高频喷射通气治疗PE—SWD兔血气和Na^＋—K^＋—ATPase图？…

为了探讨高频喷射通气（ＨＦＪＶ）治疗海水淹溺肺水肿（ＰＥ－ＳＷＤ）的作用机理,采用全自动血气酸碱分析仪和计算机图像分析系统对海水淹溺肺水肿组（ＰＥ－ＳＷＤ－Ｇ）、高频喷射通气组（ＨＦＪＶ－Ｇ）和正常对照组（ＯＮＴＲＯＬ ＧＲＯＰＵ,ｃｇ）兔ＰａＯ２、ＰａＣＯ２血氧饱和度（ＳａＯ２和兔肺内Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ进行自动检测和定量分析。结果表明,ＰＥ－ＳＷＤ经ＨＦＪＶ治疗１００ｍｉｎ,ＨＦＪＶ     

牛磺酸对缺血大鼠心肌线粒体Ca^2＋—Mg^2＋—ATP酶活性与MDA …

目的和方法：用Ｗｉｓｔａｒ大鼠皮下注射异丙肾上腺素（ＩＳＰ,５ｍｇ／ｋｇ）诱导心肌缺血模型。观测心肌线粒体（Ｍｉｔ）中丙二醛（ＭＤＡ）含量、Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－ＡＴＰ酶活性及牛磺酸（Ｔａｕ）的影响。结果：缺血组大鼠心肌Ｍｉｔ中ＭＤＡ升高８７．８３％、Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶和Ｃａ＾２＋－ＡＴＰ酶活性分别降低３７．５６％和５０．２０     

溶血磷脂酸对大鼠心肌细胞膜Na+-Ca2+交换的影响

本研究采用蔗糖梯度离心法制各大鼠心肌细胞膜,观察溶血磷脂酸（ ＬＰＡ）对心肌细胞膜 Ｎａ~＋－Ｃａ~(２＋)交换的影 响。结果发现ＬＰＡ（１～２０ｎｍｏｌ／Ｌ）呈剂量依赖性和时间依赖性刺激Ｎａ~＋一Ｃａ~（２＋）交换活性增加。Ｇｐｐ（ＮＨ）ｐ呈剂量依赖 性替代ＬＰＡ刺激的Ｎａ~＋－Ｃａ~(２＋)交换活性;ＰＴＸ可抑制ＬＰＡ对Ｎａ~＋－Ｃａ~(２＋)交换的激活;Ｇｅｎｉｓｔｅｉｎ,Ｐｒｏｐｒａｎｏｌｏｌ,Ｐｒａｚｏｓｉｎ,Ａｔｒｏｐｉｎｅ,Ｌｏｓａｒｔａｎ,ＢＱ１２３和磷脂酰胆碱对ＬＰＡ诱导的Ｎａ~＋－Ｃａ~２＋交换活性无影响,而磷脂酰丝氨酸可增加对照和ＬＰＡ 两组的 Ｎａ~＋－Ｃａ~(２＋)交换活性。这些结果表明 ＬＰＡ可通过 ＰＴＸ敏感的 Ｇ蛋白刺激大鼠心肌细胞膜 Ｎａ~＋－Ｃａ~(２＋)交换活性。     

人工细胞抗高血压因子对人脐静脉VSMC胞浆及核内Ca^2＋水平的影响

采实验用Ｆｌｕｏ－３／ＡＭ染色在激光扫描共聚焦显微镜下观察了红细胞抗高血压因子（ａｎｔｉｈｙｐｅｒｔｅｎｓｉｖｅ ｆａｃｔｏｒ,ＡＨＦ）对人脐静脉ＶＳＭＣ胞浆（〗Ｃａ＾２＋〖）及核内（〖Ｃａ＾２＋〗ｎ）游离钙离了瓣影响。结果表明：ＡＨＦ（１０＾－４ｇ／ｍＬ）明显抑制Ｂａｙ ｋ８６４４（１０＾－６ｍｏｌ／Ｌ）ＫＣｌ（６０ｍｍｏｌ／Ｌ）,ＡｎｇⅡ（１０＾－６ｍｏｌ／Ｌ）及ＩＰ３（１０＾－５ｍｏｌ／Ｌ）     

大鼠心房特殊颗粒Ca^2＋—ATP酶特性的研究

本实验对心房特殊颗粒（ＡＳＧ）膜上Ｃａ＾２＋－ＡＴＰ酶的特性进行研究，并与肌浆网（ＳＲ）膜上的Ｃａ＾２＋－ＡＴＰ酶特性进行比较。在１０ｍｍｏｌ／Ｌ Ｃａ＾２＋溶液中，二者膜上均显示酶活性，酶活性在１ｍｍｏｌ／Ｌ Ｃａ＾２＋孵育液中均减弱，并在Ｃａ＾２＋浓度降至０．１ｍｍｏｌ／Ｌ时酶反应均不显示。在加入０．１ｍｍｏｌ／Ｌ槲皮黄酮后，ＳＲ和ＡＳＧ膜上的酶活性同时被抑制；当加入０．１ｍｍｏｌ／Ｌ寡霉素后     

