抗心律失常肽对低钾低镁条件下伊布利特致尖端扭转性室性心动过速的影响

目的探讨缝隙连接开放剂抗心律失常肽(AAP10)对低钾、低镁条件下伊布利特致尖端扭转性室性心动过速(TdP)及心肌电不稳定性的影响。方法 54只日本长耳大白兔随机制备成左室楔形心肌块模型,随机分为对照组、低钾低镁组、伊布利特组、低钾低镁伊布利特组和AAP10干预组。对照组灌流正常台氏液,低钾低镁组灌流低钾低镁台氏液,伊布利特组灌流浓度2mg/l的伊布利特,低钾低镁伊布利特组灌流溶有同浓度伊布利特的低钾低镁台氏液,AAP10组给予AAP10干预的条件后灌流溶有伊布利特的低钾低镁台氏液。比较各组早期后除极(EAD)、R on T室性早搏和TdP的发生情况,以及QT间期、T波顶点到终点距离(Tp-e)和Tp-e/QT的变化。结果与对照组比较,低钾低镁伊布利特组QT间期、Tp-e和Tp-e/QT延长,EAD、R on T室性早搏、TdP的发生率明显增多。AAP10干预组,TdP、QT间期、Tp-e和Tp-e/QT比低钾、低镁伊布利特组显著减少。结论 AAP10可能通过开放缝隙连接减少跨壁复极离散度,从而起到预防伊布利特在低钾、低镁条件下的致TdP的作用。     

加替沙星致室性心律失常机制的研究

目的:探讨临床广泛使用的第四代氟喹诺酮类抗生素——加替沙星致室性心律失常的机制。方法:制作兔左室楔形心肌块模型,将30只健康新西兰长耳兔随机分为正常组、加替沙星组和低钾低镁组(低钾组),每组各10只。正常组灌流正常台式液,加替沙星组灌流19mmol/L加替沙星30min,低钾组灌流同浓度但溶于低钾低镁液的加替沙星30min。采用浮置玻璃微电极法同步记录各组内、外膜下心肌动作电位和跨壁心电图,观察灌流过程中心律失常发生率,QT间期和TDR(跨室壁离散度)的变化。结果:1与正常组比较,加替沙星组和低钾组的QT明显延长;TDR,EAD(早后除极)和TdP(尖端扭转型室速)的发生率亦明显增大(P0.05)。2与加替沙星组比较,低钾组的QT和TDR差异未见统计学意义(P0.05)。3与加替沙星组比较,低钾组的EAD和TdP的发生率明显增大(P0.05)。结论:在加替沙星合并低钾低镁条件下易诱发Tdp及EAD等恶性心律失常。     

短QT间期综合征发生室性心律失常机制探讨

目的:探讨吡那地尔(pinacidil)建立的短QT间期综合征模型致室性心律失常的机制,并观察缝隙连接激动剂抗心律失常肽(AAP10)对该模型电生理参数的影响.方法:利用pinacidil灌注家兔楔形心肌块建立短QT间期综合征模型. 将20只新西兰长耳白兔随机分成pinacidil组和AAP10组,每组10只.pinacidil组灌流10 μmol/L的pinacidil,AAP10组灌流AAP10 500 nmol/l和pinacidil 10 μmol/L的混合液,同步记录灌流前后内外膜动作电位和容积心电图,观察灌流前后QT间期,跨室壁离散度(TDR),程序性刺激观察心肌组织不应期和室性心律失常的诱发情况.结果:灌流pinacidil后,QT间期从(291±19)ms缩到(232±19) ms (P<0.05),TDR从(44±12)ms减少到(22±7)ms(P<0.05),而不应期从(164±8)ms减少到(112±14)ms(P<0.05),室性心律失常发生率从0/10增加至8/10(P<0.05).AAP10 组和pinacidil组的TDR、QT间期、不应期及室性心律失常的诱发率无显著差别.结论:TDR减小和不应期的缩短可能是pinacidil建立的短QT间期模型致室性心律失常的基础,AAP10对pinacidil诱导的短QT间期综合征模型电不稳定性无明显影响.     

