mGluR1选择性拮抗剂LY367385对脑星形胶质细胞Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶的影响

背景：脑星形胶质细胞肿胀是肝衰竭时脑水肿的特征,但其机制尚未完全阐明。目的：研究代谢型谷氨酸受体1亚型（mGluR1）选择性拮抗剂LY367385对脑星形胶质细胞Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶的影响。方法：分离、培养小鼠脑星形胶质细胞,分为谷氨酸组、谷氨酸＋LY367385组、谷氨酸＋DMSO组和空白对照组,以定磷法检测Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性,以高效液相色谱法测定ATP含量。结果：与空白对照组相比,谷氨酸组、谷氨酸＋LY367385组和谷氨酸＋DMSO组Na^＋-K^＋-ATP酶活性、Ca^2＋-Mg^2＋-ATP酶活性和ATP水平显著降低（P〈0.05）;谷氨酸＋LY367385组和谷氨酸＋DMSO组显著高于谷氨酸组（P〈0.001）,两组间则无明显差异。结论：mGluR1选择性拮抗剂LY367385可提高Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性,减少ATP消耗,从而有效保护脑星形胶质细胞,有望成为预防和治疗肝性脑病的药物。     

解毒化瘀方对内毒素血症大鼠肝细胞线粒体能量代谢的影响

目的：观察解毒化瘀方对内毒素血症（endotoxemia，ETM）大鼠肝细胞线粒体能量代谢的影响。方法：将56只大鼠随机分为正常对照组及脂多糖（LPS）注射后6、12、24小时组和解毒化瘀方6、12、24小时组。取肝组织分离线粒体，测定其Na^＋-K^＋-ATP酶、Ca^2＋～Mg^2＋-ATP酶活性。同时行高压液相色谱检测线粒体内腺苷酸含量及能荷（EC）水平。结果：在注射LPS 6小时后，线粒体Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶活性降低，ATP、ADP含量及EC值减少；24小时后，线粒体Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶活性明显降低，ATP、ADP、AMP含量及EC值明显减少。与对应的LPS组比较，经解毒化瘀方处理后，肝细胞线粒体Na^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶活性增加，ATP、ADP、AMP含量及EC值均升高。结论：解毒化瘀方能增加ETM大鼠肝线粒体Ma^＋-K^＋-ATP酶、Ca^2＋-Mg^2＋-ATP酶活性，提高线粒体氧化磷酸化水平，增加线粒体腺苷酸EC值，改善能量代谢，具有保护肝细胞的作用。     

粉防己碱对喹啉酸损伤海马神经元MDA、NOS及ATP的影响

目的 探讨粉防己碱（Tet）对喹啉酸（QA）诱导损伤的原代海马神经元丙二醛（MDA）、一氧化氮合酶（NOS）及Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶的影响。方法 采用海马神经元原代培养，生化法检测QA损伤后海马神经元MDA含量、NOS及Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性并观察Tet对损伤后海马神经元上述指标的影响。结果 与模型组相比，Tet（10^-6和10^-7mol／L）能明显降低QA损伤后原代海马神经元MDA含量及NOS活性，增加Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性（P〈0．01或0．05）。结论 Tet能浓度依赖性地明显降低QA损伤后原代海马神经元MDA含量及NOS活性，增加Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性，可能参与了其对兴奋毒导致的海马神经元损伤的保护作用。     

电针对老年性痴呆模型大鼠海马线粒体酶活性的影响

目的研究电针对老年性痴呆（AD）模型大鼠海码神经元线粒体酶活性的影响，从能量代谢的角度探讨电针治疗AD的部分作用机制。方法以D-半乳糖腹腔注射和Aβ1-40海马注射诱导形成的AD模型大鼠为研究对象，电针“百会”、“涌泉”穴，每日1次，连续20d。以通道式水迷宫测试学习记忆能力的变化，评价电针对AD的治疗效庸；以生化方法检测海马神经元线粒体琥珀酸脱氢酶、Na^＋ -K^＋ -ATP酶、Ca^2＋ -Mg^2＋ -ATP酶的活性。结果电针能有效改善AD模型大鼠学习记忆能力，提高线粒体琥珀酸脱氢酶、Na^＋ -K^＋ -ATP酶、Ca^2＋ -Mg^2＋ -ATP酶活性。结论电针可促进ATP的合成与分解利用，调节线粒体功能，改善AD能量代谢障碍。     

