阻塞性睡眠呼吸暂停低通气综合征患者血尿酸变化的临床意义

目的:了解不同程度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血尿酸水平的变化,并分析二者之间的相关性。方法:选择我院2007年3月至2009年7月就诊的OSAHS患者80例,根据睡眠监测得出的睡眠呼吸暂停低通气指数(AHI)分为轻度OSAHS组(5次/h≤AHI≤20次/h,27例)、中度OSAHS组(20次/h40次/h,34例)和对照组(AHI<5次/h,20例);观察各组年龄、性别、体质量指数(BMI)、血清胆固醇、甘油三脂、血糖、尿酸及睡眠各项指标变化,比较3组间各观察指标的差异;对OSAHS组血清尿酸水平与AHI、最低脉搏容积血氧饱和度(LSpO2)和氧减<90%的时间T90进行相关性分析。结果:组间年龄及性别相比差异均无统计学意义(P均>0.05)。轻、中度OSAHS组血尿酸水平分别为(365.30±92.37)μmol/L,(374.63±78.17)μmol/L均高于对照组(336.82±74.08)μmol/L,但差异无统计学意义;重度OSAHS组血清尿酸水平(440.26±92.14)μmol/L与对照组比较差异有统计学意义(P<0.01);OSAHS组血清尿酸水平与AHI、T90呈显著正相关(r值分别为0.441、0.309,P均<0.001)与LSpO2呈负相关(r值为-0.370,P<0.001)。结论:OSAHS患者中血清尿酸水平随着AHI的增加和缺氧程度的加重而增高,并与AHI、T90及LSpO2有较强的相关性。提示OSAHS患者反复发作低氧血症可能是心血管病高发的另一个原因。     

男性阻塞性睡眠呼吸暂停低通气综合征血浆同型半胱氨酸变化的研究

目的评估男性不同程度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与血浆同型半胱氨酸(Hcy)的关系。方法选取2008年10月至2010年12月中国医科大学附属第一医院男性OSAHS患者45例,分为轻中度组23例和重度组22例以及健康男性对照组20名,用酶联免疫吸附试验比较各组间血浆Hcy浓度。22例重度OSAHS患者在治疗1个月后再次行Hcy检测。结果OSAHS患者血浆Hcy浓度较对照组明显升高[(15.9±7.8)μmol/L对(10.0±1.2)μmol/L,P<0.01],与夜间SpO2<90%时间占总睡眠时间的百分比呈显著正相关(r=0.441,P<0.01),与夜间平均SpO2呈负相关(r=-0.393,P<0.01)。然而分组比较后,只有重度OSAHS患者Hcy浓度[(19.6±6.7)μmol/L]高于对照组(P<0.01),经治疗后虽有明显降低[(15.4±4.8)μmol/L],但仍高于对照组(P<0.01)。结论重度OSAHS可引起血浆Hcy浓度升高,与低氧程度密切相关,治疗后血浆Hcy浓度有所下降。     

黏附分子在阻塞性睡眠呼吸暂停低通气综合征合并高血压发病中的作用

目的 探讨细胞黏附分子在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)合并高血压(HT)发病中的作用。方法 应用酶联免疫吸附测定(ELISA)方法检测30例OSAHS血压正常患者(OSAHS组)、30例OSAHS合并高血压患者(OSAHS HT组)及30名健康者(正常对照组)血清中可溶性胞间黏附分子1(ICAM-1)、血管细胞黏附分子1(VCAM-1)和L-选择素的含量。结果 OSAHS HT组及OSAHS组患者血清可溶性ICAM-1[分别为(601±406)μg/,L、(513±244)μg/L]、VCAM-1含量[分别为(578±176)μg/L、(480±144)μg/L]均明显高于正常对照组[分别为(355±119)μg/L、(310±163)μg/L,q值分别为4.78,3.07;9.09,5.76,P<0.01],差异有显著性;而L-选择素与对照组相比,差异无显著性(P>0.05);OSAHS HT组的VCAM-1明显高于OSAHS组(q值为3.32,P<0.05),差异有显著性;ICAM-1水平与睡眠呼吸暂停低通气指数(AHI)及微觉醒指数呈明显的正相关(r=0.465,P<0.01,r=0.226,P<0.05);与最低血氧饱和度呈明显的负相关(r=-0.368,P<0.01)。结论 血清ICAM-1、VCAM-1水平的升高是OSAHS患者高血压发病的重要危险因子之一。     

