中频脉冲电流经皮刺激肝区对运动性疲劳大鼠肝细胞线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性的影响

目的探讨脉冲电流经皮刺激肝区对运动性疲劳大鼠肝脏线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性的影响。方法健康8周龄雄性Wistar大鼠72只,随机分为安静对照组(A组)、疲劳对照组(B组)、疲劳前刺激组(C组)、疲劳后刺激组(D组),每组18只。B、C、D组大鼠建立游泳力竭模型,C组和D组大鼠分别在游泳前和力竭后进行肝区脉冲电流刺激(频率1024Hz,电流强度10mA,间动周期1s,时间均为20min)。分别在第1、3、5周末分批处死各组动物(n=6),采用分光光度法测定大鼠肝脏线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性,采用Bradfood蛋白定量法进行大鼠肝脏线粒体蛋白定量。结果第1周末3组大鼠游泳力竭时间差异无统计学意义(P>0.05);第3周末、第5周末D组大鼠游泳力竭时间均明显长于B组和C组(P<0.05)。第1周末4组大鼠肝脏线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性差异无统计学意义(P>0.05);第3、5周末B组大鼠肝脏线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性明显低于其余3组,且C组大鼠肝脏线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性明显低于D组,差异均有统计学意义(P<0.05)。结论运动性疲劳大鼠肝脏线粒体Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶的活性降低,而脉冲电流经皮刺激肝区可以提高其活性,降低线粒体内游离钙浓度,减少线粒体钙超载,提高运动耐力及运动成绩,加速机体运动性疲劳的消除。     

脑复合剂对脑损伤大鼠Na+-K+-ATP酶、Ca2+-ATP酶活性及Ca2+调控的影响

目的 观察刨伤性脑损伤(traumatic brain injury,TBI)大鼠脑组织匀浆及线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性、神经细胞内游离Ca2+浓度及脑组织钙调蛋白(CaM)表达的动态变化,探讨脑复合剂脑保护作用的分子生物学机制.方法 建立大鼠TBI模型,分别设立假手术组、TBI组及中药治疗组.中药治疗组给予脑复合剂10 g·kg-1·d-1,假手术组及TBI组给予同等剂量等渗盐水,2次/d,连续7 d.分别于TBI后24 h、72 h、1周等3个时相点处死大鼠,动态定量分析各组大鼠脑组织匀浆及线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性、神经细胞内游离Ca2+浓度及脑组织CaM表达的变化.结果 TBI组各时相点大鼠脑组织匀浆及线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性均明显降低,于TBI后72 h后逐渐恢复,1周时仍明显低于假手术组.中药治疗组大鼠脑组织Na+-K+-ATP酶、Ca2+-ATP酶活性显著增加(P＜0.05);TBI组各时相大鼠脑组织神经细胞内游离Ca2+浓度及脑组织CaM表达均有不同程度增高,于伤后24 h达高峰,持续至72 h仍高于假手术组.而中药治疗组各时相大鼠神经细胞内游离Ca2+浓度及脑组织CaM表达明显低于TBI组(P＜0.05).结论 脑复合剂的脑保护作用可能与增加脑组织Na+-K+-ATP酶、Ca2+-ATP酶的活性,从而减轻TBI后脑细胞的能量代谢障碍,降低神经细胞内游离Ca2+浓度及脑组织CaM表达,减轻Ca2+超载所导致的继发性脑损伤有关.     