FasmAb诱导T细胞凋亡过程中胞浆游离钙的变化

采用荧光针Ｆｕｒａ－２／ＡＭ检测ＦａｓｍＡｂ诱导Ｊｕｒｋａｔ细胞ＰＣＤ过程 胞浆游离Ｃａ＾２＋的变化，探讨Ｃａ６２＋在Ｆａｓ介导ＰＣＤ中的作用。     

牛磺酸对缺血大鼠心肌线粒体Ca2+-Mg2+-ATP酶活性与MDA含量影响

目的和方法：用Ｗｉｓｔａｒ大鼠皮下注射异丙肾上腺素（ＩＳＰ,５ｍｇ／ｋｇ）诱导心肌缺血模型。观测心肌线粒体（Ｍｉｔ）中丙二醛（ＭＤＡ）含量、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性及牛磺酸（Ｔａｕ）的影响。结果：缺血组大鼠心肌Ｍｉｔ中ＭＤＡ升高８７８３％、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性分别降低３７５６％和５０２０％（Ｐ＜０．０１）。Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性与ＭＤＡ含量也呈显著负相关（ｒ＝－０．８７,Ｐ＜０．０１）。Ｃａ２＋－ＡＴＰ酶活性与ＭＤＡ含量也呈显著负相关（ｒ＝－０７９,Ｐ＜０．０１）。在注射异丙肾上腺素（ＩＳＰ）前３０ｍｉｎ腹腔注射Ｔａｕ（２００ｍｇ／ｋｇ）则Ｍｉｔ中ＭＤＡ含量、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性均未见显著异常改变。结论：Ｔａｕ可能通过抑制ＭＤＡ的生成实现其保护Ｃａ２＋－ＡＴＰ酶和Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性的作用。     

不同程度减压低氧对大鼠心功能及心肌Ca~（2＋）·Mg~（2＋）－ATPase

不同程度减压低氧对大鼠心功能及心肌Ｃａ￣（２＋）·Ｍｇ￣（２＋）－ＡＴＰａｓｅ的影响孙希武，叶益新，邓希贤（中国医学科学院基础医学研究所，北京１００００５）本文从整体、器官及细胞水平对不同程度减压低氧对大鼠心功能及心肌Ｃａ２＋·Ｍｇ２＋－ＡＴＰａｓｅ...     

长春新碱诱导的自噬性凋亡与细胞内游离Ca^2＋浓度的相关性研究

目的 研究长春新碱（ＶＣＲ）诱导的Ｌ－０２细胞自噬性凋亡细胞内游离钙离子浓度（［Ｃａ＾２＋］ｉ）的变化,以及自噬特异性抑制剂３－ｍｅｔｈｙｌａｄｅｎｉｎｅ（３ＭＡ）对此自噬性凋亡和［Ｃａ＾２＋］ｉ的影响。方法 应用已建立的ＶＣＲ诱导的Ｌ－０２细胞自噬性凋亡模型,使用电镜、流式细胞术检测细胞;用Ｆｌｕｏ－３／ＡＭ荧光探针经流式细胞仪测定Ｌ－０２细胞平均［Ｃａ＾２＋］ｉ。结果 电镜及流式细胞术检测证实     

雌激素对大鼠附睾上皮细胞非基因组作用及其机制研究

目的：研究雌激素对大鼠附睾上皮细胞非基因组作用及其机制。方法：青春期大鼠附睾上皮细胞,ＦＬＵＯ－３／ＡＭ标记,激光共聚焦显微镜技术观察。结果：１７β－雌二醇能快速诱导附睾上皮细胞内Ｃｑ＾２＋〖Ｃａ＾２＋〗ｉ升高,并且有剂量依赖性（１０＾－２～１０＾－９Ｍ）,无Ｃａ＾２＋液及２ｍＭ ＥＧＴＡ育附睾上皮细胞不影响雌二醇诱导效应;Ｃａ＾２＋通道阻活跃剂ｎｉｆｅｄｉｐｉｎｅ、ｖｅｒａｐａｍｉｌ也不影响雌二     

