乙型和丙型肝炎病毒重叠感染者外周血可溶性白细…

应用单克隆抗体夹心酶联免疫吸附试验对７５例乙型肝炎病毒和丙型肝炎病毒重叠感染者血清的白细胞介素２受体进行检测，并与单纯乙型肝炎病毒感染者和健康人做对照进行比较。结果显示，重叠感染者ｓＩＬ－２Ｒ含量明显高于正常对照组，但与乙型肝炎组比较无显著性差异，Ｐ〉０．０５。证实ＨＢＶ，ＨＣＶ重叠感染时机体免疫功能处于紊乱状态。     

慢性乙型肝炎,肝硬化患者外周血LAK细胞活性和sIL—2R测定的意义

采用＾３Ｈ－ＴｄＲ释放法测定５１例慢性肝病患者（ＣＰＨ１０例、ＣＡＨ２３例、ＬＣ１８例）外周血ＬＡＫ细胞活性，并用酶联法测定患者血清中ｓＩＬ－２Ｒ含量；与２９例正常对照组比较，发现肝病患者ＬＡＫ活性降低，ＨＢＶＤＮＡ阳性组ＬＡＫ活性较阴性组低（Ｐ〈０．０５），ｓＩＬ－２Ｒ增高，且慢性肝病组ＬＡＫ活性与ｓＩＬ－２Ｒ水平呈负相关，说明ＬＡＫ活性与机体免疫功能状态有关，ＨＢＶ的复制和高浓度的ｓＩＬ－２Ｒ     

慢性活动性乙型肝炎患者细胞免疫功能检测及其临床意义

测定了例慢性活动乙型肝炎患者外周血单个核细胞（ＰＢＭＣ）产生的白细胞介素２（ＩＬ－２）活性，其中部分病人检测了血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）水平，膜白细胞介素２受体（ｍＩＬ－２Ｒ）表达，ＬＡＫ活性及外周血Ｔ淋巴细胞亚群，并分析了它们之间的相关性，结果表明：ＩＬ－２活性，ｍＩＬ－２Ｒ表达，ＬＡＫ活性，ＣＤ４／ＣＤ８比值显著低于正常对照组（Ｐ〈０．００１），而ｓＩＬ－２Ｒ水平，ＣＤ８细胞显     

人巨细胞病毒感染对肾移植受者血清sIL－2R水平的影响

用ＰＣＲ检测ＨＣＭＶ－ＤＮＡ，ＥＬＩＳＡ法检测ＨＣＭＶ－ＩｇＭ及ＩｇＧ，以诊断肾移植受者ＨＣＭＶ感染。用双抗体夹心法ＥＬＩＳＡ检测６５例肾移植受者血清ｓＩＬ－２Ｒ水平，结果表明：ＨＣＭＶ感染后宿主血清ｓＩＬ－２Ｒ水平明显增高（Ｐ＜０．０１），且ＨＣＭＶ疾病组ｓＩＬ－２Ｒ增高程度大于无症状感染组（Ｐ＜０．０１）；６例原发性ＨＣＭＶ感染者ｓＩＬ－２Ｒ水平与ＩｇＭ水平呈正相关（ｒ＝０．９９０８），提示随感染程度增加，血清ｓＩＬ－２Ｒ水平随之增高，还发现血清ｓＩＬ－２Ｒ水平与Ｃ９４／ＣＤ８比值是负相关（ｒ＝－０．９７８９），说明ＨＣＭｖ感染后ｓＩＬ－２Ｒ水平增高与Ｔ细胞亚群改变有关，反之也说明ｓＩＬ－２Ｒ增高程度可表明体内免疫抑制状态。对于ＨＣＭＶ感染后血清ｓＩＬ－２Ｒ水平增高的机理有待进一步探讨。     

