钙对盐胁迫下冰叶日中花不同器官离子含量和根部K~+、Na~+吸收的影响

以冰叶日中花(Mesembryanthemum crystallinum L.)实生苗为材料,经NaCl、NaCl+ CaCl_2、NaCl+LaCl_3处理后,利用电感耦合等离子发射光谱仪检测叶、茎、根中Na~+、K~+、Ca~(2+)、Mg~(2+)含量,计算K~+/Na~+、Ca~(2+)/Na~+和Mg~(2+)/Na~+比值,利用非损伤微测技术测定根尖Na~+流和K~+流,研究盐胁迫下钙在维持离子平衡中的作用。结果显示,NaCl处理后,冰叶日中花各器官中Na~+含量增加,K~+、Ca~(2+)、Mg~(2+)含量降低,离子比值降低;CaCl_2处理降低了Na~+含量,提高了K~+、Ca~(2+)、Mg~(2+)含量,离子比值升高,而LaCl_3处理后的结果相反。经NaCl处理24 h后,冰叶日中花根尖Na~+和K~+明显外流,加入CaCl_2后,Na~+外流速度显著增加,K~+外流速度受到抑制,而加入LaCl_3后则降低了Na~+的外流速度,促进了K~+的外流。研究结果表明冰叶日中花受到盐胁迫后,钙参与了促进根部Na~+外排、抑制K~+外流的过程,进而保持各器官中较低的Na~+含量,表明钙在维持和调控离子平衡中起到重要作用。     

盐渍土壤大果沙枣树主要矿质阳离子的吸收和分配特征

为探明大果沙枣树体矿质离子渗透调节机制,比较分析了盐渍化生境中1～12a生树的根、枝和叶部主要矿质阳离子的吸收、分配特征。结果表明:(1)大果沙枣树体内Ca~(2+)的积累量最高(13.79 g/kg),K~+次之(5.92 g/kg),Na~+最低(1.00 g/kg);随着树龄的增大,大果沙枣根部的Na~+以及枝和叶部的K~+、Ca~(2+)、Mg~(2+)的积累量均逐渐增大,而根部的K~+含量则逐渐减少;高龄段(10～12a)树体根部的Na~+累积量显著(P0.05)高于中低龄(1～9a)段。(2)大果沙枣树体内K~+/Na~+最大(15.36),Mg~(2+)/Na~+次之(12.25),Ca~(2+)/Na~+最小(10.51),根和枝部的K~+/Na~+均随着树龄的增大而降低,叶部则表现相反。(3)土壤中的K~+和Mg~(2+)向根方向、根部K~+、Mg~(2+)和Ca~(2+)向枝方向以及根部的K~+和Mg~(2+)向叶方向的选择运移系数均随着树龄的增大呈直线上升趋势。(4)土壤中Na~+与根部Na~+含量呈极显著正相关关系(0.687,P0.01),与叶部的K~+含量呈显著正相关(0.605,P0.05);土壤中K~+含量与根部的Na~+、叶部的K~+分别呈显著和极显著正相关(0.544,0.676),与根部的Mg~(2+)呈显著负相关关系(-0.499)。研究发现,大果沙枣树生长过程中主要通过根部对Na~+的聚积作用,以及K~+、Mg~(2+)和Ca~(2+)在枝、叶部的吸收积累来维持植物体离子平衡,以适应盐渍土壤环境。     

Na^＋—K^＋—ATP酶抑制与心肌缺血后再灌注性损伤

在离体大鼠心脏灌流模型上,观察细胞内高钠对心肌缺血后再灌注性损伤的影响。在低灌流过程中,给予Na~ -K~ -ATP酶抑制剂哇巴因造成细胞内高Na~ ,可加重缺血后再灌注心脏的血液动力学障碍;增加心肌组织丙二醛含量及冠脉流出液中乳酸脱氢酶的活性;降低线粒体及胞浆液中谷胱甘肽过氧化物酶活力;并使心肌组织中Ca~(2 )超负荷及K~ 丢失严重。因此,细胞内高Na~ 可能是心肌缺血后再灌注损伤的基础。     