高频喷射通气治疗PE-SWD兔血气和Na+-K+-ATPase图像分析定量研究

为了探讨高频喷射通气（HFJV）治疗海水淹溺肺水肿（PE－SWD）的作用机理,采用全自动血气酸碱分析仪和计算机图像分析系统,对海水淹溺肺水肿组（PE－SWD－G）、高频喷射通气组（HFJV－G）和正常对照组（Con－trolgropu,CG）兔PaO2、p8CO2、血氧饱和度（SSO2）和兔肺内N －K －ATPase进行自动检测和定量分析。结果表明,PE－SWD经HFJV治疗100min后,HFJV－G中的PaO2、SaO2和肺毛细血管内皮细胞中Na －K －ATPase活性比PE－SWD－G明显升高（P＜0．01或P＜0．05）,并且HFJV－G中Na －K －ATPase的3项参数（D1、D2和G6）几乎恢复到接近CG水平。HFJV－G兔PaO2和SaO2的升高与肺内Na －K －ATPase活性的恢复密切相关。HFJV对PESWD的治疗,关键在于能较好地纠正低氧血症,因而对肺内Na －K －ATPase的恢复有明显的促进作用。     

HJ-1型一氧化氮治疗仪在救治兔海水淹溺肺水肿中的研究

采用合作研制的HJ－1型一氧化氮高频喷射通气治疗仪用于兔海水淹溺肺水肿的救治，复制兔海水淹溺肺水肿模型，将兔随机分为3组：海水淹溺肺水肿对照组、4药组（海水淹溺肺水肿动物用4种药物和高频喷射通气治疗仪救治），NO组（在4药组基础上再用HJ－1型一氧化氮高频喷射通气治疗仪救治），用血气分析仪测定Pao2,Sao2,pH值，发现NO组血氧分压和血氧饱和度比对照组显著提高，动物的存活时间大大延长，并阻止了海水淹溺肺水肿向海水型呼吸窘迫综合征的转归，提示该仪器用于救治肺水肿类疾病安全有效。     

脑益嗪抗运动病时大鼠血浆PG和小脑Na^＋—K^＋—ATPase图？…

为探讨脑益嗪抗运动病作用机理，采用放射免疫方法和计算机图像分析系统，对运动病组和脑佃嗪药物预防组大鼠血浆ＴＸＢ２，６－Ｋｅｔｏ－ＰＧＦ１α和小脑毛细血管内皮＾＋－Ｋ＾＋－ＡＴＰａｓｅ进行定量测量和分析研究。结果表明ＣＰＧ大鼠血浆ＴＸＢ２和６－Ｋｅｔｏ－ＰＧＦ１α显著低于ＭＳＧ，而小脑毛细血管内皮细胞Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ活性则明显高于。     

Alveolar epithelial beta2-adrenergic receptors

beta(2)-adrenergic receptors are present throughout the lung, including the alveolar airspace, where they play an important role for regulation of the active Na(+) transport needed for clearance of excess fluid out of alveolar airspace. beta(2)-adrenergic receptor signaling is required for up-regulation of alveolar epithelial active ion transport in the setting of excess alveolar edema. The positive, protective effects of beta(2)-adrenergic receptor signaling on alveolar active Na(+) transport in normal and injured lungs provide substantial support for the use of beta-adrenergic agonists to accelerate alveolar fluid clearance in patients with cardiogenic and noncardiogenic pulmonary edema. In this review, we summarize the role of beta(2)-adrenergic receptors in the alveolar epithelium with emphasis on their role in the regulation of alveolar active Na(+) transport in normal and injured lungs.     

Cytochemical investigation of p-NPPase activity in rat cardiac muscle.

The cytochemical demonstration of the atrial cardiac myocyte pumping activity has been made by detecting p-nitrophenylphosphatase (NPPase), which is used by investigating of Na(+)-K(+)-ATPase and H(+)-K(+)-ATPase activities. The fine ultrastructural localization of these enzymes was studied using cytochemical methods with cerium as a capturing agent. Na(+)-K(+)-ATPase was localized on the atrial muscle cell plasma membrane, T-tubule membrane, endothelial cell nuclear membrane, and cardiac myocyte nuclear membrane. H(+)-K(+)-ATPase was localized on the atrial muscle cells plasma membrane, T-tubule membrane, and sarcoplasmatic reticulum. The present findings indicate that the transporting metabolic activity of the heart as an endocrine organ is realized by the interaction between p-NPPases.     