山楂对D-半乳糖致衰小鼠抗氧化系统及钙稳态影响的实验研究

目的 观察衰老与细胞内Ca^2 含量的关系和山楂对D-半乳糖衰老小鼠抗氧化作用。方法 本实验以D-半乳糖衰老小鼠为研究对象，分别以大、中、小剂量的山楂水煎剂灌胃45d，测定了青年、老年小鼠血清总抗氧化能力(TAA)，红细胞内超氧化物歧化酶(SOD)活性、脑组织内丙二醛(MDA)含量，红细胞膜Na^ -K^ ATPase，脑组织Ca^2 含量变化，同时，观察不同剂量山楂对老年小鼠上述指标的影响。结果小鼠血清TAA，红细胞内SOD活性，红细胞膜Na^ -K^ -ATPase活性随增龄而下降；脑组织MDA含量，脑组织Ca^2 含量随增龄而上升。山楂可提高小鼠血清TAA，红细胞内SOD活性，红细胞膜Na^ -K^ -ATPase的活性，并能降低脑组织Ca^2 含量，脑组织MDA含量。在各给药组中以山楂中剂量组的抗氧化作用最强。结论 山楂能增强机体抗氧化能力，具有一定的抗衰老作用，同时，脑组织Ca^2 含量可作为衰老的一个指标。     

益气养阴活血对中国小型猪心肌梗死后早期心肌组织Na^＋-K^＋ATP酶、Ca^2＋-Mg^2＋ATP酶活性及抗氧化的作用

目的采用结扎中国小型猪冠状动脉造成急性前壁心肌梗死（AMI）模型,应用益气养阴活血中药（复方芪丹液）干预动物AMI后早期心室重构（VR）的影响,并研究其对动物心肌钙、镁离子和氧自由基的作用。方法中国小型猪28只,采取结扎冠状动脉左前降支中下1/3部,造成AMI模型。手术成功存活动物随机分为复方芪丹液大、小剂量组及卡托普利（开搏通）组、模型组、假手术组共5组,均予灌胃给药或自来水4周。4周后测定猪的血流动力学指标、心肌Na＋-K＋ATP酶、Ca2＋-Mg2＋ATP酶活性、心肌超氧化物歧化酶（SOD）、丙二醛（MDA）含量等。结果与模型组比较,复方芪丹液大剂量组的左室内压（LVP）、血压（BP）、-dp/dtmax值明显升高（P〈0.01）,复方芪丹液小剂量组及开博通组LVP显著升高（P〈0.05）,开博通组-dp/dtmax值显著升高（P〈0.05）。复方芪丹液大剂量组Na^＋-K＋ATP酶、Ca^2＋-Mg^2＋ATP含量较模型组显著升高（P〈0.05）,复方芪丹液小剂量组、开博通组与模型组相比Ca^2＋-Mg^2＋ATP酶仅有升高的趋势,未有统计学意义（P〉0.05）;复方芪丹液大剂量组、复方芪丹液小剂量组、开博通组SOD活力较模型组均显著升高（P〈0.05）。复方芪丹液大剂量组的MDA含量与模型组比较显著降低（P〈0.05）。结论益气养阴活血中药可提高中国小型猪AMI后心肌收缩力,改善血流动力学指标;增加SOD活性,降低MDA含量,提高细胞膜Ca^2＋-Mg^2＋ATP酶和Na^＋-K^＋ATP酶活力,起到干预AMI后VR和保护心肌的作用。     

葛根素对糖尿病大鼠胰腺线粒体MDA含量、SOD和ATP酶活性的影响

目的观察葛根素对实验性糖尿病大鼠胰腺线粒体丙二醛（MDA）含量、超氧化物歧化酶（SOD）和ATP酶活性的影响。方法30只Wistar大鼠随机分为正常对照组、糖尿病组和治疗组。采用四氧嘧啶腹腔注射复制糖尿病动物模型。葛根素注射液治疗8w后，测定血清葡萄糖、胰岛素、胰腺线粒体MDA、SOD含量和Na^＋-K^＋-ATP酶、Ca^2＋-ATP酶活性。结果糖尿病组大鼠血糖和MDA含量明显高于正常组（P〈0.001），而血清胰岛素、SOD、Na^＋-K^＋-ATP酶和Ca^2＋-ATP酶活性显著降低（P〈0.001）；使用葛根素治疗后，与糖尿病组比较，治疗组血糖及MDA含量降低（P〈0.05～0.001），血清胰岛素、SOD、Na^＋-K^＋-ATP酶和Ca^2＋-ATP酶活性升高（P〈0.05～0.01）。结论葛根素对糖尿病大鼠胰腺有保护作用。     

