血清层粘连蛋白、透明质酸及Ⅳ型胶原与肝纤维化不同组织学分级的关系

目的：探讨慢性肝炎血清检测指标层粘连蛋白（ Ｌ Ｎ） 、透明质酸（ Ｈ Ａ） 及Ⅳ型胶原（ Ⅳ－ Ｃ） 的临床意义及其与肝纤维化分期间的关系。方法：对１５２ 例各型肝病患者急性肝炎,慢性肝炎轻度、中度、重度及肝硬化与正常对照血清 Ｌ Ｎ、 Ｈ Ａ 及Ⅳ－ Ｃ 进行了测定,其中１０８ 例行肝脏穿刺,肝组织石蜡切片,常规 Ｈ Ｅ、网纤维及弹力纤维染色,肝纤维化病理诊断分五期（ Ｓ０ － Ｓ４） ,统计三者血清值。结果：慢性肝炎中、重度及肝硬化三者血清与对照组有显著性差异（ Ｐ＜ ０ ．０５） ,且呈现递增趋势,各病理组织学纤维化分期与血清指标成显著正相关（ｒ＝ ０ ．９８３ , Ｐ＜ ０ ．０１ ;ｒ＝ ０ ．９８０ , Ｐ＜ ０ ．０１ ;ｒ＝ ０ ．９９０ , Ｐ＜ ０ ．０１） 。结论：纤维化血清学指标有较好的临床诊断价值,血清学诊断慢性肝炎肝纤维化程度的具体数据范围可以确定,并可估计相对应病理组织学分期。     

进驻高原不同海拔高度不同时间健康青年血清心肌酶活性的变化

为探讨进驻高原不同海拔高度和不同居住时间健康青年血清心肌酶活性的变化,对从平原（海拔１４００ｍ）进驻海拔３７００ｍ和５３８０ｍ高度第７天及半年的８４名青年,进行血清ＡＳＴ、ＣＫ、ＬＤＨ．ａ－ＨＢＤＨ检测,并与平原健康青年作对照。结果表明,进驻高原ＡＳＴ、ＣＫ、ＬＤＨ及ａ—ＨＢＤＨ均显著高于平原（Ｐ＜００５或Ｐ＜００１）。进驻海拔达３７００ｍ,第七天较居住半年时ＬＤＨ显著增高（Ｐ＜００５）,ＡＳＴ、ＣＫ、ａ—ＨＢＤＨ虽然增高但无统计学差异（Ｐ＜００５）,进驻５３８０ｍ第７天较居住半年时的Ａ…     

高原肺水肿治疗前后血浆一氧化氮和心钠素含量的变化

目的：研究高原肺水肿的发生与血浆一氧化氮（ Ｎ Ｏ） 、一氧化氮合成酶（ Ｎ Ｏ Ｓ） 和心钠素（ Ａ Ｎ Ｐ） 的关系。方法：在海拔３ ７００ｍ 对１１ 例高原肺水肿患者在治疗前和治愈后分别检测其血浆 Ｎ Ｏ、 Ｎ Ｏ Ｓ和 Ａ Ｎ Ｐ含量，并与初入海拔３ ７００ ｍ 的１０ 名健康青年作对照。结果：高原肺水肿组 Ｎ Ｏ 治愈后较治疗前增高非常显著（ Ｐ＜ ０ ．０１） ， Ａ Ｎ Ｐ 降低非常显著（ Ｐ＜ ０ ．０１） ， Ｎ Ｏ Ｓ 无显著性差异（ Ｐ＞ ０ ．０５） ；治愈后 Ｎ Ｏ 和 Ａ Ｎ Ｐ显著低于健康青年组（ Ｐ＜ ０ ．０５） ，治疗前较健康青年 Ｎ Ｏ、 Ｎ Ｏ Ｓ降低非常显著（ Ｐ＜ ０ ．０１） ， Ａ Ｎ Ｐ 增高显著（ Ｐ＜ ０ ．０５） 。治疗前血浆 Ｎ Ｏ 含量与 Ｎ Ｏ Ｓ 活性呈高度正相关（ｒ＝ ０ ．８６４６ ， Ｐ＜ ０ ．０１） 。结论：血浆 Ｎ Ｏ、 Ｎ Ｏ Ｓ和 Ａ Ｎ Ｐ均参与了高原肺水肿的病理生理过程，血浆 Ａ Ｎ Ｐ含量升高可能是机体的一种保护性代偿机制。     