钙调蛋白激酶Ⅱ抑制剂对心肌肥厚兔室性心律失常的影响

目的观察钙调蛋白激酶Ⅱ抑制剂KN-93对心肌肥厚兔室性心律失常的影响。方法雌性新西兰大白兔随机分为4组：假手术组（Sham组）、心肌肥厚组（LVH组）、心肌肥厚＋KN-93组（KN-93组）、心肌肥厚＋KN-92组（KN-92组）,每组10只。LVH、KN-93及KN-92组通过缩窄腹主动脉制备兔心肌肥厚模型,Sham组仅游离腹主动脉未进行缩窄。8周后制备兔左室楔形心肌块的灌注模型,同步记录心内、外膜动作电位及跨壁心电图,观察低钾（2mmol／L）、低镁（0．25mmol／L）台氏液灌流及慢频率刺激条件下各组早期后除极（EAD）和尖端扭转型室性心动过速（Tap）的发生率,并记录在不同起搏周期下QT间期、动作电位时程（APD）及跨室壁复极离散度（TDa）的变化。结果在低钾、低镁台氏液灌流及2000～4000hi8慢频率刺激下,Sham、LVH、KN-92组（0．5μmol／L）及KN-93组（0．5μmol/L）EAD的发生率分别为0／10、10／10、9／10和5／10,Tdp的发生率分别为0／10、5／10、4／10和1／10;当KN-92组及KN-93组中药物浓度增至1μmol／L时,EAD的发生率分别为9／10和3／10,Tdp的发生率分别为4／10和1／10。而且KN-93组、KN-92组对QT间期、APD及TDR无明显影响（P〉0．05）。结论钙调蛋白激酶Ⅱ特异性抑制剂KN-93能够有效抑制心肌肥厚兔室性心律失常的发生,其主要作用机制是通过减少EAD的发生来实现。     

门冬氨酸钾镁对肥厚心肌室性心律失常的抑制作用

目的:观察口服门冬氨酸钾镁对肥厚心肌室性心律失常的影响并探讨门冬氨酸钾镁抗心律失常的作用机制。方法:将家兔随机分为假手术组、心肌肥厚组和门冬氨酸钾镁组。假手术组开腹但不行腹主动脉缩窄术,心肌肥厚组和门冬氨酸钾镁组采用腹主动脉缩窄术制备家兔心肌肥厚模型,喂养8周,制备兔左心室楔形心肌块,利用浮置玻璃微电极法同步记录楔形心肌块跨壁心电图和内、外膜心肌细胞跨膜动作电位,观察各组QT间期和内、外膜心肌细胞跨膜动作电位以及跨室壁复极离散度(TDR),程序电刺激诱发室性心律失常,记录早期后除极(EAD)和尖端扭转型室性心动过速(TDP)的诱发率。结果:门冬氨酸钾镁组和心肌肥厚组QT间期和内、外膜心肌细胞跨膜动作电位复极90%时程(APD90)和TDR较假手术组明显延长(均P<0.01)。门冬氨酸钾镁组与心肌肥厚组相比以上各项指标均明显缩短(均P<0.05)。假手术组、心肌肥厚组和门冬氨酸钾镁组EAD的发生率分别为0、100%和50%,TDP的发生率分别为0、40%和10%。心肌肥厚组与假手术组相比差异有统计学意义(P<0.01),门冬氨酸钾镁组与心肌肥厚组相比EAD和TDP的发生率明显降低(P<0.01)。结论:肥厚心肌TDR增大,心律失常的发生率显著升高。门冬氨酸钾镁降低TDR,可明显降低EAD和TDP的发生率。     

Langendorff逆灌流制备特非那丁诱发尖端扭转室性心动过速模型

目的对临床易发尖端扭转型室性心动过速(TDP)的情况进行模拟,利用Langendorff逆灌流技术灌注离体兔心,研究特非那丁促TDP的机制。方法烧灼法制备Ⅲ°房室传导阻滞离体兔心模型,应用不同浓度的特非那丁低钾镁台氏液,利用Langendorff逆灌流技术灌注兔心,以不同周长起搏,利用慢频率和刺激周长骤变方法诱发早期后除极(EADs)、TDP。结果基础台氏液和低钾镁台氏液(MT)灌流下均未见EADs、TDP;各浓度特非那丁低钾镁台氏液灌流都可延长QT间期和单向动作电位复极达90%时限(MAPD90),10/18例记录到EADs,起搏周长1 400~2 400 ms。10/18例诱发出TDP,7/18例经过刺激周长骤变诱发出TDP,以300~2 300 ms为多(6/18例),MT+特非那丁浓度8×10-6mmol/L时诱发TDP频率最高,为66.7%。结论在离体兔心,特非那丁MT灌注呈浓度及频率依赖性延长MAPD90;EAD及其引起的触发活动(TA)是诱发TDP的基础。     