巨细胞病毒感染与可溶性白细胞介素2受体的关系

应用酶联免疫吸附试验（ＥＬＩＳＡ）对１０４例育龄妇女的血清进行了巨细胞病毒（ＨＣＭＶ）ＩｇＧ、ＩｇＭ抗体的检测，同时用ＥＬＩＳＡ双抗体夹心法测定了不同感染状态下血清中可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）的水平，并将ｓＩＬ－２Ｒ水平与未感染ＨＣＭＶ的正常育龄妇女进行了比较。结果，育龄妇女中抗－ＨＣＭＶＩｇＧ的阳性率为８９．４％，ＩｇＭ的阳性率为９．６％，感染ＨＣＭＶ的妇女血清中ｓＩＬ－２Ｒ水平均大于未感染的对照组（１７８．１±５７．３Ｕ／ｍｌ），Ｐ＜０．０５，其中ＩｇＭ阳性者和ＩｇＭ、ＩｇＧ同时阳性者血清中ｓＩＬ－２Ｒ水平最高，分别为９１０±４６５．６Ｕ／ｍｌ和９０５±３４７．８Ｕ／ｍｌ，两者间的差异无显著性意义（Ｐ＞０．０５），但均大于仅抗－ＨＣＭＶＩｇＧ阳性者（４４６．８±１５８．９Ｕ／ｍｌ），Ｐ均＜０．０５。表明，ＨＣＭＶ感染可致ｓＩＬ－２Ｒ水平升高，并且活动性感染者上升明显。提示：ｓＩＬ－２Ｒ可能参与了ＨＣＭＶ的免疫致病机制。     

急性丙型肝炎患者免疫状况的研究

用间接免疫荧光法、酶联免疫吸附试验（ＥＬＩＳＡ）及ＬＤＨ释法，对１６例急性输血后丙型肝炎（抗－ＨＣＶ、ＨＣＶ－ＲＮＡ均阳性）患者，分别进行外周血单个核细胞（ＰＢＭＣ）的Ｔ细胞亚群计数、Ｔ４／Ｔ８比值、Ｔａｃ受体的检测及血清可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）ＮＫ细胞活性的测定。并与正常人组比较，经ｔ检验发现，急性丙型肝炎患者的Ｔ４亚群所占百分比、Ｔ４／Ｔ８比值及ＰＢＭＣＴａｃ受体表达均明显低于正常人组（Ｐ＜０．０５），而ＮＫ细胞活性、血清ｓＩＬ－２Ｒ明显高于正常人组（Ｐ＜０．０５）。患者的这些免疫状态改变，可能对其发病机理的研究有一定意义。     

肝硬化患者血清透明质酸含量与sIL－2R水平的观察

本文用放射免疫测定法及双抗体夹心法测定了２５例健康人，３０例肝硬化患者血清透明质酸（ＨＡ）的含量及可溶性白细胞介素２受体（ｓＩＬ－２Ｒ）水平。结果表明：（１）肝硬化组血清ＨＡ含量及ｓＩＬ－２Ｒ水平均高于对照组（Ｐ值均＜０．０１）；（２）肝硬化组血清ＨＡ与ｓＩＬ－２Ｒ水平间呈正相关关系（ｒ＝０．５１９２，Ｐ＜０．０１）。提示：肝硬化组患者血清ｓＩＬ－２Ｒ水平增高与肝损害程度有关，可能是由于肝细胞受损而对ＳＩＬ－２Ｒ清除能力降低所致。     

急性早幼粒细胞白血病患者诱导分化治疗前后血清IL—2受体的…

ＥＬＩＳＡ法检测２７例急性早幼粒细胞白血病患者（ＡＰＬ）血清白细胞介素２受体（ｓＩＬ－２Ｒ）水平。结果表明ＡＰＬ患者血清ｓＩＬ－２Ｒ高于正常对照（Ｐ〈０．０１），经维甲酸治疗后逐渐降低，但治疗中期患者血清ｓＩＬ－２Ｒ仍高于正常和治疗后（缓解期）患者血清ｓＩＬ－２Ｒ（Ｐ〈０．０５）。治疗后血清ｓＩＬ－２Ｒ虽略高于正常对照。却已恢复正常范围（Ｐ〈０．０５）。同时发现治疗中ＷＢＣ却明显升高，治疗后又下降     