健身锻炼对老年男子身体素质的影响——Ⅱ.酶和自由基

为探讨健身锻炼对老年男子酶和自由基的影响,对照了５１名健身锻炼和４８名非锻炼老年男子血清酶活性和自由基水平。发现老年男子血清氧化还原酶活性处于成人正常值的中、下水平,血清ＳＯＤ活性低于成人正常值下限,血清ＭＤＡ含量接近成人正常值上限,健身锻炼可提高血清ＡＬＴ活性（Ｐ＜０．０５）,提高血清ＣＫ活性（Ｐ＜０．０５）,提高血清ＣＫ ＭＢ活性（Ｐ＜０．００１）,提高血清ＡＳＴ活性（Ｐ＞０．０５）,提高血清ＧＧＴ活性（Ｐ＞０．０５）,降低血清ＡＬＰ活性（Ｐ＜０．０５）,降低血清ＬＤＨ活性（Ｐ＜０．０５）,同时还可以提高血清ＳＯＤ活性（Ｐ＜０．０５）,降低血清ＭＤＡ含量。提示健身锻炼可改善老年男子酶代谢能力,有利于提高新陈代谢和抗氧化能力     

绞股蓝总皂甙对肝脏四氯化碳损伤保护作用的实验研究

给慢性四氯化碳（ＣＣ１＿４）肝损害小鼠灌喂绞股蓝总皂甙（ＧＰｓ），剂量为每次７５ｍｇ／ｋｇ或１５０ｍｇ／ｋｇ（每周５次，共３周），均能明显减轻肝组织损害，与未治疗组比较差异有显著意义（Ｐ＜０．０５和Ｐ＜０．０１）。用ＧＰｓ治疗的两组小鼠血清丙氨酸转氨酶（ＡＬＴ）活性均较未治疗组降低，血清白蛋白含量和Ａ／Ｇ比值较未治疗组升高。在原代培养大鼠肝细胞损伤模型上，预先用浓度为１０ｍｇ／Ｌ和４０ｍｇ／Ｌ的ＧＰｓ处理大鼠肝细胞，肝细胞ＤＮＡ合成速率分别从ＣＣ１＿４损伤组的３１．９％升高到６７．６％（Ｐ＜０．０５）和８２．４％（Ｐ＜０．０１）；肝细胞培养液中ＡＬＴ活性均明显低于损伤组（Ｐ＜０．０１）。表明ＧＰｓ能减轻ＣＣ１＿４诱导的小鼠慢性肝损害和离体大鼠肝细胞损伤，改善肝脏合成白蛋白的功能，保护肝细胞ＤＮＡ合成。     

高原肺水肿治疗前后几种血清酶和尿酸的变化

目的：探讨高原肺水肿治疗前后几种血清酶和尿酶的变化。方法：在海拔３７００ｍ对８例高原肺水肿患者在治疗前和临床治愈后检测其血清天冬氨酸氨基转移（ＡＳＴ），α－羟丁酸脱氢酶（α－ＨＢＤＨ）、肌酸激酶（ＣＫ）、乳酸脱氢酶（ＬＤＨ），血尿酸（ＵＡ）和尿液尿酸（ＵＵＡ）的含量，并以初入相同海拔高度第１０天的１０名健康青年为对照，。结果：治疗前较治愈后ＡＳＴ、ＵＡ、ＵＵＡ增高非常显著（Ｐ〈０．０１），α－ＨＢ     

L-精氨酸对缺氧性肺动脉高压大鼠内皮素释放的影响

为了探讨Ｌ—精氨酸（Ｌ－Ａｒｇ）对缺氧性肺动脉高压（ＨＰＨ）大鼠血浆内皮素释放的影响。本文建立了ＨＰＨ大鼠模型,将Ｗｉｓｔａｒ大鼠４０只分为;对照组、缺氧组、缺氧＋Ｎ－硝基Ｌ精氨酸甲脂（ＬＮＡＭＥ）组和缺氧ＬＡｒｇ组四组进行研究,结果显示：缺氧组的肺动脉平均压（ｍＰＡＰ）显著高于对照组（Ｐ＜００５）,缺氧组＋Ｌ－Ａｒｇ组的ＭＰＡＰ显著低于缺氧组（Ｐ＜００５）及缺氧＋Ｌ－ＮＡＭＥ组（Ｐ＜００１）,缺氧组的ＲＶ／（ＬＶ＋Ｓ）比值显著高于对照组（Ｐ＜００１）,缺氧＋ＬＮＡＭＥ组的ＰＶ…     