新生儿高胆红素血症中胱抑素C临床意义

目的探讨测定胱抑素C(Cys C)在新生儿高胆红素血症的临床价值。方法以74例高胆红素血症患儿(高胆红素血症组)和45例非高胆红素血症新生儿(对照组)作为研究对象,对两组新生儿的血尿素氮(BUN)、肌酐(CR)和Cys C进行测定。结果高胆红素血症组新生儿的BUN、CR检测指标和对照组比较,差异均无统计学意义(P>0.05);而高胆红素血症组新生儿的Cys C检测指标高于非高胆红素血症组,两组比较,差异有显著统计学意义(P<0.01);轻、中、重度高胆红素血症组新生儿Cys C检测指标逐渐增高,组间比较差异有显著统计学意义(P<0.01)。结论高胆红素血症时,Cys C水平随病情严重程度及时间增长而升高。     

模拟高强度军事训练对大鼠肾组织Na+,K+-ATP酶活性的影响

目的:探讨模拟高强度军事训练对大鼠肾组织Na+,K+-ATP酶活性的影响.方法:①一次性力竭运动:大鼠随机分对照组(A组)、一次性力竭运动组(B组).B组模拟军事训练行一次性力竭跑台运动,检测运动结束即刻(B1组)及24h后(B2组)尿液指标及肾组织Na+,K+-ATP酶活性.②递增负荷跑台运动:大鼠随机分对照组(C组)、递增负荷跑台运动组(D组).D组模拟军事训练行递增负荷跑台运动,检测4周末(C1组、D1组)和8周末(C2组、D2组)尿液指标及肾组织Na+,K+-ATP酶活性.结果:①一次性力竭运动结束即刻,B1组尿蛋白、尿N-乙酰-β-D-葡萄糖苷酶(NAG酶)较A组显著升高(P＜0.05),肾组织Na+,K+-ATP酶活性显著降低(P＜0.05),24h后有所恢复但仍低于A组(P＜0.05).②递增负荷跑台运动4周末D1组尿蛋白、尿NAG酶、肾组织Na+,K+-ATP酶活性均较C1组显著升高(P＜0.05);8周末D2组尿蛋白、尿NAG酶较C2组显著升高,肾组织Na+,K+-ATP酶活性显著降低(P＜0.05),且与尿NAG酶排泄呈负相关.结论:模拟高强度军事训练可引起大鼠肾组织Na+,K+-ATP酶活性的不同改变.     

DWI及常规MR在新生儿高胆红素血症及胆红素脑病诊断中的应用

目的 探讨DWI及常规MR在新生儿高胆红素血症及胆红素脑病诊断中的应用.方法 分析19例新生儿高胆红素血症及13例新生儿胆红素脑病患儿和8例健康新生儿(对照组)DWI及常规MR检查资料.结果 新生儿胆红素脑病常规MR表现:T1加权像可见苍白球对称性高信号,T2加权像可见苍白球呈等信号,13例病人中12例有此项MR表现,另外有6例新生儿胆红素脑病患儿底丘脑在T1加权像呈高信号,T2加权像呈等信号.13例新生儿胆红素脑病患儿苍白球及底丘脑DWI及ADC图信号均未见异常.19例高胆红素血症患儿苍白球及底丘脑T1加权像、T2加权像及DWI信号均未见异常.新生儿胆红素脑病组基底节区和丘脑ADC值较对照组和高胆红素血症组相比均稍微升高,但是3组差别无统计学意义(P＞0.05).结论 常规磁共振检查对从新生儿高胆红素血症患儿中早期发现新生儿胆红素脑病患儿并对新生儿胆红素脑病早期诊断可提供有益的帮助.DWI对于新生儿胆红素脑病患儿的早期诊断没有意义.     