不同严重度阻塞性睡眠呼吸暂停低通气综合征女性血压影响因素分析

目的:探讨不同严重度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)女性患者血压的影响因素。方法:将190例2009至2011年就诊于上海交通大学医学院附属瑞金医院睡眠中心的女性打鼾患者按睡眠呼吸暂停低通气指数(AHI)分成4组:非OSAHS组、轻度OSAHS组、中度OSAHS组和重度OSAHS组,比较这4组患者的一般特征、多导睡眠图(PSG)监测指标及血压的差异,并分析不同OSAHS严重度组血压影响因素。结果:非OSAHS组43例,轻度OSAHS组52例,中度OSAHS组30例,重度OSAHS组65例。随着AHI升高,各组血压值呈升高趋势。各组血压比较,重度OSAHS组收缩压与非OSAHS组比较有显著差异(P<0.05);重度OSAHS组舒张压高于非OSAHS组及轻度OSAHS组(P     

阻塞性睡眠呼吸暂停低通气综合征对血压及心律失常的影响

目的观察阻塞性睡眠呼吸暂停低通气综合征(Obstructive sleep Apnea-hypopnea Syndrome,OSAHS)对血压及心律失常的影响。方法 117例OSAHS患者按照按其睡眠呼吸暂停低通气指数(AHI)及经皮血氧饱和度(SPO2)的变化情况分为轻度、中度、重度组,随机选取35例无OSAHS患者作为对照组。所有入选对象均行多导睡眠图(Polysomnogram,PSG)检查,监测睡前及醒后血压,同时行动态心电图监测。结果睡前及醒后血压水平在OSAHS患者中明显高于对照组(P0.01),并且各组间相比差异均有统计学意义(P0.05)。睡前及醒后血压相比:对照组无显著差异(P0.05),轻度OSAHS组收缩压无显著差异(P0.05),舒张压有显著差异(P0.05),中度及重度OSAHS组收缩压及舒张压水平均有显著差异(P0.05)。中重度OSAHS组心律失常发生率明显高于对照组和轻度OSAHS组,差异有统计学意义(P0.05)。结论 OSAHS本身可以引起夜间血压的升高,且血压的变化随着OSAHS程度的加重而加大。OSAHS在睡眠时有较大的心率变异性,夜间可见明显的高频峰,心率变异夜间大于白天。     

急性脑梗死合并阻塞性睡眠呼吸暂停低通气综合征患者超敏C反应蛋白与同型半胱氨酸水平的变化

目的探讨急性脑梗死(ACI)与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的关系。方法采用乳胶增强免疫比浊法检测33例ACI、32例ACI合并OSAHS患者血清超敏C反应蛋白(hs-CRP)水平,采用循环酶法检测血清同型半胱氨酸(Hcy)水平,并记录呼吸暂停低通气指数(AHI)。结果 ACI合并OSAHS组患者血清hs-CRP及Hcy分别为:(5.35±0.77)mg/L、(23.38±7.96)μmol/L,均高于ACI组(P0.05),且hs-CRP、Hcy与AHI均呈正相关。结论 OSAHS可能通过炎症反应的途径促进ACI的发生发展。     