褪黑素对盐胁迫下香椿幼苗生长及离子吸收和光合作用的影响

以香椿幼苗为材料,采用水培法研究不同浓度褪黑素(0、50、100、200和400μmol/L)对盐(150 mmol/L NaCl)胁迫下香椿幼苗生长指标、矿质元素离子(Na~+、K~+、Ca~(2+)和Mg~(2+))含量、净光合速率(P_n)、蒸腾速率(T_r)、气孔导度(G_s)和胞间CO_2浓度(C_i)等光合作用指标的影响,以探究外源物质褪黑素对盐胁迫下香椿幼苗生长和生理的调控作用。结果表明:(1)在盐胁迫条件下,香椿幼苗的生长受到显著抑制,叶绿素含量和P_n显著降低,叶片和根系中Na~+含量比对照(CK)显著增加,而K~+、Mg~(2+)和Ca~(2+)含量以及离子含量的比值(K~+/Na~+、Mg~(2+)/Na~+和Ca~(2+)/Na~+)则明显下降,且丙二醛含量显著增加。(2)施加适宜浓度褪黑素能显著促进盐胁迫下香椿植株生长,降低其叶片和根系中Na~+含量,提高其K~+、Ca~(2+)、Mg~(2+)含量和离子含量比值以及叶片P_n、T_r、水分利用效率(WUE)和G_s和C_i,但却降低了气孔限制值(L_s)。(3)适宜浓度褪黑素使盐胁迫下香椿植株叶片的丙二醛积累明显下降,叶绿素含量显著上升。研究发现,外施适宜浓度的褪黑素能降低盐胁迫下香椿幼苗叶片和根系内Na~+浓度,增加K~+、Mg~(2+)和Ca~(2+)浓度,调控植物体内细胞的离子平衡状态,增强对营养元素的吸收,提高光合作用效率,从而提高香椿幼苗对盐胁迫的抗性,并以100μmol/L褪黑素处理的效果最佳。     

NaCl胁迫对圆柏幼苗生长和离子吸收及分配的影响

以当年生圆柏幼苗为实验材料,采用温室调控盆栽土培法研究了不同浓度NaCl(0、100、200、300mmol·L-1)胁迫21d对其生长情况及不同器官(根、茎、叶)中K~+、Na~+、Ca~(2+)和Mg~(2+)的吸收和分配的影响,以探讨圆柏幼苗对盐环境的生长适应性及耐盐机制。结果表明:(1)随着NaCl胁迫浓度的增加,圆柏幼苗生长,包括株高、地径、相对生长量以及生物量的积累均呈下降趋势,而其根冠比却增加。(2)在各浓度NaCl胁迫处理下,圆柏幼苗根、茎、叶中Na~+含量较对照均显著增加,而且叶中Na~+含量显著高于茎和根,叶中Na~+含量是根中的5倍。(3)随着NaCl胁迫浓度的升高,圆柏幼苗各器官中K~+、Ca~(2+)和Mg~(2+)含量以及K~+/Na~+、Ca~(2+)/Na~+及Mg~(2+)/Na~+比值均呈下降趋势。(4)在NaCl胁迫条件下,圆柏幼苗根系离子吸收选择性系数SK,Na、SCa,Na、SMg,Na显著提高,茎、叶离子转运选择性系数SCa,Na、SMg,Na则逐渐降低,叶中离子转运选择性系数SK,Na则随着NaCl胁迫浓度的升高显著降低,大量Na~+进入地上部,减缓了盐胁迫对根系的伤害。研究认为,圆柏幼苗的盐适应机制主要是通过根系的补偿生长效应及茎、叶对Na~+的聚积作用来实现的,同时也与根对K~+、Ca~(2+)、Mg~(2+)的选择性运输能力增强和茎、叶稳定的K~+、Ca~(2+)、Mg~(2+)的选择性运输能力有关。     