卡巴胆碱对烫伤大鼠肠内补液时肠黏膜血流量、Na+-K+-ATP酶活性和水通道蛋白-1表达的影响

目的研究卡巴胆碱对烫伤早期大鼠肠内补液时肠黏膜血流量(IMBF)、Na -K -ATP酶活性和水通道蛋白-1(AQP1)表达的影响。方法雄性Wistar大鼠50只,随机分为假烫组、单烫组、肠内卡巴胆碱组、肠内补液组和肠内补液 卡巴胆碱组,每组10只。大鼠经35% TBSA Ⅲ度烫伤后,麻醉状态下进行十二指肠和回肠插管,与输液泵相连形成闭合回路进行小肠补液(灌流)。肠内补液时于烫伤后0.5h开始灌注葡萄糖-电解质溶液,灌注液总量为2ml/(kg.1% TBSA),于3.5h内在智能输液泵控制下匀速输入。卡巴胆碱(60μg/kg)于烫伤后0.5h肠内注射。伤后4h用激光多普勒血流仪测定IMBF,然后处死动物,取肠组织进行Na -K -ATP酶活性和AQP1免疫组化测定。结果IMBF、Na -K -ATP酶活性和AQP1表达肠内卡巴胆碱组和肠内补液组均显著高于单烫组(P<0.01),但低于肠内补液 卡巴胆碱组(P<0.05)。结论35%TBSAⅢ度烫伤肠内补液时给予卡巴胆碱能增加肠黏膜血流量和Na -K -ATP酶活性,促进AQP1表达,有助于肠道对口服液体的吸收。     

冷应激游泳和冷适应游泳对大鼠心肌和脑组织ATP酶、钙离子及自由基代谢的影响

目的:探讨冷应激游泳和冷适应游泳对大鼠心肌和脑自由基代谢、ATP酶活性和钙离子含量的影响。方法:30只健康雄性SD大鼠随机分成3组,每组10只。对照组不运动。冷应激游泳组前5周不运动,第6周末进行3天适应性游泳,每天1次,水温30℃,时间15 min。第7周在8℃水温中游泳1次,时间8 min,运动后即刻处死。冷适应游泳组适应性游泳3天,每天1次,水温30℃,时间15 min。之后进入正式训练:每天1次,起始水温30℃,时间40 min,从第2天起每天水温下降2℃,时间缩短3 min,每周训练6天,持续2周;从第3周起水温和时间保持在10℃、5 min,持续4周;第7周在8℃水温中游泳1次,时间8 min,运动后即刻处死。取材检测心肌和脑组织MDA含量、SOD活性、Na+-K+-ATP酶、Ca2+-ATP酶活性和Ca2+含量。各组大鼠每周称重1次。结果:冷适应游泳组大鼠体重较对照组和冷应激组显著降低。冷应激游泳组大鼠心肌和脑组织MDA含量较对照组显著升高,SOD、Na+-K+-ATP酶和Ca2+-ATP酶活性显著下降,心肌组织Ca2+含量升高,脑组织Ca2+含量显著升高。冷适应游泳组大鼠心肌和脑组织MDA含量较冷应激游泳组显著下降,SOD、Na+-K+-ATP酶和Ca2+-ATP酶活性显著升高,心肌、脑组织Ca2+含量下降。结论:冷适应游泳有减重效果,能明显降低心肌和脑组织脂质过氧化损伤,提高其抗氧化系统能力,改善ATP酶活性,维持心肌和脑的正常钙含量。     

补充几丁聚糖对一次力竭游泳小鼠红细胞自由基代谢及ATP酶活性的影响

目的:探讨补充4周几丁聚糖对一次力竭运动小鼠红细胞自由基代谢及ATP酶活性的影响。方法:昆明系小鼠36只随机分为安静组、力竭组和药物组,每组12只。药物组补充几丁聚糖,每日按0.33g/kg体重的剂量灌胃,补充4周后力竭组和药物组进行一次力竭游泳测试,记录游泳至力竭时间,测定运动后即刻各组红细胞MDA含量和SOD、GPH-Px、Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性。结果:药物组小鼠游泳至力竭时间与力竭组相比明显延长。力竭组小鼠红细胞MDA含量显著高于安静组,红细胞SOD、Na+-K+-ATP酶及Ca2+-Mg2+-ATP酶活性均显著低于安静组;药物组红细胞MDA含量显著低于力竭组,红细胞SOD、Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性均显著高于力竭组;三组间GSH-Px活性均无显著性差异。结论:补充几丁聚糖能降低力竭运动导致的红细胞自由基过氧化损伤、提高红细胞抗氧化酶活性、抵抗力竭运动导致的红细胞ATP酶功能下降,延长小鼠游泳至力竭时间。     