促红细胞生成素和血管紧张素转换酶抑制剂对血透患者贫血的影响

目的：了解促红细胞生成素和血管紧张素转换酶抑制剂对维持性血透（HD）患者红细胞的影响,为临床更合理治疗肾性贫血提供依据。方法：78例维持性HD患者随机分成HD组、HD＋EPO组、HD＋ACEI组和HD（Na^ -K^ ATP酶,Ca^2 -ATP酶）活性、血浆谷光甘肽过氧化物酶（GSH－PX）活力及红细胞脂质过氧化物丙二醛（MDA）含量。结果：与HD组比较,HD－EPO组治疗后,Hb,Hct,红细胞ATP酶（Na^ -K^ ATP酶,Ca^2 -ATP酶）活性和血浆GSH－PX活力明显升高,差异显著（P＜0．01）;红细胞MDA明显降低,差异显著（P＜0．01）。HD＋ACEI治疗后,Hct有所下降,存在差异（P＜0．05）,而Hb,红细胞ATP酶（Na^ -K^ ATP酶,Ca^2 -ATP酶）活性、血浆GSH－PX活力,红细胞MDA含量均无明显差异（P＞0．05）。结论：CRF维持性HD患者经促红细胞生成素治疗后,不仅红细胞数量明显升高,而且通过提高红细胞ATP酶活性、血浆谷光甘肽过氧化物酶活力,减少红细胞脂质过氧化物含量红细胞的形态和功能,延长红细胞寿命,纠正贫血。而血管紧张素转换酶抑制剂则有减少红细胞数量,加重贫血的趋势,但其对红细胞的形态和功能影响不大。     

首灵健脑胶囊治疗老年性痴呆小鼠的机制研究

目的探讨首灵健脑胶囊治疗老年性痴呆小鼠的机制.方法腹腔注射AlCl3复制慢性铝中毒老年痴呆模型,同时灌胃给予相应药物.给药结束后测试脑中单胺类递质去甲肾上腺素（NE）、多巴胺（DA）、5-羟色胺（5-HT）、丙二醛（MDA）、超氧化物歧化酶（SOD）、Na^＋-K^＋-ATP酶及胆碱酯酶含量.结果模型组小鼠脑中的单胺类递质、MDA、SOD、胆碱酯酶及Na^＋-K^＋-ATP酶含量与正常对照组比较均有统计学意义（P〈0.05或P〈0.01）;用药后与模型组比较,高、中剂量的首灵健脑胶囊和双氢麦角碱（喜得镇）对单胺类递质、MDA、SOD、Na^^＋-ATP酶和胆碱酯酶的含量均有显著的影响（P〈0.05或P〈0.01）;低剂量的首灵健脑胶囊对NE的含量有显著增加（P〈0.05）.结论首灵健脑胶囊减轻脑神经元的损伤,发挥防治老年性痴呆的作用.     

复方银杏滴丸抗脑功能衰退作用及作用机制探讨

目的　探讨复方银杏滴丸 (CO GBE)的抗脑功能衰退作用 ,并分析其可能的作用机制。方法　小鼠颈背部皮下注射D 半乳糖 (D galactose ,D gal) 4 9d ,测定模型组和给药组小鼠的学习记忆能力、胸腺和脾脏指数、脑组织超氧化物歧化酶 (SOD)活力、谷胱甘肽过氧化物酶 (GSH Px)活力、丙二醛 (MDA)和脂褐素含量的变化。结果　CO GBE 1 5mg/kg、30mg/kg、60mg/kg可以不同程度地改善模型小鼠的学习记忆能力 ;抑制模型小鼠胸腺萎缩 ;增强模型小鼠脑组织SOD、GSH Px活力 ,降低MDA和脂褐素含量 (P <0 0 5 ,P <0 0 1 )。结论　增强脑组织的抗脂质过氧化能力 ,可能是CO GBE改善学习记忆能力 ,抑制胸腺指数下降 ,抗脑功能衰退的作用机制     