高压氧与一氧化氮对高原脱适应青年血流动力学的影响

目的：研究高压氧（ＨＢＯ）与一氧化氮（ＮＯ）对高原脱适应青年血流动力学的影响。方法：将海拔５０００ｍ以上居住１年返回海拔１４００ｍ的３６名青年随机分为：对照组;ＨＢＯ治疗组;ＮＯ治疗组。治疗前后分别用ＸＧⅢ型血液循环功能自动测试仪检测血流动力学。结果：对照组前后差别不显著（Ｐ＞０．０５）;ＨＢＯ组ＢＶ增加显著（Ｐ＜０．０５）,Ｐ、ＳＶ增加非常显著（Ｐ＜０．０１）,η降低非常显著（Ｐ＜０．０１）;ＮＯ组Ｐ、ＢＶ、ＳＶ、ｍＡＰ增加非常显著（Ｐ＜０．０１）,ＡＬＴ、ＰＡＷＰ降低显著（Ｐ＜０．０５）,ＴＰＲ、η降低非常显著（Ｐ＜０．０１）。结论：ＨＢＯ与ＮＯ对久居特高海拔返回后脱适应青年低排高阻性血流动力学有明显的增排降阻作用,吸入ＮＯ较ＨＢＯ效果更好     

HAPC患者红细胞2,3—二磷酸甘油酸的变化和红细胞ATP酶的活性

目的：了解红细胞２，３－二磷酸甘油酸、红细胞膜ＡＴＰ酶在高原红细胞增多症（ＨＡＰＣ）的变化及二者关系。方法：ＨＡＰＣ患者２４例，正常对照１９例，分别测定红细胞２，３－二磷酸甘油酸，红细胞膜ＡＴＰ酶（Ｎａ＋－Ｋ＋－ＡＴＰ酶，Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性。结果：ＨＡＰＣ组及对照组红细胞２，３－二磷酸甘油分别为：３．２１ｍｍｏｌ／Ｌ±０．１３ｍｍｏｌ／Ｌ，４．８７ｍｍｏｌ／Ｌ±０．０７ｍｍｏｌ／Ｌ，（Ｐ＜０．０５）；Ｎａ＋－Ｋ＋－ＡＴＰ酶活性分别为：４．１±０．０１３λΒ／μｍｏｌ·ｈ－１·ｇ－１，７．４±０．１９λΒ／μｍｏｌ·ｈ－１·ｇ－１（Ｐ＜０．０１）；Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性分别为１５．１±１．７０λΒ／μｍｏｌ·ｈ－１·ｇ－１，２５．３±２．３１λΒμｍｏｌ·ｈ－１·ｇ－１（Ｐ＜０．０１）；相关分析显示：２，３－二磷酸甘油酸与Ｎａ＋－Ｋ＋－ＡＴＰ酶呈正相关（ｒ＋０．４８１７，Ｐ＜０．０１）与Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶呈正相关（ｒ＝０．４７８３，Ｐ＜０．０１）。结论：ＨＡＰＣ患者红细胞２，３－二磷酸甘油酸的减少，红细胞膜ＡＴＰ酶活力降低，反映机体缺氧状况，体细胞代谢异常     

21天头低位(-6°)卧床前后下体负压和头高位倾斜暴露时的心血管反应

目的探讨２１天头低位（ＨＤＴ）卧床对人体立位应激下心血管反应的影响,以及比较下体负压（ＬＢＮＰ）和头高位倾斜（ＨＵＴ）两种立位应激下心血管反应的差异。方法６名受试者在２１天ＨＤＴ前、后分别进行ＬＢＮＰ（－４．００ｋＰａ／３ｍｉｎ、－６．６７ｋＰａ／３ｍｉｎ及－９．３３ｋＰａ／３ｍｉｎ）和ＨＵＴ试验（３０°／３ｍｉｎ、４５°／３ｍｉｎ、６０°／３ｍｉｎ及７５°／３ｍｉｎ）,以比较两种检测方法的血压（ＢＰ）和心率（ＨＲ）的变化情况。结果与ＬＢＮＰ（或ＨＵＴ）前相比：①ＬＢＮＰ（ＨＵＴ）时ＨＲ显著增加（Ｐ＜０．０１）,ＳＢＰ显著降低（Ｐ＜０．０５）;卧床后相应的变化量增加。②ＬＢＮＰ时ＤＢＰ降低（卧床后达显著,Ｐ＜０．０５）;而ＨＵＴ时ＤＢＰ增加（卧床后达显著,Ｐ＜０．０５）。③ＬＢＮＰ时ＭＡＰ均显著降低（Ｐ＜０．０５）;而ＨＵＴ时在卧床前无变化（Ｐ＞０．０５）,在卧床后显著增加（Ｐ＜０．０５）。结论ＬＢＮＰ和ＨＵＴ引起的ＣＶＳ反应并不相同。笔者认为,ＨＵＴ更能促进心血管系统对立位应激的调节作用。     