NaCl处理对西伯利亚白刺幼苗生长及离子平衡的影响

以1年生西伯利亚白刺水培幼苗为材料,研究了不同浓度NaCl(0、200、400mmol·L~(-1))处理对幼苗生长及不同器官(根、茎、叶)中Na~+、K~+、Ca~(2+)、Mg~(2+)的吸收、运输与分配的影响,探讨西伯利亚白刺的盐适应机制。结果表明:(1)200mmol·L~(-1) NaCl处理促进了西伯利亚白刺幼苗的生长及叶片肉质化程度,400mmol·L-1 NaCl处理显著抑制其生长。(2)随着NaCl处理浓度的升高,西伯利亚白刺幼苗根、茎、叶中Na~+含量显著增加,且叶中Na~+含量显著高于茎和根中;根系中K~+含量显著增加;根、茎、叶中Ca~(2+)、Mg~(2+)含量在200mmol·L~(-1) NaCl处理下保持平稳或上升,而在400mmol·L-1 NaCl处理下显著下降。(3)各器官中K~+/Na~+、Ca~(2+)/Na~+和Mg~(2+)/Na~+比值总体随NaCl处理浓度的升高呈下降趋势,且根部离子比值始终高于叶片和茎。(4)随着NaCl处理浓度的升高,西伯利亚白刺幼苗根-茎SK,Na显著下降,而根-茎SCa,Na、SMg,Na及茎-叶SK,Na、SCa,Na、SMg,Na逐渐提高。研究发现,西伯利亚白刺的盐适应机制主要是通过植株的补偿生长效应及叶片对Na~+的聚积作用实现的,同时也与根系对K~+的扣留及茎叶对K~+、Ca~(2+)、Mg~(2+)选择性运输能力增强有关。     

盐胁迫对高丛越橘幼苗生长及离子平衡的影响

以高丛越橘"双迪"2年生扦插苗为材料,在盆栽条件下经0、100、200和300mmol·L~(-1)Na Cl溶液处理40天后,研究了幼苗干物质积累量、叶片受害情况以及矿质离子(Na~+、K~+、Ca~(2+)、Mg~(2+)和Cl~-)含量变化及其在根、茎、叶中积累、运输与分布特征,以揭示其盐适应生理机制,为耐盐越橘品种选育及合理栽培提供依据。结果表明:在低盐(100mmol·L~(-1))处理下总干物质量没有明显降低,在中高盐(200～300 mmol·L~(-1))处理下总干物质量明显降低,盐害指数随盐胁迫的加重而明显增大;在低盐处理下,茎和叶对K~+、茎对Mg~(2+)以及根对Ca~(2+)的吸收保持稳定;在中高盐胁迫下,Na~+和Cl~-在叶中大量积聚,显著降低了根对K~+、Ca~(2+)和Mg~(2+)以及茎和叶对K~+的吸收能力,显著降低了植株从根到叶K~+、Ca~(2+)和Mg~(2+)的整体运输能力,从而破坏了叶的离子平衡,导致离子毒害和生长受阻。     

关于溴氰菊酯神经毒作用的生物化学研究

 本文利用生物化学的手段,对大鼠进行了急性和亚急性毒性实验,研究溴氰菊酯对动物中枢神经系统离子调节作用的影响。急性实验结果表明:<1>溴氰菊酯能显著抑制脑微粒体上的Ca~(2+)+Mg~(2+)-ATP酶和Na~++K~+-ATP酶活性,但并不降低ecto-Ca~(2+)-ATP酶(细胞表面的Ca~(2+)-ATP酶)的活性;<2>溴氰菊酯对大鼠小脑组织中的环腺苷酸含量无明显影响,但却能显著升高与其作用相反的环鸟苷酸含量。体外实验证明,溴氰菊酯能够减少线粒体对Ca~(2+)的主动摄取。在对大鼠进行的亚急性实验中,发现溴氰菊酯中毒组与对照组大鼠的Ca~(2+)+Mg~(2+)-ATP酶、Na~++K~+-ATP酶和ecto-Ca~(2+)-ATP酶的活性均无显著性差异。根据以上结果推测,在急性中毒的条件下,溴氰萄酯能引起大鼠脑神经细胞内Ca~(2+)和Na~+的浓度增高,致使神经兴奋性发生改变。     

黄河三角洲柽柳植株周围土壤盐分离子的分布

为探讨柽柳的盐分富集效应及其对不同盐分离子分布的影响,以黄河三角洲盐碱地柽柳为研究对象,分析了离植株不同距离不同土层中的盐分离子组成、含量、离子比及不同离子之间的相关性。研究结果表明:各土层阳离子中Na~+含量最高,其次是Ca~(2+)和Mg~(2+),K~(+)最低,Cl~(-)在阴离子中的含量最高,SO_4~(2-)次之,HCO_3~-最低,而未检测到CO_3~(2-)。在柽柳植株周围,尤其是表层土壤中,离植株越近盐分含量越高,显示出柽柳对盐分的富集效应,其中对不同阳离子的富集程度表现为K~+Na~+Mg~(2+)Ca~(2+),而对阴离子的富集程度表现为HCO_3~-Cl~-SO_4~(2-)。冠层下凋落物中盐分的释放和树干径流可能是导致盐分在柽柳植株周围水平方向上存在差异的主要原因。土壤总可溶性盐含量随着土层的加深而升高。阳离子和阴离子向下迁移程度分别表现为Na~+Mg~(2+)Ca~(2+)K+和Cl~-SO_4~(2-)≈HCO_3~-,因而随土层加深而升高的Na~+、Ca~(2+)、Mg~(2+)和Cl~-,显示出底聚特征,而K+、SO_4~(2-)和HCO_3~-含量则随着土层的加深而降低,具有表聚特征。降水淋溶、盐分离子迁移速率的差别和各土层中不同生物量根系对盐分吸收的差异可能是造成盐分在垂直方向上含量变化的主要因素。     