苦参碱和阿苯达唑联合治疗小鼠泡球蚴病的机制探讨

目的 探讨泡球蚴病小鼠经苦参碱（matrine, Mat）阿苯达唑（albendazole, ABZ）及两药 联用治疗后机体的免疫应答状态和小鼠肝酶代谢的变化。 方法 泡球蚴病小鼠（AE小鼠）经Mat、ABZ及其联合用药治疗60 d后，检测小鼠血清中白细胞介素-2（IL-2）、IL-4、IL-6、肿瘤坏死因子-α（TNF-α）及肝组织匀浆中NO、一氧化氮合酶（NOS）、诱导型一氧化氮合酶（iNOS）、乳酸（LD）、乳酸脱氢酶（LDH）、钠钾ATP酶和钙镁ATP酶的含量及活性。 结果 药物治疗组血清中IL?鄄4、IL-6和TNF-α的含量较感染对照组降低（P<0.05），IL?鄄2的含量高于感染对照组（P<0.05），其中联合用药组IL-4和TNF-α下降较感染对照组明显（P<0.05）；各用药组肝组织LDH、NO、NOS和iNOS均较感染对照组明显下降（P<0.05），iNOS在Mat组及联合用药组下降幅度明显大于ABZ组（P<0.05），LD仅在联合用药组下降（P<0.05）；各用药组钠钾ATP酶和钙镁ATP酶较之对照组升高（P<0.05），且Mat组及联合用药组钙镁ATP酶与ABZ组差异有统计学意义（P<0.05）。 结论 AE小鼠经治疗后，Th1型细胞因子分泌增加，Th2型细胞因子分泌减少，说明Mat能提高小鼠机体的免疫力，并能显著改善小鼠肝功能，这可能与Mat作用钙离子通道和逆转耐药性有关。     

金莲花中荭草苷和牡荆苷对D-半乳糖致衰小鼠细胞膜转运能力的影响

目的研究金莲花中有效成分单体荭草苷和牡荆苷在D-半乳糖致衰小鼠体内组织细胞膜转运能力的保护作用。方法采用D-半乳糖腹腔注射致亚急性衰老小鼠为模型,8 w造模成功后,分成模型组,维生素E对照组,荭草苷和牡荆苷高、中、低各三个剂量组,给药后进行药理学研究。结果通过Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶试剂盒来测定金莲花单体荭草苷和牡荆苷对D-半乳糖致衰小鼠肝、脑、肾组织中Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶的活性,通过对酶系的检测,探究金莲花有效成分单体荭草苷和牡荆苷对动物体内细胞膜转运能力的影响以及筛选出最佳药物的构效关系。结论金莲花单体荭草苷和牡荆苷具有明显提高Na+-K+-ATP酶、Ca2+-Mg2+-ATP酶的活性,保护组织细胞膜转运能力,但荭草苷中、低剂量组的抗氧化活性高于牡荆苷。     

黄龙通络胶囊对大鼠心肌缺血再灌注心律失常的影响

目的探索黄龙通络胶囊对心肌缺血再灌注所致大鼠心律失常模型的保护作用。方法采用结扎大鼠冠状动脉前降支,引起心肌缺血再灌注所致心律失常模型,记录各组大鼠Ⅱ导联心电图,并测定心肌组织中Na+-K+-ATPase、Ca2+-Mg2+-ATPase的活性。结果黄龙通络胶囊有稳定QRS间期、PR间期的作用,能降低抬高的ST段;能显著提高线粒体膜Na+-K+-ATPase、Ca2+-Mg2+-ATPase活性。结论黄龙通络胶囊可能是通过保持缺血-再灌注心肌细胞膜的稳定性,改善缺血心肌能量代谢障碍,而发挥其抗心律失常的作用。     

肝硬化大鼠膈肌功能改变的实验研究

目的研究肝硬化大鼠膈肌损伤的作用机制。方法SD大鼠16只被随机分成对照组(n=8)和实验组(n=8)。实验组大鼠皮下注射40?l4制备肝硬化动物模型,共成模8只。应用体外灌流大鼠膈肌条的方法,分别测量其单收缩力(Pt),最大强直张力(Po),峰值收缩时间(CT),半舒张时间(1/2RT),张力最大上升速率( dT/dtmax),张力最大下降速率(-dT/dtmax),并测量在10、20、40、60、100Hz的张力,绘制力—频率曲线,同时测定膈肌组织中SOD、SDH、NOS、Na -K -ATPase、Ca2 -Mg2 ATPase的活性及MDA含量,并观察膈肌的形态学变化。结果肝硬化大鼠膈肌Pt,Po, dT/dtmax,-dT/dtmax均低于对照组(P<0.01);CT,1/2RT高于对照组(P<0.05);给予10、20、40、60、100Hz的电压刺激膈肌时,肝硬化大鼠膈肌张力明显低于对照组(P<0.05);肝硬化大鼠膈肌组织SOD、SDH、Na -K -ATPase,Ca2 -Mg2 ATPase活性明显低于对照组(P<0.05),而MDA含量和NOS活性显著高于对照组(P<0.05);肝硬化大鼠膈肌肌纤维断裂,溶解。结论肝硬化大鼠膈肌肌纤维结构受到破坏,收缩功能下降,可能与SOD,SDH,Na -K -ATPase,Ca2 -Mg2 ATPase活性降低,NOS活性和MDA含量增高有关。     