阻塞性睡眠呼吸暂停低通气综合征患者血浆白细胞介素-18水平与动脉粥样硬化的关系

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆IL-18水平与动脉粥样硬化的关系.方法 选取就诊的男性OSAHS患者52例,年龄26～77岁,分为轻度组16例,中度组18例,重度组18例,另选对照组18例.对其中OSAHS组中20例中重度患者进行持续气道内正压(CPAP)治疗,并检测颈动脉内膜中膜厚度(IMT),测定血浆白细胞介素-18(IL-18)的水平.采用方差分析、配对t检验及Pearson相关分析进行统计学处理.结果 轻度、中度和重度OSAHS组的IL-18水平分别为(352±76)ng/L、(600±84)ng/L和(798±110)ng/L,均明显高于对照组的(250±76)ng/L,且OSAHS各组间均有明显差别.重度OSAHS组颈动脉IMT较对照组和轻度OSAHS组明显增厚.血浆IL-18水平与颈动脉IMT、呼吸暂停低通气指数(AHI)呈显著正相关(r值分别为0.486、0.865,P均＜0.001),与最低脉搏氧饱和度呈显著负相关(r=-0.664,P＜0.001).CPAP治疗后OSAHS患者血浆IL-18水平明显降低,颈动脉IMT未见明显改变.结论 OSAHS患者颈动脉IMT增厚,血浆IL-18水平升高,两者密切相关.血浆IL-18水平升高与OSAHS严重程度相关,OSAHS相关炎症反应可能与动脉粥样硬化的进程相关.CPAP治疗能够改善患者AHI和最低脉搏氧饱和度,降低血浆IL-18水平.     

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。     

阻塞性睡眠呼吸暂停低通气综合征与高血压

目的　探讨阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)与高血压的关系。方法　 398例患者用Sullivan Auto监测仪行夜间 (≥ 7小时 )睡眠监测 ,并行睡前、醒后血压测定。呼吸暂停通气指数 (AHI) <5为对照组 ,AHI≥ 5为 OSAHS组 ,比较两组之间睡眠呼吸参数和睡眠前、后血压改变。结果　 OSAHS组醒后血压 14 6 .35± 16 .2 8/96 .5 1± 10 .31mm Hg比睡前血压 131± 18.37/81± 11.0 9mm Hg明显升高 (P<0 .0 5 ) ,较对照组睡前血压 12 2± 16 .2 8/79± 11.4 5 mm Hg明显升高 (P<0 .0 5 )。 OSAHS组最低 Sa O2 5 4± 18.0 4 %较对照组 80± 12 .1%明显降低 (P<0 .0 5 )。结论　 OSAHS引起的夜间低氧血症可能是部分高血压病病因之一。     

血尿酸水平与冠状动脉病变程度的关系

目的:探讨血清尿酸水平与冠脉病变程度的关系。方法:216例经过冠脉造影确诊为冠心病的患者,以冠脉病变程度分组,同时检测空腹血尿酸水平。结果:冠状动脉正常组血尿酸水平为(293.98±74.49)μmol/L,冠状动脉单支病变组血尿酸水平为(309.65±50.98)μmol/L,冠状动脉双支病变组血尿酸水平为(358.28±79.08)μmol/L,冠状动脉多支病变组血尿酸水平为(366.71±92.24)μmol/L。狭窄组患者的血尿酸水平(348.45±)μmol/L明显高于对照组(293.98±74.49)μmol/L,P<0.01,差异有统计学意义。血尿酸水平与冠心病的病变血管数目呈正相关(r=0.324,P<0.01)。结论:随着冠状动脉病变程度的增加,血尿酸水平也逐渐升高。     