特布他林对海水浸泡人肺泡上皮细胞钠钾泵及钠通道的影响

目的 探讨特布他林对海水浸泡的人肺泡上皮细胞(A549)钠水转运通道的影响.方法 将常规培养的A549细胞分为海水处理(SG)组、特布他林(20 μmol/L孵育6h)处理(TG)组和阴性对照(NG)组.采用甲基噻唑基四唑(MTT)法检测细胞存活率,流式细胞仪检测细胞的凋亡和坏死情况,Western blotting法检测钠钾泵α1亚单位(Na+/K+-adenosine triphosphatase-α1,NKA-α1)、钠通道α亚单位(epithelail sodium channds-α,α-ENaC)的表达,水解比色法检测Na+-K+-ATP酶(Na-/K+-exchanging ATPase,NKA)活性.结果 MTT法及流式细胞仪检测结果均显示,特布他林处理对海水孵育后细胞的存活率无影响.NG组的NKA-α1和α-ENaC蛋白表达显著高于SG组(P＜0.01)和TG组(t=3.71,3.78,P＜0.01),TG组显著高于SG组(t=2.58,2.64;P＜0.05).与NG组NKA酶活性[(31.298±5.779)μmol/(mg·h)]比较,SG组[(14.211±3.885)μmol/(mg·h)]和TG组[(19.521±1.648)μmol/(mg·h)]明显降低(t=2.54,2.71;P＜0.05);TG组的NKA酶活性[(19.521±1.648)μmol/(mg·h)]较SG组升高(t=2.51,P＜0.05).结论 特布他林不影响人肺泡上皮细胞存活,并且可以抑制海水浸泡引起的α-ENaC、NKA-α1含量及NKA活性的下降.     

妈咪爱和鲁米那对早产儿儿胆红素代谢的影响

目的:治疗妈咪爱和鲁米那对早产儿胆红素代谢的影响.方法:将115例早产儿分为治疗组和对照组,治疗组出生1 d内口服妈咪爱和鲁米那,对照组不加任何干预,治疗组黄疸降至正常日龄,达到高胆红素血症标准(经皮测胆红素256.5 umol/L)的人数,5 d后血清总胆红素值.结果:治疗组降至正常日龄(8±1.8)d,对照组黄疸降至正常日龄(18±1.5)d;治疗组高胆红素血症3例;对照组高胆红素血症28例;治疗组和对照组在治疗5 d后血清总胆红素值分别为(44.8±18.2)μmol/L,(95.5±33.2)μmol/L.结论:早期服用妈咪爱和鲁米那能有效降低早产儿胆红素水平,促进黄疸消退,对预防早产儿高胆红素血症及胆红素脑病发生有一定作用.     

Recovery to +1Gz and +2Gz following +Gz-induced loss of consciousness: operational considerations

With the development of aircraft autorecovery technology, the need to understand the effects of potential inflight recovery profiles on human physiology has become important. Eight male volunteer subjects were exposed to +7Gz with an onset rate of 6 G.s-1 until they were unconscious. The subjects did not wear anti-G suits and did not perform anti-G straining maneuvers. The subjects controlled the centrifuge utilizing an F-16A stick, thereby deliberately self-inducing their unconsciousness. Following +Gz-induced loss of consciousness (G-LOC), recovery to the usual +1Gz level was compared to recovery to a +2Gz level by comparing absolute, relative, and total incapacitation times. The mean (+/- S.D.) absolute incapacitation time (period of unconsciousness) was 11.9 +/- 2.9 s for recovery to a +1Gz level and 12.9 S (+/- 6.9 S.D.) for recovery to a +2Gz level. The mean relative incapacitation time (period of confusion/disorientation) was 3.6 +/- 2.3 s for recovery to a +1Gz level as compared to 2.9 +/- 0.8 s for recovery to a +2Gz level. The total incapacitation time (sum of the absolute and relative incapacitation) was 15.6 +/- 2.7 s for recovery to a +1Gz level and 16.0 s (+/- 6.8 S.D.) for recovery to a +2Gz level. No significant differences in any of the incapacitation times were found when comparing recovery to +1Gz and +2Gz. The mean time from the onset of +Gz-stress to the onset of unconsciousness was approximately 7 s.(ABSTRACT TRUNCATED AT 250 WORDS)     