HBcAg/HBeAg对慢性乙型肝炎患者PBMC中Th1/Th2类细胞应答的影响

目的 探讨ＨＢｃＡｇ／ＨＢｅＡｇ对慢性乙型肝炎患者ＰＢＭＣ中Ｔｈ１／Ｔｈ２类细胞应答的影响。方法 用套式ＰＣＲ法检测６４便慢性ＨＢＶ感染者ＰＢＭＣ中ＨＶＢ ＤＮＡ;分别用ＰＨＡ、ＨＢｃＡｇ和ＨＢｅＡｇ体外培养;ＥＬＩＳＡ法检测ＰＢＭＣ产生Ｔｈ１类细胞因子（ＩＬ－２、ＩＦＮ－γ）和Ｔｈ２类细胞因子（ＩＬ－４、ＩＬ－１０）的含量。结果 表明ＨＢＶ ＤＮＡ阳性组和阴性组相比,无论是在ＰＨＡ还是在ＨＢｃＡ     

乙型肝炎患者白细胞介素6和自身免疫反应

测定４４例不同类型乙型肝炎患者外周血单个核细胞产生的白细胞介素６（ＩＬ－６）活性水平及其与血清抗肝细胞膜脂蛋白（ＬＳＰ）浓度、肝功能和乙肝病毒复制指标的关系。主要发现重型肝炎、慢活肝患者的ＩＬ－６活性水平和抗ＬＳＰ浓度明显增高（Ｐ＜０．０１），慢迁肝、急性肝炎患者则无明显改变（Ｐ＜０．０５），ＩＬ－６活性水平与抗ＬＳＰ浓度呈正相关（Ｐ＜０．０１）。ＩＬ－６活性水平与ＨＢＶ－ＤＮＡ及ＨＢｅＡｇ呈负相关（Ｐ＜０．０５）。     

The separation of three antibody populations from anti-poly(A).poly(U) antibodies elicited in mice or rabbits and antigenic features of poly(A).poly(U))

Anti-poly(A).poly(U) antibodies in ascitic fluid of DDY mice immunized with poly(A).poly(U)-methylated bovine serum albumin complexes were fractionated into three major antibody populations, Ab-1, Ab-2 and Ab-3, by precipitating with poly(I).poly(C), poly(A).poly(U), and poly(A).2 poly(U), respectively. Antibody population one, Ab-2, reacted with various double-stranded RNAs [poly(I).poly(C), poly(A).poly(U), and rice dwarf virus ribonucleic acid (RDV-RNA)] and poly(A).2 poly(U). Ab-2 reacted with poly(A).poly(U) and poly(A).2 poly(U). Although both Ab-1 and Ab-2 reacted with poly(A).poly(U), the two populations were distinguishable by their different reactivities against chemically modified antigens and oligonucleotides. In contrast to Ab-2, acetylation at the furanose 2'-position of poly(U) resulted in a dramatic decrease in the complement fixation reactivity of Ab-2. Also, Ab-2 was capable of binding with complexes of hexa- to heptaadenylates and poly(U), whereas Ab-1 required oligoadenylates of longer chain lengths (9-10 chain length) for binding. Therefore, it appears that poly(A).poly(U) possesses unique antigenic determinants which are recognizable only by Ab-2, in addition to those determinants which are common to a variety of double-stranded RNAs.     