黄精多糖对力竭训练小鼠肝组织损伤的保护作用

通过观察小鼠力竭训练后血ALT、AST,肝组织抗氧化指标、一氧化氮系统及ATP酶生化指标,探讨黄精多糖对小鼠运动性肝组织损伤的保护作用。研究以昆明雄性小鼠30只为研究对象,适应游泳训练后,随机分为3组(每组10只):安静组、运动组、对照组,除安静组外,运动组、运动给药组进行20 d,隔天一次的一次性力竭游泳训练,运动给药组小鼠灌服150 g/kg·d黄精多糖,其他两组小鼠灌服同体积的生理盐水。测定小鼠血清ALT、AST,肝组织MDA、GSH-PX、SOD、CAT、NO、总NOS、iNOS、eNOS、Na~+/K~+-ATP、Ca~(2+)/Mg~(2+)-ATP。测定结果显示:运动组与安静组比较,ALT、AST、MDA、NO、总NOS、iNOS升高,GSH-PX、SOD、CAT、Na~+/K~+-ATP、Ca~(2+)/Mg~(2+)-ATP降低;运动给药组与运动组相比,ALT、AST、MDA、NO、总NOS、iNOS降低,GSH-PX、SOD、CAT、Na~+/K~+-ATP、Ca~(2+)/Mg~(2+)-ATP升高。研究提示:黄精多糖能抑制过度训练引起的肝组织自由基增多,提高抗氧化酶的活性,通过调节i NOS、e NOS的活性,平衡NO的生成量,提高Na~+/K~+-ATP、Ca~(2+)/Mg~(2+)-ATP活性,保持较高的能量供给,维持细胞内外Na~+、K~+、Ca~(2+)、Mg~(2+)的正常分布与运转,对运动性肝组织伤有一定的保护作用。     

SMT对大鼠在体心脏缺血-再灌注损伤超微结构的保护作用

目的：研究ＳＭＴ对心脏缺血－再灌注损伤（ＩＲＩ）心肌超微结构的影响。方法：ＳＤ大鼠１８只,体重３２０￣３８０ｇ,随机分为三组：①缺血－再灌注组（ＩＲ）：夹闭冠状动脉左前降支６０ｍｉｎ,松夹２０ｍｉｎ。②缺血－再灌注＋ＳＭＴ组（ＳＭＴ）：再灌注前５ｍｉｎ,股静脉注射ｉＮＯＳ抑制剂Ｓ－ｍｅｔｈｙｌｉｓｏｔｈｉｏｕｒｅａ ｓｕｌｆａｔｅ（ＳＭＴ ５ｍｇ／ｋｇ ｗ）,余同ＩＲ组;③对照组（Ｃ）：暴露心脏后     

Endothelin A and B receptor antagonist bosentan reduces postischemic myocardial injury in the rat: critical timing of administration

The purpose of this study was to investigate the effects of bosentan, a mixed endothelin receptor A and B subtype antagonist, on myocardial ischemia-reperfusion injury and to explore the influence of the timing of bosentan administration on its cardioprotective effects. Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit solution (KH) at a constant flow rate at 10 mL/min. Global myocardial ischemia was induced by stopping KH perfusion for 40 min, and this was followed by 60 min of reperfusion. Hearts were randomized to 1 of 3 experimental groups (n = 7 each): untreated control; treatment with bosentan 1 micromol/L 10 min prior to, during 40 min global ischemia, and for 15 min of reperfusion (BOS); or treatment with bosentan 1 micromol/L after 15 min of reperfusion (BOS-R). We observed that BOS-R, but not the BOS treatment regimen, significantly reduced the release of cardiac-specific creatine kinase and postischemic myocardial infarct size (P < 0.05 vs. control) without affecting myocardial contractility. Left ventricular developed pressure in the BOS group was significantly (P < 0.01) lower than that in the control group throughout reperfusion. It is concluded that pharmacologically delayed antagonism of endothelin-1 during reperfusion attenuates postischemic myocardial injury. Endothelin-1 antagonist application during early reperfusion may exacerbate postischemic myocardial dysfunction.     