High altitude pulmonary hypertension: role of K+ and Ca2+ channels

Global alveolar hypoxia, as experienced at high-altitude living, has a serious impact on vascular physiology, particularly on the pulmonary vasculature. The effects of sustained hypoxia on pulmonary arteries include sustained vasoconstriction and enhanced medial hypertrophy. As the major component of the vascular media, pulmonary artery smooth muscle cells (PASMC) are the main effectors of the physiological response(s) induced during or following hypoxic exposure. Endothelial cells, on the other hand, can sense humoral and hemodynamic changes incurred by hypoxia, triggering their production of vasoactive and mitogenic factors that then alter PASMC function and growth. Transmembrane ion flux through channels in the plasma membrane not only modulates excitation- contraction coupling in PASMC, but also regulates cell volume, apoptosis, and proliferation. In this review, we examine the roles of K+ and Ca2+ channels in the pulmonary vasoconstriction and vascular remodeling observed during chronic hypoxia-induced pulmonary hypertension.     

ESR study of Gd3+ and Mn2+ ions sorbed on hydroxyapatite.

Adsorption of Gd3+ and Mn2+ into hydroxyapatite (HAP (Ca5(PO4)3(OH)2) was studied by ESR, ion chromatography and ICP-AES to investigate the U-uptake model. HAP absorbed Gd3+ via a cation exchange reaction and resulted in a signal width of 240 mT. The growth of the thermally stable Gd3+ signal in HAP was also fitted by saturation and diffusion equations. The ESR signals of Gd3+ and Mn2+ were observed overlapping the CO2- signals, however, the dose-response curves of the CO2- signal were similar to that of control HAP.     

Effects of extracellular Na+ and Ca2+ ions and Ca2+ channel modulators on the cell-associated activity of 99mTc-MIBI and 99mTc-tetrofosmin in tumour cells

Our aim was to determine whether the Ca2+ ion or cell membrane Ca2+ and Na+/Ca2+ ion transport systems are involved in maintaining the cell-associated activity of technetium-99m-hexakis-methoxy-isobutyl-isonitrile (99mTc-MIBI) and technetium-99m-ethylene-bis[bis(2-ethoxyethyl)phosphin] (99mTc-tetrofosmin) in tumour cell lines. The cell-associated activities of 99mTc-MIBI and 99mTc-tetrofosmin were assessed in various buffers, with or without Na+ and/or with different concentrations of Ca2+, in Lewi's murine lung cell carcinoma and human glioma cell lines. Different Ca2+ channel modulators, such as verapamil, flunarizine and 3,4-dichlorobenzamil (DCB), were used to assess the effect of Ca2+ channels on the cell-associated activity of 99mTc-MIBI and 99mTc-tetrofosmin. Despite significant differences between cell lines, the cell-associated activity of 99mTc-MIBI was higher in buffers without extracellular Ca2+ and Na+. The cell-associated activity of 99mTc-MIBI was significantly lower in all buffers containing high concentrations of Ca2+ in both cell lines. The cell-associated activity of Tc-tetrofosmin was also significantly higher in buffers without Ca2+, and was significantly decreased in buffers with high concentrations of Ca2+. All modulators significantly increased the cell-associated activity of 99mTc-MIBI in both cell lines in all buffers. All modulators increased the cell-associated activity of 99mTc-tetrofosmin, particularly in buffers containing Ca2+. The cell-associated activities of both 99mTc-MIBI and 99mTc-tetrofosmin may be dependent on verapamil-, flunarizine- and DCB-sensitive Ca2+ channels.