低压缺氧对大鼠肾脏功能和结构的影响

目的 观察急性低压缺氧对大鼠肾脏的损害。方法 将３６只雄性Ｗｉｓｔａｒ大鼠随机平均分为Ａ、Ｂ、Ｃ三级。Ａ组为对照组,将Ｂ、Ｃ且置低压舱内上升至５０００ｍ,停留３０ｍｉｎ,予以缺氧。下降后Ｂ组２０ｍｉｎ后,Ｃ组２４ｈ后取静脉血及肾组织,用全自动生化分析仪测定血清尿素氮、肌酐、碱怀磷酸酶、氯离子,并用放免法测定肾组织内皮素。切取肾皮质做光镜及电镜下的病理检查。结果 实验组血清尿素氮和肌酐明显增多（Ｐ〈     

Reduced pulmonary vascular reactivity after cold exposure to acute hypoxia: a role of nitric oxide (NO)

Exposure to high altitude causes pulmonary hypertension and alterations in pulmonary vascular reactivity. Among the environmental factors, cold exposure has been suggested to be involved in the development of pulmonary hypertension. However, little information is available about pulmonary vascular reactivity after cold exposure. We examined whether cold exposure can cause changes in pulmonary vascular reactivity to acute hypoxia and the possible participation of endogenous nitric oxide. We measured mean systemic (Psa) and pulmonary artery pressures (Ppa) in conscious rats after 1-week cold exposure (3.5 +/- 1.0 degrees C). Subsequently, we investigated hypoxic pulmonary vasoconstriction (HPV) with and without endogenous NO inhibition using N(G)-nitro-L-arginine methyl ester (3 mg/kg) or 7-nitroindazole (1 mg/kg). Cold exposure for 1 week caused a small but significant increase in Ppa, but not in Psa. Neither Ppa nor Psa showed significant changes after both NO inhibitions in rats exposed to cold. However, cold exposure caused a blunted HPV and an increase in plasma nitrite-nitrate concentration compared with rats kept in a neutral environment (24.0 +/- 1.0 degrees C). In addition, NO inhibition by N(G)-nitro-L-arginine methyl ester partially restored the blunted HPV in rats exposed to cold, but not 7-nitroindazole, a selective inhibitor of neuronal NO synthase. We concluded that cold exposure alters pulmonary vascular reactivity to acute hypoxia, and augmented endothelial NO bioactivity plays a counterregulatory role in response to acute hypoxia during cold exposure in rats.     

Acclimation to intermittent hypobaric hypoxia modifies responses to cold at sea level

INTRODUCTION: Residence at high altitude modifies thremoregulatory responses to cold stress upon return to lower altitude. These changes are difficult to explain since several stresses related to high altitude may interact, including hypoxia, cold, solar radiation, and physical exertion. We hypothesized that adaptation to hypoxia without cold exposure would produce at least part of the observed changes. METHODS: Five men underwent acclimation to intermittent hypoxia (AIH) in a hypobaric chamber (8 h daily for 4 d, and 6 h on the last day, 4500 to 6000 m) at 24 degrees C. Cold stress responses were tested during a whole-body standard cold air test (1 degrees C, 2 h at rest at sea level) both before and after AIH. RESULTS: Increased reticulocyte counts and percentages confirmed acclimation to hypoxia after AIH. Changes in thermoregulation during the cold test included lower mean skin temperature after 60-80 min (18.8 +/- 0.7 degrees C vs. 19.4 +/- 0.7 degrees C); higher mean metabolic heat production (127 +/- 8 W x m(-2) vs. 118 +/- 6 W x m(-2)); and lower heat debt (7.7 +/- 1.3 kJ x kg(-1) vs. 10.3 +/- 1.2 kJ x kg(-1)), without significant change in rectal temperature. Time to onset for continuous shivering decreased after AIH (12 +/- 5 min vs. 21 +/- 6.3 min), and shivering activity occurred at higher mean skin but not rectal temperatures. CONCLUSION: AIH in comfortable ambient temperature leads to a normothermic-insulative-metabolic general cold adaptation. We conclude that AIH modifies the thermoregulatory responses to cold at sea level without cold exposure leading to a cross-adaptation.     