门冬氨酸钾镁对家兔缺血再灌注心肌室性心律失常的影响

目的观察门冬氨酸钾镁注射液对家兔缺血再灌注心肌室性心律失常的抑制作用并探讨其抗心律失常作用机制.方法30只家兔随机分为正常组、心肌缺血组和治疗组,每组10只, 制备兔左心室楔形心肌块.正常组持续灌流台氏液,心肌缺血组和治疗组灌流台氏液1 h后停灌0.5 h,造成心肌缺血,0.5 h后复灌台氏液并程序刺激诱发心律失常,治疗组复灌的台氏液中含有浓度为2.42 mg/L的门冬氨酸钾镁.采用浮置玻璃微电极法同步记录楔形心肌块内、外膜心肌细胞跨膜动作电位和跨壁心电图,观察正常组、心肌缺血组和治疗组再灌注0.5 h的QT间期和内、外膜心肌细胞跨膜动作电位时程以及跨室壁复极离散度(TDR),记录正常组、心肌缺血组和治疗组缺血再灌注时室性心律失常的诱发率.结果①心肌缺血组较正常组和治疗组TDR明显延长(P＜0.05),治疗组与正常组相比,TDR差异无统计学意义(P＞0.05).②正常组无一例发生心律失常、心肌缺血组和治疗组室性心律失常的发生率分别为90%(9/10)、10%(1/10),心肌缺血组和治疗组间差异有统计学意义(P＜0.05).结论门冬氨酸钾镁可改善再灌注心肌的各项异常的电生理指标,特别是减小TDR,并能够明显降低再灌注心肌室性心律失常的发生率.     

Ⅲ度房室传导阻滞患者交感神经张力与多形性室性心动过速的关系

目的:探讨Ⅲ度房室传导阻滞(AVB)患者交感神经张力、QT间期和QT离散度(QTd)与多形性室性心动过速(Tdp)的关系。方法:选择永久起搏器治疗的Ⅲ度AVB患者93例,以术前是否发生晕厥和(或)Tdp史分为Tdp组和对照组。观察2组患者置入起搏器前1周内的R-R间期、P-P间期、QRS间期、QT间期和QTd以及置入起搏器后第1、2天与第5、6天的P-P间期、QT间期和QTd。结果:2组在术前R-R间期和QRS间期差异无统计学意义,但Tdp组P-P间期较对照组明显缩短,分别为(601±72)与(720±68)ms,P<0.01,QT间期和QTd较对照组明显延长,QT间期分别为(617±62)与(519±53)ms,P<0.01,QTd分别为(98±27)与(56±15)ms,P<0.01。在置入起搏器后第1、2天2组间QT间期和QTd差异有统计学意义,第5、6天则差异无统计学意义。结论:Ⅲ度AVB伴晕厥史患者P-P间期明显缩短,QT间期和QTd明显延长,置入起搏器后这种差异逐渐消除。     

缝隙连接对心肌肥厚兔室性心律失常的影响

目的研究兔慢性压力超负荷模型中缝隙连接(G J)对室性心律失常的影响。方法30只兔随机分为假手术组(Sham组)、心肌肥厚组(LVH组)和抗心律失常肽组(AAP10组)。LVH组和AAP10组通过缩窄腹主动脉制备兔左室压力超负荷心肌肥厚模型,Sham组仅游离腹主动脉未进行缩窄。动物饲养3个月后制备兔左室楔形心肌块的灌注模型,Sham组和LVH组灌流台氏液,AAP10组灌流含AAP10的台氏液,记录不同起搏周长下容积心电图、跨室壁离散度(TDR)及刺激反应间期(SR I),并观察早期后除极(EAD)及室性心律失常的发生率。结果在不同频率起搏下,LVH组SR I和TDR与Sham组比较均明显增加(P<0.05)。而AAP10组的SR I和TDR与LVH组比较明显减小(P<0.05)。Sham组无1例诱发EAD和室性心律失常;在5 000 m s起搏时LVH组和AAP10组EAD的发生率分别为10/10、3/10,室性心律失常发生率分别为4/10,1/10,两组比较差异有显著性(P<0.05)。结论G J激动剂AAP10减轻了心肌肥厚时SR I的延长和TDR增加,相应的减少了EAD和室性心律失常的发生率。     