Effect of hypoxia and dexamethasone on inflammation and ion transporter function in pulmonary cells

Dexamethasone has been found to reduce the incidence of high-altitude pulmonary oedema. Mechanisms explaining this effect still remain unclear. We assessed the effect of dexamethasone using established cell lines, including rat alveolar epithelial cells (AEC), pulmonary artery endothelial cells (RPAEC) and alveolar macrophages (MAC), in an environment of low oxygen, simulating a condition of alveolar hypoxia as found at high altitude. Inflammatory mediators and ion transporter expression were quantified. Based on earlier results, we hypothesized that hypoxic conditions trigger inflammation. AEC, RPAEC and MAC, pre-incubated for 1 h with or without dexamethasone (10(-7) mol/l), were subsequently exposed to mild hypoxia (5% O(2), or normoxia as control) for 24 h. mRNA and protein levels of cytokine-induced neutrophil chemoattractant-1, monocyte chemoattractant protein-1 and interleukin-6 were analysed. mRNA expression and functional activity of the apical epithelial sodium channel and basolateral Na(+)/K(+)-ATPase were determined using radioactive marker ions. In all three types of pulmonary cells hypoxic conditions led to an attenuated secretion of inflammatory mediators, which was even more pronounced in dexamethasone pretreated samples. Function of Na(+)/K(+)-ATPase was not significantly influenced by hypoxia or dexamethasone, while activity of epithelial sodium channels was decreased under hypoxic conditions. When pre-incubated with dexamethasone, however, transporter activity was partially maintained. These findings illustrate that long-term hypoxia does not trigger an inflammatory response. The ion transport across apical epithelial sodium channels under hypoxic conditions is ameliorated in cells treated with dexamethasone.     

Identification and properties of pathways for K+ transport in guinea-pig and rat alveolar epithelial type II cells.

86Rb+ was used to study potassium uptake and efflux in type II pneumocytes freshly isolated from adult guinea-pig and rat lung. Both species exhibited a substantial ouabain-sensitive component of potassium influx. In rats, most of the ouabain-resistant influx was abolished by bumetanide and removal of extracellular chloride elicited no further effect. In contrast, only a proportion of the ouabain-insensitive uptake was inhibitable by bumetanide in guinea-pigs and this species showed an additional component of influx, which was chloride dependent and which was reduced by either the K(+)-H(+)-ATPase inhibitor, omeprazole, or by the stilbene derivative, 4,4'-diisothiocyanostilbene-2,2'-disulphonate (DIDS). The chloride-dependent component was also apparent in efflux experiments in guinea-pigs, but was absent in rats. Ouabain-insensitive ATPase activity was assayed in highly purified apical membranes from guinea-pig type II pneumocytes. This activity was inhibitable by omeprazole (apparent inhibition constant, Ki, was approximately 40 microM), was potassium dependent (apparent activation constant, Ka, was approximately 200 microM) and was doubled by the addition of nigericin. While potassium transport in rat type II cells is adequately accounted for by Na(+)-K(+)-ATPase and Na(+)-K(+)-2Cl- cotransport, our data suggest the additional presence of K(+)-Cl- cotransport and K(+)-H(+)-ATPase in guinea-pig type II pneumocytes. A model of how alveolar subphase acidification may occur is proposed.     

Ionic mechanisms of regulatory volume increase (RVI) in the human hepatoma cell-line HepG2

We studied the effects of hypertonic stress on ion transport and cell volume regulation (regulatory volume increase; RVI) in the human tumor cell-line HepG2. Ion conductances were monitored in intracellular current-clamp measurements with rapid ion-substitutions and in whole-cell patch-clamp recordings; intracellular pH buffering capacity and activation of Na(+)/H(+) antiport were determined fluorometrically; the rates of Na(+)-K(+)-2Cl(-) symport and Na(+)/K(+)-ATPase were quantified on the basis of time-dependent and furosemide- or ouabain-sensitive (86)Rb(+) uptake, respectively; changes in cell volume were recorded by means of confocal laser-scanning microscopy. It was found that hypertonic conditions led to the activation of a cation conductance that was inhibited by Gd(3+), flufenamate as well as amiloride, but not by benzamil or ethyl-isopropyl-amiloride (EIPA). Most likely, this cation conductance was non-selective for Na(+) over K(+). Hypertonic stress did not change K(+) conductance, whereas possible changes in Cl(-) conductance remain ambiguous. The contribution of Na(+)/H(+)antiport to the RVI process appeared to be minor. Under hypertonic conditions an approximately 3.5-fold stimulation of Na(+)-K(+)-2Cl(-)symport was observed but this transporter did not significantly contribute to the overall RVI process. Hypertonic stress did not increase the activity of Na(+)/K(+)-ATPase, which even under isotonic conditions appeared to be working at its limit. It is concluded that the main mechanism in the RVI of HepG2 cells is the activation of a novel non-selective cation conductance. In contrast, there is little if any contribution of K(+) conductance, Na(+)/H(+) antiport, Na(+)-K(+)-2Cl(-) symport, and Na(+)/K(+)-ATPase to this process.