冷冻和缺氧对大鼠血清肌酸激酶活性的影响

为探讨冷冻和缺氧对大鼠机体的影响，本文以血清肌酸激酶（ＣＫ）活性为指标，观察了冷习服，缺氧习服及低氧冷暴露４周的Ｗｉｓｔａｒ大鼠，在常和模拟６０００ｍ低氧条件下实验性冻伤后组织损伤的严重程度，结果表明，冷习服大鼠抗冻能力增强，损伤减轻；缺氧习服大鼠抗冻能力明显减弱，损伤加重，即缺氧与寒冷之间为负交叉习服，低氧冷暴露４周大鼠冻后血清ＣＫ活性变化与缺氧习服大鼠基本一致，与冷习服大鼠明显不同。表明在本实     

Exercise-induced angina in the cold

Exercise-induced angina (AP) is a common complaint of cardiac patients, particularly when exercising in the cold. To investigate the effects of environmental and inspired air temperature on AP, 9 patients with a history of cold-induced AP underwent progressive cycle ergometry tests in a climatic chamber on 4 separate occasions: (1) room environment (RE) (24 degrees C), and room inspired air (RA) (22.5 degrees C); (2) RE and cold inspired air (CA) (0.7 degrees C); (3) cold environment (CE) (-7.5 degrees C) and RA; and (4) CE and CA. Measurements of oxygen consumption, heart rate, blood pressure, and ventilation were made every minute and at test endpoint, which was either AP (85%) or fatigue (15% of all tests). Expired air temperature and skin temperature at 5 sites were also recorded. Results indicated that angina occurred sooner, and mean exercise time was significantly reduced in both RA/CE (-24%) and CA/CE (-15%) when compared with the RA/RE. Breathing CA in the RE did not significantly reduce exercise tolerance. Skin temperature was lower in both CE's compared to the RE's at all sites. Submaximal systolic blood pressure and calculated rate-pressure product were significantly higher in the CE's vs RE's. The adverse effects of cold on exercising angina patients are due to the earlier onset of angina, which appears to be induced more by the effects of exposure to the cold environment (-7.5 degrees C) than by cold air inhalation (0.7 degrees).     

缺氧条件下冻伤对大鼠血液凝固系统某些因素的影响

为研究高原冻伤的发病机理及防治措施，探讨了缺氧条件下冻伤大鼠血液凝固系统的变化，将雄性Ｗｉｓｔａｒ大鼠（２００±２０ｇ）随机分为四组，冻后４ｈ－３ｄ测定血液的出血，凝血时间，血块回缩率，前列环素，血栓素含量及Ｔ／Ｐ比值，结果表明，冻伤后各组大鼠出血和凝血时间缩短，血块回缩率降低，血浆中ＰＧＩ２和ＴＸＡ２含量增加，Ｔ／Ｐ比值升高，且缺氧习服冻伤大鼠各项指标的改变尤为明显，提示，冻伤可使血凝系统发生改     

Effects of acute cold exposure on submaximal endurance performance

The purposes of this study were to assess VO2max and submaximal endurance time to exhaustion (ET) during acute cold-air exposure. Eight male subjects (means age = 19.9 yr) were alternately exposed in groups of four to chamber temperatures of +20 degrees C and -20 degrees C for 30 h each. A week was allowed between exposures. Maximum oxygen uptake was measured using a mechanically-braked cycle ergometer, and ET was determined on the same ergometer using a 17-min/3-min exercise/rest schedule until the subject was unable to maintain pedal rate. Maximum oxygen uptake was not significantly different between conditions: 3.43 +/- 0.09 l X min-1 at +20 degrees C and 3.35 +/- 0.10 l X min-1 at -20 degrees C. During endurance exercise, intensities equaled 77.1 +/- 1.4% and 78.9 +/- 2.0% of VO2max at +20 degrees C and -20 degrees C, respectively. Heart rate and VO2 values obtained between 8 and 10 min of the endurance run were not significantly different (156 +/- 2 bpm and 2.63 +/- 0.08 l X min-1 at +20 degrees C and 158 +/- 3 bpm and 2.65 +/- 0.11 l X min-1 at -20 degrees C). Endurance time to exhaustion however, decreased 38% (P less than 0.05) from 111.9 +/- 22.8 min at +20 degrees C to 66.9 +/- 13.6 min at -20 degrees C. The data support the contention that aerobic capacity is not altered by cold exposure but suggest a marked decrease in submaximal endurance performance.     