LQT2模型尖端扭转型室性心动过速的发生机制

目的探讨LQT2模型早期后除极(EAD)、跨壁折返以及尖端扭转型室性心动过速(Tdp)的发生机制。方法采用冠状小动脉灌注兔左室心肌楔形组织块标本,应用浮置玻璃微电极动作电位及ECG同步记录技术,以IKr阻断剂d-sotalol作为工具药模拟LQT2,并与延迟整流钾电流IK阻滞剂azimilide对比,观察两者对兔心内膜和外膜层心肌细胞动作电位时程(APD)、跨壁复极离散度(TDR)、EAD、R-on-T早搏和Tdp的作用。结果d-sotalol和azimilide均显著延长心内膜和外膜层心肌细胞APD和QT间期;d-sotalol显著增加TDR,诱发EAD、R-on-T早搏和自发性Tdp的发生率分别为7/7,7/7和3/7;azimilide不增加TDR和不形成跨壁折返,但可诱发EAD和R-on-T早搏。结论通过冠状小动脉灌注兔左室心肌组织块LQT2模型,发现整体心室肌组织在QT延长的条件下,2相EAD是触发并引起Tdp的机制;TDR增加是产生EAD和形成折返的基础。     

钙调蛋白激酶Ⅱ信号转导途径在儿茶酚胺敏感性室性心动过速中的作用

目的研究钙调蛋白激酶Ⅱ(CaMKⅡ)特异性抑制剂KN-93对异丙肾上腺素和咖啡因诱导的晚期后除极(DAD)和触发活动的影响,探讨CaMKⅡ磷酸化途径在儿茶酚胺敏感性室性心动过速(CPVT)发生中的作用。方法酶解法分离家兔心室肌细胞,应用全细胞膜片钳技术记录动作电位(AP),采用含1μmol/L异丙肾上腺素和0.3mmol/L咖啡因的正钙台氏液灌流心室肌细胞,在快频率(3Hz)电刺激下,诱发DAD和触发活动,建立CPVT细胞模型。在此基础上应用KN-93(1μmol/L)和KN-92(1μmol/L)进行灌流,观察KN-93和KN-92对DAD和触发活动诱发率的影响。结果在1μmol/L异丙肾上腺素和0.3mmol/L咖啡因的正钙台氏液灌流下,3Hz时DAD和触发活动的诱发率达到18/20和6/20,建模成功。KN-93组、KN-92组DAD的发生率为8/20、18/20,触发活动的发生率为6/20、19/20。结论CaMKⅡ信号转导途径可能是CPVT发生的主要作用机制之一。     

Correction of hypomagnesemia by dapagliflozin in patients with type 2 diabetes: A post hoc analysis of 10 randomized,placebo-controlled trials

AimsHypomagnesemia (serum magnesium [Mg] <0.74 mmol/L [<1.8 mg/dL]) is commonly observed in patients with type 2 diabetes (T2D). This study investigated the effect of treatment with dapagliflozin 10 mg on Mg concentrations in patients with T2D.MethodsIn this post hoc analysis, we used pooled data from 10 placebo-controlled studies of dapagliflozin over 24 weeks of treatment in patients with T2D. We evaluated the change in Mg in patients receiving dapagliflozin vs. placebo overall, and in subgroups with baseline hypomagnesemia and normal/hypermagnesemia (≥0.74 mmol/L [≥1.8 mg/dL]). We determined the proportion of patients with baseline hypomagnesemia who achieved Mg ≥0.74 mmol/L (≥1.8 mg/dL).ResultsA total of 4398 patients with T2D were included. The mean change from baseline to week 24 in Mg was significantly larger with dapagliflozin vs. placebo; difference, 0.06 mmol/L (95% confidence interval [CI]: 0.05, 0.06). The proportion of patients with Mg within the population reference range after 24 weeks of treatment was significantly higher with dapagliflozin vs. placebo; difference, 47.8% (95% CI: 41.4, 53.9). The proportion of patients displaying hypermagnesemia did not increase with dapagliflozin treatment.ConclusionsTreatment with dapagliflozin 10 mg resulted in correction of Mg concentrations in patients with T2D and hypomagnesemia.     