Investigations of cardiac sarcolemmal ATPase activity in rabbits with acute myocarditis produced by scorpion venom (Buthus tamulus)

Acute myocarditis is produced in rabbits with scorpion (Buthus tamulus) (a common scorpion found in South India) venom. Acute myocarditis is confirmed by changes in the ECG taken before and after venom injection. The atrial and ventricular sarcolemmal Na+-K+ ATPase, Mg++ ATPase, and Ca++ ATPase activities are assayed in control and venom injected rabbits. Atrial and ventricular sarcolemmal ATPase activities are similar in control animals. A significant reduction in atrial Ca++ ATPase activity is seen in venom treated rabbits. Animals injected with 2 mg/Kg venom exhibited significant increases in Mg++ ATPase and Ca++ ATPase activities in the ventricular sarcolemma. However, significant reductions in Na+-K+ ATPase and Ca++ ATPase activities are observed in ventricular tissue from rabbits treated with 4 mg/Kg of venom.     

地精子皂甙抗缺血再灌性心律失常的作用机制研究

目的研究地精子皂甙对心律失常的作用机制.方法借助缺血-再灌注诱发心律失常大鼠模型,观察地精子皂甙对心律失常大鼠心肌组织乳酸代谢、Ca2 浓度、脂质过氧化损伤及心肌细胞膜Na -K -ATPase和Ca2 -Mg2 -ATPase活性的影响.结果心律失常大鼠心肌组织乳酸大量堆积,脂质过氧化增强,Ca2 含量增高,而心肌细胞膜Na -K -ATPase、Ca2 -Mg2 -ATPase活性明显降低;与模型组比较,地精子皂甙大、中剂量治疗组心肌组织乳酸含量明显降低,心肌组织丙二醛(MDA)含量也明显较低,而超氧歧化酶(SOD)活性升高(P＜0.05),其中地精子皂甙大、中剂量和维拉帕米皆可明显提高心肌细胞膜Na -K -ATPase、Ca2 -Mg2 -ATPase活性,并能明显降低心肌组织Ca2 含量(P＜0.05).结论地精子皂甙具有明显抗心律失常的作用,其作用机制是通过改善缺血再灌注心肌乳酸代谢,对抗脂质过氧化损伤,提高缺血心肌细胞ATP含量,提高心肌细胞膜Na -K -ATPase、Ca2 -Mg2 -ATPase活性,抑制了Ca2 超负荷,从而发挥其抗心律失常的作用.     

Sarcolemmal Ca2+-binding and enzyme activities in myocardium from hypothyroid rat

Effects of hypothyroidism on heart sarcolemmal activities were examined by using membrane preparations obtained by two different methods from rats treated with propylthiouracil for 6 to 8 weeks. ATP-independent Ca2+ binding, sialic acid and phospholipid content, Ca2+ ATPase, Mg2+ ATPase and adenylate-cyclase were not altered in membranes isolated by the hypotonic shock-LiBr treatment method from hypothyroid hearts. On the other hand, depressed activities of ouabain sensitive Na+-K+ ATPase and 5'-nucleotidase were observed in this hypothyroid preparation. Sarcolemma isolated by the sucrose density gradient procedure from hypothyroid hearts exhibited lower ouabain-sensitive Na+-K+ ATPase and higher ATP-dependent Ca2+ binding as well as Ca2+ stimulated ATPase without any changes in the 5'-nucleotidase, adenylate cyclase and Mg2+-ATPase activities. The activation of ATP-dependent Ca2+ binding and Ca2+ stimulated ATPase by calmodulin in the hypothyroid preparation was greater than the control; these effects of calmodulin were blocked by trifluoperazine. The results suggest some specific changes in the heart sarcolemmal Ca2+-pump during the development of hypothyroidism.     