Three layer functional model and energy exchange concept of aging process

Relying on a certain degree of abstraction, we can propose that no particular distinction exists between animate or living matter and inanimate matter. While focusing attention on some specifics, the dividing line between the two can be drawn. The most apparent distinction is in the level of structural and functional organization with the dissimilar streams of ‘energy flow’ between the observed entity and the surrounding environment. In essence, living matter is created from inanimate matter which is organized to contain internal intense energy processes and maintain lower intensity energy exchange processes with the environment. Taking internal and external energy processes into account, we contend in this paper that living matter can be referred to as matter of dissipative structure, with this structure assumed to be a common quality of all living creatures and living matter in general. Interruption of internal energy conversion processes and terminating the controlled energy exchange with the environment leads to degeneration of dissipative structure and reduction of the same to inanimate matter, (gas, liquid and/or solid inanimate substances), and ultimately what can be called ‘death.’ This concept of what we call dissipative nature can be extended from living organisms to social groups of animals, to mankind. An analogy based on the organization of matter provides a basis for a functional model of living entities. The models relies on the parallels among the three central structures of any cell (nucleus, cytoplasm and outer membrane) and the human body (central organs, body fluids along with the connective tissues, and external skin integument). This three-part structural organization may be observed almost universally in nature. It can be observed from the atomic structure to the planetary and intergalactic organizations. This similarity is corroborated by the membrane theory applied to living organisms. According to the energy nature of living matter and the proposed functional model, the decreased integrity of a human body's external envelope membrane is a first cause of the structural degradation and aging of the entire organism. The aging process than progresses externally to internally, as in single cell organisms, suggesting that much of the efforts towards the restoration and maintenance of the mechanisms responsible for structural development should be focused accordingly, on the membrane, i.e., the skin. Numerous reports indicate that all parts of the human body, like: bones, blood with blood vessels, muscles, skin, and so on, have some ability for restoration. Therefore, actual revival of not only aging tissue of the human body's membrane, but the entire human body enclosed within, with all internal organs, might be expected. We assess several aging theories within the context of our model and provide suggestions on how to activate the body's own anti-aging mechanisms and increase longevity. This paper presents some analogies and some distinctions that exist between the living dissipative structure matter and inanimate matter, discusses the aging process and proposes certain aging reversal solutions.     

Unusual responses of nocturnal pineal melatonin synthesis and secretion to swimming: Attempts to define mechanisms

Abstract: The effect of swimming at night on rat pineal melatonin synthesis was compared with that of light exposure at night. Rats were forced to swim at 0030 hr (lights out at 2000 hr) and sacrificed by decapitation 15 and 30 min later, immediately after swimming. Other groups of animals were exposed to white light (650μW/cm²) for 15 and 30 min at same time. Swimming caused a rapid and highly significant drop in the melatonin content in the pineal gland; however, the activity of N-acetyltransferase (NAT), the supposed rate limiting enzyme in the melatonin production, was not changed. Despite the drop in pineal melatonin levels, serum concentrations of the indole remained elevated in the rats that swam. In contrast, melatonin levels in the pineal and serum of light exposed rats fell precipitously, accompanied by a significant suppression of NAT activity. Since we anticipated that the strenuous exercise associated with swimming may induce release of artrial natriuretic peptide (ANP) from the heart, which in turn could cause the release of pineal melatonin, in a second study we injected physiological saline intravenously to stretch the cardiac muscle and release ANP. Three milliliters of normal saline was injected during the day into the jugular vein of anesthetized rats that were pretreated with isoproterenol to stimulate pineal melatonin production. Animals were killed 15 min after the saline injection, and pineal NAT activity and pineal melatonin levels were measured. The saline injections caused no alteration in the elevated levels of either NAT or melatonin. These data suggest that the disparity in pineal NAT activity (which was high) and pineal melatonin (which was low), in animals swum at night, may not be caused by ANP which is released during strenuous exercise such as swimming.     

The immunoneuroendocrine role of melatonin

Abstract: A tight, physiological link between the pineal gland and the immune system is emerging from a series of experimental studies. This link might reflect the evolutionary connection between self-recognition and reproduction. Pinealectomy or other experimental methods which inhibit melatonin synthesis and secretion induce a state of immunodepression which is counteracted by melatonin. In general, melatonin seems to have an immunoenhancing effect that is particularly apparent in immunodepressive states. The negative effect of acute stress or immunosuppressive pharmacological treatments on various immune parameters are counteracted by melatonin. It seems important to note that one of the main targets of melatonin is the thymus, i.e., the central organ of the immune system. The clinical use of melatonin as an immunotherapeutic agent seems promising in primary and secondary immunodeficiencies as well as in cancer immunotherapy. The immunoenhancing action of melatonin seems to be mediated by T-helper cell-derived opioid peptides as well as by lymphokines and, perhaps, by pituitary hormones. Melatonin-induced-immuno-opioids (MHO) and lymphokines imply the presence of specific binding sites or melatonin receptors on cells of the immune system. On the other hand, lymphokines such as -γ-interferon and interleukin-2 as well as thymic hormones can modulate the synthesis of melatonin in the pineal gland. The pineal gland might thus be viewed as the crux of a sophisticated immunoneuroendocrine network which functions as an unconscious, diffuse sensory organ.     