Effects of tetrandrine on calcium and potassium currents in isolated rat hepatocytes

AIM: To study the effects of tetrandrine (Tet) on calciumrelease-activated calcium current (ICRAC), delayed rectifierpotassium current (IK), and inward rectifier potassiumcurrents (IK1) in isolated rat hepatocytes.METHODS: Hepatocytes of rat were isolated by usingperfusion method. Whole cell patch-clamp techniques wereused in our experiment.RESULTS: The peak amplitude.of ICRAC was -508±115 pA(n＝15), its reversal potential of ICRAC was about 0 mV. At thepotential of -100 mV, Tet inhibited the peak amplitude ofICRAC from -521±95 pA to -338±85 pA (P＜0.01 vs control,n＝5), with the inhibitory rate of 35 % at 10 μmol/L andfrom -504±87 pA to -247±82 pA (P＜0.01 vscontrol, n＝5),with the inhibitory rate of 49 % at 100 μmol/L, withoutaffecting its reversal potential. The amplitude of ICRAC wasdependent on extracellular Ca2+ concentration. The peakamplitude of ICRAC was -205±105 pA (n＝3) in tyrode's solutionwith Ca2+ 1.8 mmol/L (P＜0.01 vs the peak amplitude ofICRAC in external solution with Ca2+ 10 mmol/L). Tet at theconcentration of 10 and 100 μmol/L did not markedly changethe peak amplitude of delayed rectifier potassium currentand inward rectifier potassium current (P＞0.05 vs control).CONCLUSION: Tet protects hepatocytes by inhibiting ICRAC,which is not related to I K and IK1.     

锌对砷中毒小鼠肝脏Fas和FasL表达影响的实验研究

目的 探讨砷对小鼠肝脏Fas、FasL表达的影响及锌的拈抗作用.方法 选用健康昆明种小鼠60只,按体质量分成5组:阴性对照组(不给砷也不给锌),单纯给砷组(55 mg/L NaAsO2溶液),砷+低锌组、砷+中锌组、砷+高锌组均给55 mg/L NaAsO2溶液,并分别给20、40、80 mg/L ZnSO4溶液.经口连续灌胃(按体质量灌胃量为0.02 ml/g.1次/d)6周,待实验结束后处死小鼠,采用免疫组化法测定小鼠肝脏巾凋亡因子Fas、FasL表达.结果 干预组随着给锌量的增加,肝脏Fas、FasL的表达率逐渐降低.低、中锌+砷组的Fas的表达率[83.33%(10/12)、50%(6/12)]、FasL表达率[66.67%(8/12)、41.67%(5/12)]与阴性对照组Fas[8.33%(1/12)]、FasL[0.00%(0/12)]表达率比较,差异有统计学意义(P均<0.05);中、高锌+砷组的Fas的表达率[50%(6/12)、25%(3/12)]与阳性对照组[8.33%(1/12)]比较,差异有统计学意义(P均<0.01),中、高锌+砷组的FasL的表达率[41.67%(5/12)、16.67%(2/12)]与阳性对照组[91.67%(11/12)]比较,差异有统计学意义(P均<0.05).结论 砷可使小鼠肝脏Fas、FasL的表达率增高,促进肝脏的凋亡,锌可拮抗砷对细胞凋亡的作用.

Abstract：

Objective To investigate the effects of arsenic on liver Fas/FasL expression in mice and to observe the antagonize effect of zinc. Methods Sixty health Kunming mice were divided into five groups according to their body mass: negative control group(no arsenic and no zinc), arsenic group(55 mg/L NaAsO2 solution), low dose zinc intervention group(55 mg/L NaAsO2 solution and 20 mg/L ZnSO4 solution), middle dose zinc intervention group (55 mg/L NaAsO2 solution and 40 mg/L ZnSO4 solution), and high dose zinc intervention group (55 mg/LNaAsO2 solution and 80 mg/L ZnSO4 solution). Everyday the solution was given by oral gavage at a dose of 0.02 ml/g body weight for six weeks. The expression of Fas/FasL in mice liver was examined by immunohistochemistry.Results With the amount of zinc increasing, the expression of both Fas and FasL in mice liver decreased gradually. The expression rates of Fas[83.33%(10/12), 50%(6/12)] and FasL[66.67%(8/12), 41.67%(5/12)]in low dose zinc intervention group and middle dose zinc intervention group, respectively, were different from the expression rate of Fas[8.33%(1/12)] and FasL[0.00%(0/12)] in the negative control group(all P < 0.05). The Fas expression rate of middle dose zinc intervention group[50%(6/12)] and the high dose zinc intervention group [25%(3/12)] was compared with the arsenic group[8.33%(1/12)], and the difference was statistically significant (all P < 0.01 ). The FasL expression rate of the middle dose zinc intervention group [41.67% (5/12 )] and the high dose zinc intervention group[16.67%(2/12)] was compared with positive control group[91.67%(11/12)], and the difference was statistically significant (all P < 0.05). Conclusions Arsenic can increase the expression of Fas and FasL in mice liver, and promote apoptosis in liver, zinc may antagonize the effect of arsenic.     