In vitro exposure to carbon dioxide induces oxidative stress in human peritoneal mesothelial cells

BACKGROUND: The objective of this study was to verify whether in vitro exposure of human peritoneal mesothelial cells to carbon dioxide (CO(2)) influences the levels of 8-isoprostaglandin F(2alpha) (8-iso-PGF(2alpha)), a marker of oxidative stress. METHODS: Mesothelial cells were exposed to either: (i). 100% CO(2) for 4 h; (ii). 100% helium (an alternative gas with which to create hypoxic conditions) for 4 h; (iii). 100% CO(2) for 24 h; or (iv). standard conditions (control). After gas exposure, mesothelial cells were returned to standard conditions and harvested immediately (T(0)), and at 1-(T(1)) and 3 (T(3)) h afterwards. Cell viability and culture medium pH were monitored throughout the experiments. 8-iso-PGF(2alpha) was assayed by enzyme-linked immunosorbent assay (ELISA). RESULTS: Exposure to CO(2) decreased the culture medium pH whereas helium increased the pH. 8-iso-PGF(2alpha) levels in all treated groups were significantly higher than in the control group: in the 4 h CO(2) group at T(1); in the 24 h CO(2) group at T(0) and T(1); and in the 4 h helium group at T(0), T(1) and T(3). 8-iso-PGF(2alpha) levels following 4 h CO(2) exposure were significantly lower than after 24 h CO(2) exposure at T(1), and lower than following 4 h helium exposure at all time points. CONCLUSIONS: Exposure to both CO(2) and helium induces oxidative stress in mesothelial cells. Hypoxia-reoxygenation may play a role in this process.     

The effect of various menopausal hormone therapies on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins in healthy postmenopausal women

OBJECTIVE: Androgenic progestins such as norethisterone acetate (NETA) may influence the effect of estradiol (E(2)) therapy. We compared the influence of oral E(2), with and without NETA, and transdermal E(2) on markers of coagulation, fibrinolysis, and inflammation and on lipids and lipoproteins in healthy postmenopausal women. DESIGN: A total of 112 healthy postmenopausal women were randomized to receive treatment with either oral E(2), with or without NETA, transdermal E(2), or placebo. At baseline and after 28 weeks, levels of serum lipids and lipoproteins and markers of coagulation, fibrinolysis, and inflammation were determined. RESULTS: Of the fibrinolytic parameters, oral E(2) (P < 0.05) and E(2) with NETA (P < 0.01) shortened euglobulin clot lysis time. Oral E(2) decreased plasminogen activator inhibitor-1 activity (P < 0.05). Oral E(2) with NETA reduced plasminogen activator inhibitor-1 antigen levels (P < 0.01) and increased D-dimer antigen levels (P < 0.001). All three modes of menopausal hormone therapy reduced tissue type plasminogen activator antigen. Of the coagulation parameters, both routes of E(2) therapy decreased fibrinogen levels (P = 0.002 for oral and P = 0.007 for transdermal E(2)), whereas E(2) with NETA showed no effect. The decrease of fibrinogen was larger after oral E(2) (P = 0.02). Oral E(2) with NETA reduced antithrombin III (P < 0.001) and protein C (P < 0.001) activity. Oral E(2) (P = 0.04) and E(2) with NETA (P < 0.01) increased C-reactive protein (CRP). Transdermal E(2) showed no influence on CRP. The addition of NETA influenced the change in CRP, as the increase in CRP was more pronounced after E(2) without NETA (P = 0.005). The levels of serum amyloid A, interleukin-6, and tumor necrosis factor-alpha did not change significantly after any of the modes of hormone therapy. Of the lipids and lipoproteins, oral E2 decreased low-density lipoprotein cholesterol (P < 0.01), lipoprotein (a) (P < 0.05), and increased high-density lipoprotein cholesterol (P < 0.05). Transdermal E(2) decreased triglycerides (P < 0.02) and increased high-density lipoprotein cholesterol (P < 0.03). Oral E(2) with NETA decreased total cholesterol (P < 0.01) and high-density lipoprotein cholesterol (P < 0.005). CONCLUSIONS: Oral E(2), with or without NETA, produced no net activation of coagulation but improved fibrinolysis. Both modes of oral menopausal hormone therapy have a greater impact on markers of inflammation, coagulation, fibrinolysis, lipids, and lipoproteins than transdermal E(2). NETA attenuates some E(2) effects. Further studies are needed to elucidate the impact of these effects on clinical endpoints.     