Heart sarcolemmal ATPase and calcium binding activities in rats fed a high cholesterol diet

ATPase and calcium binding activities were studied in sarcolemmal membranes from hearts of male rats fed either a control or 2% cholesterol diet for different time periods. Studies with isolated membrane revealed a significant increase in Na+-K+ ATPase activity, sialic acid content and ATP-independent calcium binding capacity in the presence of 1.25 mM CaCl2 in the 6 week cholesterol fed group. By 12 weeks, Na+-K+ ATPase, Mg2+-ATPase and Ca2+-ATPase activities as well as ATP-independent calcium binding in the presence of 0.05 mM CaCl2 were increased in membranes from cholesterol fed rats. A significant increase (P less than 0.05) in the sarcolemmal cholesterol/phospholipid molar ratio, which is an indicator of a decrease in membrane fluidity, was also noted in the 12 week cholesterol fed group. Concanavalin A, which is believed to decrease membrane fluidity, stimulated both Mg2+ and Ca2+-dependent ATPase activities and increased ATP-independent calcium binding in control sarcolemmal preparations and these changes resembled those observed in the sarcolemma from cholesterol fed rats. Since concanavalin A did not alter the activity of Na+-K+ ATPase, it appears that some of the observed differences in sarcolemmal activities upon cholesterol feeding did not correlate well with changes in membrane order. At 24 weeks, there was a generalized depression in the sarcolemmal ATPase activities of the cholesterol group; both Mg2+ ATPase and Ca2+ ATPase were significantly less than in control.(ABSTRACT TRUNCATED AT 250 WORDS)     

Alterations of Na+-K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase activities in erythrocyte, muscle, and liver of traumatic and septic patients

Na+-K+-ATPase, Ca2+-ATPase and Mg2+-ATPase activities of erythrocyte membrane, microsomal fractions of rectus muscle, and liver were measured colorimetrically in the biopsy specimens of 14 control, 7 uncomplicated trauma (group 2), and 14 severe trauma or septic patients (groups 3-A and 3-B). In erythrocytes, these three ATPase activities in group 2 were not significantly changed but sepsis of both the acute (group 3-A) and ongoing type (group 3-B) decreased all of the ATPase activities. In muscle, there was a significant loss of three ATPase activities in the acute insult of severe trauma or sepsis (group 3-A), while Na+-K+-ATPase and Mg2+-ATPase activities were not significantly changed in ongoing, severe trauma (group 3-B). In the liver, a tendency for all three ATPase activities to decrease is noted in the severe traumatic group. However, a statistical difference between the control and severe traumatic group showed only for Na+-K+ ATPase and Mg2+-ATPase in group 3-A and Ca2+-ATPase in group 3-B. Correlation coefficients between erythrocyte, muscle, and liver for three ATPase activities are between 0.4 and 0.5. The mechanism which alters ATPase activity remains unknown in this study, but it may account for the variation in traumatic insult, in hemodynamic and hormone changes, and in tissue energy stores.     

Abnormalities in heart membranes and myofibrils during bacterial infective cardiomyopathy in the rabbit.

We studied hearts from sham-operated and uninfected catheterized rabbits as well as from rabbits at early and late stages of cardiomyopathy and failure after 3 and 6 days of infection with Streptococcus viridans. No ultrastructural abnormalities or biochemical changes in membrane and myofibrillar activities were seen in 3-day uninfected hearts. In 6-day uninfected hearts there were decreased sarcolemmal M2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding and uptake, and myofibrillar Ca2+-stimulated ATPase as well as increased mitochondrial calcium uptake. Slight ultrastructural changes also were apparent in 6-day uninfected hearts. At both early and late stages of infective cardiomyopathy and failure there were varying degrees of depression in sarcolemmal Mg2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding, calcium uptake and basal ATPase, and myofibrillar Ca2+-stimulated ATPase activities. However, sarcolemmal Ca2+ ATPase and myofibrillar Mg2+ ATPase activities were decreased only after 6 days of infection. Mitochondrial calcium binding and uptake were increased in early stages but decreased in late stages of disease. Furthermore in infected hearts there were defects in mitrochondrial respiration and phosphorylation. Generalized severe myocardial cell damage involving myofibrils, mitochondria, and the sarcotubular system was seen only in late stages of infection. The results demonstrate impairment of different membrane and contractile protein functions as well as ultrastructural abnormalities in bacterial cardiomyopathic hearts which were absent or of lesser magnitude in hearts with only hypertrophy. The findings reported here suggest to use that there is an association between heart failure and changes in function of cellular components during bacterial infective cardiomyopathy.