The value of serum magnesium determination in hypertensive patients receiving diuretics

Some clinicians contend that hypomagnesemia is a common problem in patients receiving diuretic therapy and that routine serum magnesium determinations may be indicated in such patients. We determined serum magnesium (Mg++) levels in 354 patients with uncomplicated hypertension. No significant difference was observed in the mean Mg++ between the 245 diuretic-treated patients and the 109 patients not receiving diuretics, 0.965 vs 0.97 mmol/L (1.93 vs 1.94 mEq/L). When analyzed by type of diuretic, there were statistically significant differences in the mean serum Mg++ concentrations between those receiving thiazides, 0.94 mmol/L (1.87 mEq/L); those receiving no diuretics, 0.97 mmol/L (1.94 mEq/L); and those receiving triamterene-containing diuretics, 1.01 mmol/L (2.01 mEq/L). These absolute differences, however, were clinically quite small, and hypomagnesemia was uncommon. Neither patient age, the duration of diuretic use, nor the serum potassium level correlated with Mg++. With respect to dose, those receiving 100 mg/d of hydrochlorothiazide had the lowest Mg++ concentrations and the greatest prevalence of hypomagnesemia (12%), defined as Mg++ less than 0.75 mmol/L (1.5 mEq/L). Serum Mg++ need not routinely be determined in patients with uncomplicated hypertension who are receiving triamterene-containing diuretics or low-dose (50 mg/d or less) hydrochlorothiazide.     

N-乙酰半胱氨酸对日本血吸虫病小鼠肝组织中丙二醛和超氧化物歧化酶的影响

将90只小鼠随机分为健康对照组(18只)、感染对照组(18只)、长期服药组1(18只)、长期服药组2(18只)、短期服药组1(9只)和短期服药组2(9只),共6组。除正常对照组外,余各组小鼠经腹部皮肤感染日本血吸虫尾蚴30条。于感染的同时给长期服药组1和长期服药组2小鼠分别灌胃200 mg/kg、400 mg/kg N-乙酰半胱氨酸(N-acetylcysteine,NAC)(溶于0.2 ml蒸馏水),2次/d,共56 d;短期服药组1和短期服药组2小鼠在感染的第42天开始分别灌胃200 mg/kg、400 mg/kg NAC(溶于0.2 ml蒸馏水),2次/d,共14 d。正常对照组和感染对照组小鼠于感染同时灌胃0.2 ml生理盐水,2次/d,共56 d。正常对照组、感染对照组、长期服药组1和长期服药组2小鼠分别在感染后第42天和56天各处死9只;短期服药组1和短期服药组2于感染后第56天全部处死。观察各组小鼠肝组织中日本血吸虫单个虫卵肉芽肿个数和面积、血清和肝组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)的活性。结果表明,小鼠肝组织中炎症细胞浸润程度为+级单个虫卵肉芽肿个数以长期服药组1最少,平均为...     

人参二醇组皂甙在抗心肌缺血再灌注损伤作用中的钙拮抗剂效应

目的研究适宜浓度的人参二醇组皂甙(Panaxadiol Sapanins,PDS)在抗心肌缺血再灌注损伤作用中的钙拮抗剂效应。方法大耳白兔30只,体重(2.5±0.3)kg,随机分为对照组与4个实验组,每组6只,制成离体作功兔心模型。St.Thomas心脏停搏液用于对照组,该停搏液内分别加入浓度为40、80、160、320mg/L的PDS用于4个实验组(以PDS 40 mg/L组、PDS 80 mg/L组、PDS 160 mg/L组、PDS 320 mg/L组表示)。在阻断升主动脉即刻和心脏停搏30min、60min时分别灌注心脏停搏液。于心脏停搏前10min和心脏复搏后心脏作功30min时取心肌标本测定心肌钙离子含量。结果再灌注后PDS 40 mg/L组、PDS 80 mg/L组、PDS 160 mg/L组三个实验组的心肌钙离子含量均明显低于对照组(P<0.05或P<0.01),尤以PDS 160mg/L为著。而PDS 320mg/L组的心肌钙离子含量与对照组无显著差异(P>0.05),甚至有增高倾向。结论在抗心肌缺血再灌注损伤作用中,作为心脏停搏液的添加剂,PDS在40~160mg/L的浓度范围,有钙拮抗剂样作用,且在一定范围内随着浓度递增,该作用增强。但当PDS浓度增至320mg/L时,钙拮抗剂样作用消失。