基质金属蛋白酶-2、金属蛋白酶组织抑制因子-2表达与滑膜肉瘤转移、肿瘤血管生成的关系及其预后意义

目的探讨滑膜肉瘤肿瘤细胞中基质金属蛋白酶-2（MMP-2）和金属蛋白酶组织抑制因子-2（TIMP-2）的表达情况及其预后意义。方法采用免疫组织化学SP法检测72例滑膜肉瘤肿瘤细胞中MMP-2、TIMP-2的表达情况,收集每例临床病理学参数并统计生存率、以CD31标记检测微血管密度（MVD）并分析与生存率的关系。结果（1）MMP-2、TIMP-2的表达阳性率分别为84．7％（61／72）和83．3％（60／72）,二者表达强度呈负相关关系（r=-0．290,P=0．013）。（2）有转移病例出现MMP-2高表达和TIMP-2低表达的比例明显高于无转移病例（分别P=0．010,P=0．002）。（3）MMP-2高表达病例的MVD明显大于其低表达者（P=0．005）,TIMP-2高表达病例的MVD明显小于其低表达者（P=0．048）。（4）单因素和多因素生存分析均显示TIMP-2低表达与患者预后不良有关（分别P=0．002,P=0．016）。结论MMP-2和TIMP-2表达异常可能与滑膜肉瘤的转移及肿瘤血管生成有关,TIMP-2低表达可能提示患者预后不良。     

Self-setting properties and in vitro bioactivity of Ca3SiO5/CaSO4.1/2H2O composite cement

In this study, a biphasic injectable bone substitute, based on tricalcium silicate (Ca(3)SiO(5)) and plaster (CaSO(4).1/2H(2)O), is presented. The addition of CaSO(4).1/2H(2)O could accelerate the hydration of Ca(3)SiO(5), decrease the setting time, and improve the strength of the cement. The workable Ca(3)SiO(5)/CaSO(4).1/2H(2)O pastes with a liquid to powder (L/P) ratio of 0.8-1.0 mL g(-1) could be injected for 2-20 min (nozzle diameter 2.0 mm) and enabled initial setting times of 9-60 min. The setting process yielded cellular structures with compressive strength of 12.4-31.5 MPa after 2-28 days. The in vitro bioactivity of the paste was investigated by soaking in simulated body fluid (SBF) for 7 days. The result showed that although large amount of CaSO(4).1/2H(2)O (30%) was added, the paste showed good ability to induce the formation of hydroxyapatite (HA). Furthermore, the Ca(3)SiO(5)/CaSO(4).1/2H(2)O paste could degrade in Ringer's solution, and the dissolution extracts of the paste also had a stimulatory effect on L929 cell growth in certain concentration range. Our results indicated that Ca(3)SiO(5)/CaSO(4).1/2H(2)O paste was bioactive and degradable, and showed excellent mechanical properties after self-setting. Therefore, it may be a potential candidate for further investigation as injectable tissue repairing substitute.     