Triiodothyronine concomitantly inhibits calcium overload and postischemic myocardial stunning in diabetic rats.

Acute effects of triiodothyronine (T3) on postischemic myocardial stunning and intracellular Ca2+ contents were studied in the isolated working hearts of streptozotocin-induced diabetic rats and age-matched controls. After two weeks of diabetes, serum T3 and T4 levels were decreased to 62.5% and 33.9% of control values. Basal preischemic cardiac performance did not differ between diabetic and control rats. In contrast, during reperfusion after 20-min ischemia, diabetic rats exhibited an impaired recovery of heart rate (at 30-min reperfusion 57.5% of baseline vs. control 88.5%), left ventricular (LV) systolic pressure (44.1% vs. 89.5%), and cardiac work (23.1% vs. 66.0%). When 1 and 100 nM T3 was added before ischemia, heart rate was recovered to 77.2% and 81.8% of baseline, LV systolic pressure to 68.3% and 81.9%, and cardiac work to 50.8% and 59.0%, respectively. Diabetic rat hearts showed a higher Ca2+ content in the basal state and a further increase after reperfusion (4.96+/-1.17 vs. control 3.78+/-0.48 micromol/g, p<0.01). In diabetic hearts, H+ release was decreased after reperfusion (5.24+/-2.21 vs. 8.70+/-1.41 mmol/min/g, p<0.05). T3 administration caused a decrease in the postischemic Ca2+ accumulation (lnM T3 4.66+/-0.41 and 100 nM T3 3.58+/-0.36) and recovered the H+ release (lnM T3 16.2+/-3.9 and 100 nM T3 11.6+/-0.9). T3 did not alter myocardial O2 consumption. Results suggest that diabetic rat hearts are vulnerable to postischemic stunning, and T3 protects the myocardial stunning possibly via inhibiting Ca2+ overload.     

胰岛素保护缺血/再灌注心脏:PI3-K/Akt和JNKs信号通路间的交互作用

我们前期研究表明胰岛素可激活细胞内信号转导机制如磷脂酰肌醇3．激酶．蛋白激酶B．内皮型一氧化氮合酶．一氧化氮（P13-K-Akt-eNOS-NO）信号通路,减轻心肌缺血／再灌注（ischemia／reperfusion,I／R）损伤,改善缺血后心肌功能恢复。然而c-Jun氨基末端激酶（c-JunNH2-terminal kinase,JNK）信号通路在胰岛素保护I／R心肌中的作用尚不清楚,本研究旨在探讨JNK信号通路在胰岛素保护I／R心肌中的作用及其与P13．K／Akt信号通路间的相互关系。离体Sprague-Dawley大鼠心脏缺血30min后施行2h或4h的再灌注,缺血前用LY294002（15mmol／L）和SP600125（10mmol／L）灌注15min,分别阻断P13．K／Akt和磷酸化JNK（phosphorylated．JNK,p-JNK）活化,观测心脏功能、心肌梗死、细胞凋亡和蛋白磷酸化水平。与对照组相比,胰岛素再灌注2h后,心率、左心室发展压和左心室收缩／舒张最大速率均明显增加,梗死面积减少约16．1％[（28．9±2．0）％vs（45．0±4．0）％,n=6,P〈O．01],细胞凋亡指数从（27．6±113）％减少到（16．0±0．7）％（n=6,P〈O．01）,Akt的活性增加1．7倍（n=6,P〈0．05）,同时JNK活性增加1．5倍铆=6,P〈O．05）。用LY294002处理后,胰岛素对I／R心肌的保护作用消失;而用SP600125处理可增强胰岛素的保护作用,且可部分逆转LY294002的抑制作用。进一步观察发现SP600125减弱了Akt的磷酸化m=6,P〈0．05）。上述结果表明,在I／R心肌中,胰岛素可同时激活P13．K／Akt及JNK信号通路,且通过后者进一步增加Akt活化,从而减轻I／R损伤,改善心肌功能。这种P13．K／Akt与JNK信号通路交互机制对胰岛素保护I／R心肌有重要意义。     