Changes in cardiac autonomic activity during a passive 8 hour acute exposure to 5 500 m normobaric hypoxia are not related to the development of acute mountain sickness

Alterations in the autonomic nervous system after ascent to high altitude may be related to the development of acute mountain sickness (AMS). So far, the time course of cardiac autonomic modulation in relation to AMS development during the early hours at altitude is not well established. As AMS develops sometimes as early as 1 h and typically within 6 to 10 h at altitude, evaluating this time period provides information on cardiac autonomic responses with regard to AMS development. Prior studies exclusively investigated autonomic modulations in hypobaric hypoxia. Because barometric pressure per se might influence autonomic nervous system activity, the evaluation of cardiac autonomic alterations caused by hypoxia alone might give new insights on the role of the autonomic nervous system in AMS development. To assess the early responses of acute hypoxia on cardiac autonomic modulation and its association to the development of AMS, 48 male subjects were exposed for 8 h to acute normobaric hypoxia (FiO2 11.0%, 5?500 m respectively). Heart rate variability (HRV) was determined by 5-min recordings of successive NN-intervals in normoxia and after 2, 4, 6 and 8 h in hypoxia. Compared with normoxia, acute exposure to hypoxia decreased total power (TP), high frequency (HF) and low frequency (LF) components as well as the standard deviation of all NN intervals (SDNN), the root mean square of differences of successive NN intervals (rMSSD) and the proportion of differences between adjacent NN intervals of more than 50 ms (pNN50). LF:HF ratio, heart rate (HR) and blood lactate (LA) were augmented, indicating an increase in cardiac sympathetic activity. No differences were found between those who developed AMS and those who did not. Our results confirm reduced HRV with a shift towards sympathetic predominance during acute exposure to hypoxia. However, changes in cardiac autonomic modulations are not related to AMS development in acute normobaric hypoxia.     

Cardiovascular regulation response to hypoxia during stepwise decreases from 21% to 15% inhaled oxygen

INTRODUCTION: The classical view states that hypoxia beyond an oxygen concentration of about 17% induces tachycardia. However, few studies have investigated the dose-dependent effects of acute normobaric hypoxia on autonomic nervous regulation of the cardiovascular system. Therefore, we evaluated the effects of stepwise hypoxia on cardiovascular neural regulation and postulated that acute normobaric hypoxia causes vagal withdrawal and sympathetic activation from 17% 02. METHODS: There were 18 healthy men who were exposed to acute stepwise normobaric hypoxia (21%, 19%, 17%, 15% 02). Spectral analysis of the RR interval and BP variability were used. RESULTS: BP was not altered. Heart rate significantly increased at 15% (21%, 59 +/- 2; 15%, 62 +/- 2 bpm). The low-frequency power of systolic BP variability (an index of vasomotor sympathetic nerve activity) significantly increased at 15% (21%, 6.1 +/- 1.3; 15%, 9.9 +/- 1.3 mmHg2). The low-frequency power of the RR interval variability significantly increased from 17% (21%, 1036 +/- 233; 17%, 1892 +/- 409; 15%, 1966 +/- 362 ms2), However, the high-frequency power of RR interval variability (an index of cardiac parasympathetic nerve activity) did not change. Associated with these changes, the ratio of low- to high-frequency power of RR interval variability as an index of relative cardiac autonomic balance significantly shifted toward sympathetic dominance (21%, 1.5 +/- 0.3; 15%, 2.2 +/- 0.3). All indices of cardiac baroreflex function (transfer function and sequence gains) were unchanged. DISCUSSION: These results suggest that acute exposure to normobaric mild hypoxia (O2 > or = 15%) induces increases in sympathetic vasomotor activity and cardiac sympathetic dominance resulting in an increased heart rate. However, 15% O2 hypoxia might not induce changes in static BP, vagal activity, or spontaneous arterial-cardiac baroreflex function.