Inhibitory effects of PGE(2) on K(+) currents and Ca(2+) oscillations in rat pancreatic acinar cells

Prostaglandin E(2) (PGE(2)) inhibits pancreatic enzyme secretion and shows a protective action against pancreatitis. In this study, we tested the effects of PGE(2) on the slowly activating voltage-dependent K(+) channel current ( I(Ks)) and cholecystokinin (CCK)-induced oscillations of cytosolic [Ca(2+)] ([Ca(2+)](i)) in rat pancreatic acini (RPA). I(Ks) in RPA is reportedly augmented by both Ca(2+)- and cAMP-mediated secretagogues. PGE(2) (10(-7) M) decreased the amplitude of I(Ks), an effect that was more prominent following prior stimulation with secretin. The application of the membrane-permeable cAMP analogue 8-Br-cAMP prevented the effect of PGE(2) on I(Ks). The Ca(2+)-mediated augmentation of I(Ks) by ACh was unaffected by pretreatment with PGE(2). Using fura-2 fluorescence ratiometry to assess [Ca(2+)](i), CCK (相似文献   

Development of anthropometry-based equations for the estimation of the total body water in Koreans

For developing race-specific anthropometry-based total body water (TBW) equations, we measured TBW using bioelectrical impedance analysis (TBW(BIA)) in 2,943 healthy Korean adults. Among them, 2,223 were used as a reference group. Two equations (TBW(K1) and TBW(K2)) were developed based on age, sex, height, and body weight. The adjusted R2 was 0.908 for TBW(K1) and 0.910 for TBW(K2). The remaining 720 subjects were used for the validation of our results. Watson (TBW(W)) and Hume-Weyers (TBW(H)) formulas were also used. In men, TBW(BIA) showed the highest correlation with TBW(H), followed by TBW(K1), TBW(K2) and TBW(W). TBW(K1) and TBW(K2) showed the lower root mean square errors (RMSE) and mean prediction errors (ME) than TBW(W) and TBW(H). On the Bland-Altman plot, the correlations between the differences and means were smaller for TBW(K2) than for TBW(K1). On the contrary, TBW(BIA) showed the highest correlation with TBW(W), followed by TBW(K2), TBW(K1), and TBW(H) in females. RMSE was smallest in TBW(W), followed by TBW(K2), TBW(K1) and TBW(H). ME was closest to zero for TBW(K2), followed by TBW(K1), TBW(W) and TBW(H). The correlation coefficients between the means and differences were highest in TBW(W), and lowest in TBW(K2). In conclusion, TBW(K2) provides better accuracy with a smaller bias than the TBW(W) or TBW(H) in males. TBW(K2) shows a similar accuracy, but with a smaller bias than TBW(W) in females.     

Modulation of perfusion and oxygenation by red blood cell oxygen affinity during acute anemia

Responses to exchange transfusion using red blood cells (RBCs) with modified hemoglobin (Hb) oxygen (O(2)) affinity were studied in the hamster window chamber model during acute anemia to determine its role on microvascular perfusion and tissue oxygenation. Allosteric effectors were introduced in the RBCs by electroporation. Inositol hexaphosphate (IHP) and 5-hydroxymethyl-2-furfural (5HMF) were used to decrease and increase Hb-O(2) affinity. In vitro P50s (partial pressure of O(2) at 50% Hb saturation) were modified to 10, 25, 45, and 50 mm Hg (normal P50 is 32 mm Hg). Allosteric effectors also decreased the Hill coefficient. Anemic condition was induced by isovolemic hemodilution exchanges using 6% dextran 70 kD to 18% hematocrit (Hct). Modified RBCs (at 18% Hct in 5% albumin solution) were infused by exchange transfusion of 35% of blood volume. Systemic parameters, microvascular perfusion, capillary perfusion (functional capillary density, FCD), and microvascular Po(2) levels were measured. RBcs with P50 of 45 mm Hg increased tissue Po(2) and decreased O(2) delivery (Do(2)) and extraction (Vo(2)) and RBCs with P50 of 60 mmHg reduced FCD, microvascular flow, tissue Po(2), Do(2) and Vo(2). Erythrocytes with increased Hb-O(2) affinity maintained hemodynamic conditions, Do(2) and decreased tissue Po(2). This study shows that in an anemic condition, maximal tissue Po(2) does not correspond to maximal Do(2) and Vo(2).     