Apelin-13 limits infarct size and improves cardiac postischemic mechanical recovery only if given after ischemia

We studied whether apelin-13 is cardioprotective against ischemia/reperfusion injury if given as either a pre- or postconditioning mimetic and whether the improved postischemic mechanical recovery induced by apelin-13 depends only on the reduced infarct size or also on a recovery of function of the viable myocardium. We also studied whether nitric oxide (NO) is involved in apelin-induced protection and whether the reported ischemia-induced overexpression of the apelin receptor (APJ) plays a role in cardioprotection. Langendorff-perfused rat hearts underwent 30 min of global ischemia and 120 min of reperfusion. Left ventricular pressure was recorded. Infarct size and lactate dehydrogenase release were determined to evaluate the severity of myocardial injury. Apelin-13 was infused at 0.5 μM concentration for 20 min either before ischemia or in early reperfusion, without and with NO synthase inhibition by N(G)-nitro-l-arginine (l-NNA). In additional experiments, before ischemia also 1 μM apelin-13 was tested. APJ protein level was measured before and after ischemia. Whereas before ischemia apelin-13 (0.5 and 1.0 μM) was ineffective, after ischemia it reduced infarct size from 54 ± 2% to 26 ± 4% of risk area (P < 0.001) and limited the postischemic myocardial contracture (P < 0.001). l-NNA alone increased postischemic myocardial contracture. This increase was attenuated by apelin-13, which, however, was unable to reduce infarct size. Ischemia increased APJ protein level after 15-min perfusion, i.e., after most of reperfusion injury has occurred. Apelin-13 protects the heart only if given after ischemia. In this protection NO plays an important role. Apelin-13 efficiency as postconditioning mimetic cannot be explained by the increased APJ level.     

Chronically administered acetaminophen and the ischemia/reperfused myocardium

Male and female Hartley strain guinea pigs weighing 280 +/- 10 g were given acetaminophen-treated water ad libitum for 10 days. Sham-treated control animals were given similar quantities of untreated tap water (vehicle-treated control group). On Day 10, hearts were extracted, instrumented, and exposed to an ischemia (low-flow, 20 min)/reperfusion protocol. Our objective was to compare and contrast ventricular function, coronary circulation, and selected biochemical and histological indices in the two treatment groups. Left ventricular developed pressure in the early minutes of reperfusion was significantly greater in the presence of acetaminophen, e.g., at 1 min, 40 +/- 4 vs 21 +/- 3 mmHg (P < 0.05). Coronary perfusion pressure was significantly less from 3 to 40 min of reperfusion in the presence of acetaminophen. Creatine kinase release in vehicle-treated hearts rose from 42 +/- 14 (baseline) to 78 +/- 25 units/liter by the end of ischemia. Corresponding values in acetaminophen-treated hearts were 36 +/- 8 and 44 +/- 14 units/liter. Acetaminophen significantly (P < 0.05) attenuated release of creatine kinase. Chemiluminescence, an indicator of the in vitro production of peroxynitrite via the in vivo release of superoxide and nitric oxide, was also significantly attenuated by acetaminophen. Electron microscopy indicated a well-preserved myofibrillar ultrastructure in the postischemic myocardium of acetaminophen-treated hearts relative to vehicle-treated hearts (e.g., few signs of contraction bands, little or no evidence of swollen mitochondria, and well-defined light and dark bands in sarcomeres with acetaminophen; opposite with vehicle). We conclude that chronic administration of acetaminophen provides cardioprotection to the postischemic, reperfused rodent myocardium.     

白藜芦醇甙对大鼠心脏缺血/再灌注损伤的保护作用

本文利用冠脉结扎/放松方法和Langendorff灌注技术,建立在体和离体大鼠心脏缺血/再灌注(ischemia/reperfusion,I/R)损伤模型,探讨白藜芦醇甙(polydatin)对大鼠I/R心肌损伤的保护作用及其机制.观察白藜芦醇甙对缺血和再灌注心律失常、心肌梗死面积、心脏收缩功能、心肌超氧化物歧化酶(superoxide dismutase,SOD)活性、丙二醛(malondialdehyde,MDA)含量、NO含量以及一氧化氮合酶(nitric oxide synthase,NOS)活性的影响.结果显示:与对照组相比,白藜芦醇甙组大鼠缺血和再灌注心律失常明显降低(P<0.05,P<0.01);心肌梗死面积显著减少(P相似文献   