Melatonin and photoperiodic time measurement: Seasonal breeding in the sheep

Abstract: Well-established circadian physiology supports the view that photoperiodic time measurement utilizes the coincidence between the presence of light and a photosensitive phase of a 'biological clock' to alter reproductive status—the so-called external coincidence model of seasonal breeding. In this review, we examine the mechanism whereby photoperiod interacts with presumed suprachiasmatic nuclei activity to allow endogenous melatonin to normally synchronize reproductive activity to the optimal time of year. The Romney Marsh sheep is particularly explored as an experimental model. It is suggested that the on/off activity of seasonal reproduction may be a robust mechanism able to be predictably manipulated by the judicious use of the light/dark cycle and exogenous melatonin, but firmly based on circadian principles.     

Response of rat pineal melatonin to calcium, magnesium, and lithium is circadian stage dependent

Abstract: Herein we documented the response of pineal melatonin production to electrolytes known to be effective on pineal function in view of a possible circadian stage dependence. We studied the release of melatonin by perifused rat pineal glands at 2 different circadian stages corresponding to the middle of the light and dark periods, i.e., respectively, 7 and 19 HALO (Hours After Light Onset, L:D = 12:12). The initial efflux rates were, as expected, much higher in the perifusates of glands removed from rats sacrificed during the dark phase than of those removed during the light phase. After 3 hr of perifusion, melatonin release reached similar levels which were found constant up to the 8th hr of perifusion, whatever the circadian stage. Perifusion of the glands with physiological concentrations for the rat of calcium (5.2 mmol/1) and magnesium (1.34 mmol/1) resulted in a stimulatory effect on the pineal glands removed from rats sacrificed in the middle of the dark period (19 HALO), whereas no effects were observed on the pineal glands removed from rats sacrificed during the light (7 HALO). Lithium (0.28 and 0.55 mmol/1) was ineffective on melatonin release in pineal glands removed 7 and 19 HALO. Our results show differences in the initial efflux rates of melatonin and in the response of perifused pineal glands to calcium and magnesium according to the circadian stage.     

Conservative management of perforated duodenal diverticulum： A case report and review of the literature

Duodenal diverticula are a relatively common condition. They are asymptomatic, unless they become complicated, with perforation being the rarest but most severe complication. Surgical treatment is the most frequently performed approach. We report the case of a patient with a perforated duodenal diverticulum, which was diagnosed early and treated conservatively with antibiotics and percutaneous drainage of secondary retroperitoneal abscesses. We suggest this method could be an acceptable option for the management of similar cases, provided that the patient is in good general condition and without septic signs.     

Changes in connexin43, the gap junction protein of astrocytes, during development of the rat pineal gland

Abstract: The abundance of gap junctions between rat pineal astrocytes formed by connexin43 (Cx43) was studied during development. Levels and distribution of Cx43 were measured by immunoblotting and indirect immunofluorescence, respectively. The amount of Cx43 in cells located within the gland was low until about the 7th postnatal day and increased to adult values between the 14th and 21st days postpartum. Although astrocytes, recognized by their vimentin immunoreactivity, were scarce before birth, they were abundant by the 7th postnatal day suggesting that the low levels of Cx43 found at this age corresponded to a low expression of this protein. Localization of the immunoreactivity to Cx43 and vimentin showed a close correlation, indicating that mature or immature pineal astrocytes form gap junctions made of Cx43. Since Cx43 levels attained their adult values at about the time the innervation and the functional state of the gland reached maturity (2–3 weeks after birth), it is proposed that astrocyte gap junctions are involved in the function of the adult rat pineal gland.