (PMP) are increased during sleep in patients with OSAS. METHODS: In vivo platelet activation and PMP formation was determined using flow cytometry in 12 patients with untreated OSAS during and after sleep (4 and 7 a.m.). To study the effect of treatment with continuous positive airway pressure (CPAP), the measurements were repeated at the same time points after initiation of CPAP therapy. Healthy volunteers served as controls (n = 6). RESULTS: Patients with OSAS had an increased percentage of platelets positive for the activation-dependent epitopes CD63 and CD62P during sleep (4 a.m.) compared to controls (4.8 +/- 0.8 vs. 1.9 +/- 0.4% for CD63, p < 0.01, and 2.0 +/- 0.5 vs. 1.1 +/- 0.3% for CD62P, p < 0.05). In OSAS patients, the amount of CD63- and CD62P-positive platelets was significantly elevated at 4 compared to 7 a.m. (4.8 +/- 0.8 vs. 2.6 +/- 0.4% for CD63 and 2.0 +/- 0.5 vs. 1.1 +/- 0.2% for CD62P, p < 0.05), but not in the control group. The levels of PMP were similar in patients with OSAS and controls at 4 and 7 a.m. After 1 night of CPAP therapy, there was a trend to reduced levels of CD63- and CD62P-positive platelets at 4 a.m. CONCLUSIONS: Patients with OSAS have increased in vivo platelet activation during sleep, which may contribute to the increased incidence of cardiovascular events in patients with OSAS.     

Continuous positive airway pressure treatment improves baroreflex control of heart rate during sleep in severe obstructive sleep apnea syndrome

The role of the arterial baroreflex in the cardiovascular changes associated with the obstructive sleep apnea syndrome (OSAS), and the effect of nasal continuous positive airway pressure (CPAP) treatment on baroreflex function during sleep are unknown. Baroreflex control of heart rate was studied in 29 normotensive patients with OSAS under no treatment, in 11 age-matched control subjects, and in 10 patients at CPAP withdrawal after 5.5 +/- 3.7 (range 3-14) months of treatment. Baroreflex control of heart rate was assessed by "sequence method" analysis of continuous blood pressure recordings (Finapres) obtained during nocturnal polysomnography. In untreated OSAS, baroreflex sensitivity (BRS) was low during wakefulness and non-rapid eye movement (REM) stage 2 sleep compared with control subjects, and correlated inversely with mean lowest Sa(O(2)) and the blood pressure increase after apneas. After CPAP treatment, the apnea-hypopnea index was lower, and mean lowest Sa(O(2)) higher than before treatment. After CPAP, patients were more bradycardic, blood pressure and its standard deviation decreased as Sa(O(2)) improved in non-REM stage 2 sleep, and BRS increased (nocturnal wakefulness: +59%; non-REM stage 2 sleep: +68% over pretreatment values). Our data suggest that baroreflex dysfunction in OSAS may be at least partly accounted for by nocturnal intermittent hypoxemia, and can be reversed by long-term CPAP treatment.