Hyperosmotic pretreatment reduces infarct size in the rat heart

Preconditioning of the heart can be achieved by an ischemia/reperfusion stimulus, but also by stretching of the heart by an acute volume overload. Since manipulations of the extracellular osmolality affects cell size, we hypothesized that hyperosmotic pretreatment of the isolated perfused rat heart could reduce infarct size following regional ischemia (RI). Langendorff perfused rat hearts were subjected to 30 min RI by ligature of the main branch of the left coronary artery followed by 120 min reperfusion (control group). Ischemic preconditioning (IP-5') was achieved by 5 min total global ischemia and 5 min reperfusion prior to RI. Hyperosmotic pretreatment was accomplished by perfusion with a hyperosmotic buffer (600 mOsm/kg H2O by adding mannitol) for 1 min, 2 min or 5 min. At the end of the experiments, the hearts were cut into 2 mm slices, incubated with triphenyltetrazoliumchloride before scanning and computerized for estimation of infarct size. The average infarct size (as percentage of area at risk) in the control group was 42% and was significantly reduced to 16% by ischemic preconditioning and to 17% by 2 min hyperosmotic pretreatment. Neither 1 min nor 5 min hyperosmotic pretreatment reduced infarct size as compared to the controls. The infarct reducing effect of 2 min hyperosmotic pretreatment was not blunted by inhibition of protein kinase C (chelerytrine chloride), the Na+/H+-exchanger (HOE 694) or stretch-activated anion channels (gadolinium chloride). The results indicate that short-lasting hyperosmotic perturbations of the extracellular environment may precondition the heart to a subsequent ischemic insult.     

Apomorphine prevents myocardial ischemia/reperfusion-induced oxidative stress in the rat heart

This study examined the hypothesis that low-concentration apomorphine improves postischemic hemodynamic and mitochondrial function in the isolated rat heart model by attenuating oxidation of myocardial proteins. Control and apomorphine-treated hearts were subjected to 35 min of perfusion, 25 min of normothermic global ischemia, and 60 min of reperfusion. Apomorphine (2 microM) was introduced into the perfusate for 20 min starting from the onset of reperfusion. Apomorphine significantly (p <.05) improved postischemic hemodynamic function: work index of the heart (product of LVDP and heart rate) was twice as high in apomorphine-treated hearts compared to controls at the end of reperfusion (p <.01). After isolation of cardiac mitochondria, the respiratory control ratio (RCR) was calculated from the oxygen consumption rate of State 3 and State 4 respiration. Apomorphine significantly improved postischemic RCR (87% of preischemic value vs. 39% in control, p <.05). Using an immunoblot technique, carbonyl content of multiple unidentified myocardial proteins (mitochondrial and nonmitochondrial) was observed to be elevated after global ischemia and reperfusion. Apomorphine significantly attenuated the increased protein oxidation at the end of reperfusion. These results support the conclusion that apomorphine is capable of preventing ischemia/reperfusion-induced oxidative stress and thereby attenuating myocardial protein oxidation and preserving mitochondrial respiration function.     

Cardioprotective mechanisms of Prunus cerasus (sour cherry) seed extract against ischemia-reperfusion-induced damage in isolated rat hearts

The effects of kernel extract obtained from sour cherry (Prunus cerasus) seed on the postischemic cardiac recovery were studied in isolated working rat hearts. Rats were treated with various daily doses of the extract for 14 days, and hearts were then isolated and subjected to 30 min of global ischemia followed by 120 min of reperfusion. The incidence of ventricular fibrillation (VF) and tachycardia (VT) fell from their control values of 92% and 100% to 50% (not significant) and 58% (not significant), 17% (P<0.05), and 25% (P<0.05) with the doses of 10 mg/kg and 30 mg/kg of the extract, respectively. Lower concentrations of the extract (1 and 5 mg/kg) failed to significantly reduce the incidence of VF and VT during reperfusion. Sour cherry seed kernel extract (10 and 30 mg/kg) significantly improved the postischemic recovery of cardiac function (coronary flow, aortic flow, and left ventricular developed pressure) during reperfusion. We have also demonstrated that the extract-induced protection in cardiac function significantly reflected in a reduction of infarct size. Immunohistochemistry indicates that a reduction in caspase-3 activity and apoptotic cells by the extract, beside other potential action mechanisms of proanthocyanidin, trans-resveratrol, and flavonoid components of the extract, could be responsible for the cardioprotection in ischemic-reperfused myocardium.