Excess CO(2) output response during and after short-term intensive exercise in sprinters and long-distance runners

The purpose of the present study was to examine the response of excess CO(2) output to short-term intensive exercise in sprinters (SPR) and long-distance runners (LDR). End-tidal CO(2) pressure (PETCO(2)) increased up to about 20 s postexercise and then returned to the resting level at about 2-3 min postexercise. Thereafter, PETCO(2) remained below the resting level. VCO(2) excess, defined as the difference between VCO(2) and VO(2) was integrated from the start of exercise until PETCO(2) returned to the resting level. This integrated VCO(2) excess was defined as the first phase of CO(2) excess (1st CO(2) excess). The subsequent integrated VCO(2) excess until 10 min postexercise was defined as the second phase of CO(2) excess (2nd CO(2) excess). The ratio of 1st CO(2) excess to the lactate rise from rest to the peak value was significantly lower in SPR than in LDR, whereas 2nd CO(2) excess was significantly greater in SPR than in LDR. The decrease in PETCO(2) at 10 min postexercise was significantly larger in SPR than in LDR. The 2nd CO(2) excess was closely related to the decrease in PETCO(2). The results in the second phase suggest that the difference in the response of excess CO(2) output is derived from the difference in the respiratory chemosensitivity to lactic acid rise.     

Behavior of junction channels between rat glomus cells during normoxia and hypoxia

The activity of gap junction channels between cultured and clustered carotid body glomus cells of the rat was studied with dual voltage clamping during normoxia (PO(2) 300 Torr) and hypoxia induced by sodium dithionite (Na(2)S(2)O(4)) or 100% N(2). Na(2)S(2)O(4) reduced the saline PO(2) to approximately 10 Torr, whereas 100% N(2) reduced ambient O(2) to approximately 60 Torr. The following observations were made. 1) In normoxia, the intercellular macroconductance (G(j) = 3.0 +/- 1.01 ns, mean +/- SE) was changed unevenly (increased and decreased) under hypoxic conditions by either agent, although N(2) produced the largest changes. 2) The intercellular microconductances of the channels (g(j) = 104.44 +/- 10.16 pS under normoxic conditions) significantly decreased in 100% N(2) but showed depressions and enhancements in Na(2)S(2)O(4). 3) The conductance of single-junction channels (SChs), calculated as g(j) variance/mean g(j), yielded a mean of approximately 17.6 pS. Larger values were obtained with manual measurements of the data (approximately 34 pS). Hypoxic hypoxia (induced by 100% N(2)) significantly depressed the conductance of SChs when calculated from digitized records or from manual measurements. Hypoxia induced by Na(2)S(2)O(4) did not significantly change junctional conductance. 4) The number of intercellular channels, calculated as g(j)/SCh g(j), had a mean of approximately 452 (range 1 to 2,471). During N(2)-induced hypoxia, this number significantly decreased to approximately 84 but remained unchanged during Na(2)S(2)O(4) hypoxia. 5) The mean open time of junction channels varied from 4 to 30 ms in different experiments, having an overall mean of mu = 11.33 +/- 0.33 ms. This value was significantly reduced by 100% N(2) but was not changed by Na(2)S(2)O(4). 6) Intracellular calcium ([Ca(2+)](i)), 46.2 +/- 4.84 nM under normoxia, significantly increased to 77.32 +/- 11.27 nM with Na(2)S(2)O(4) and to 66.39 +/- 11.64 nM with 100% N(2). It is concluded that 100% N(2) uncouples glomus cells by significantly reducing intercellular macro- and microconductances. Hypoxia induced by Na(2)S(2)O(4) had variable effects. The coupling effects of hypoxia may depend on, or be aided by, increases in [Ca(2+)](i) and/or intracellular pH changes. However, secreted transmitters and ATP plus the effects of hypoxia on second messengers and other cytoplasmic components may also play an important role in this phenomenon.