糖尿病大鼠右心室乳头肌收缩功能的研究

目的: 研究不同时期糖尿病大鼠右心室乳头肌收缩功能状态。方法: 以四氧嘧啶复制大鼠糖尿病模型,在糖尿病大鼠的第2、4、6、8周, 游离右心室乳头肌, 置于氧合台氏液中, 电刺激状态下, 记录乳头肌收缩功能, 与对照组大鼠进行比较。结果: 糖尿病大鼠第4周的右心室乳头肌+dT/dt_max、-dT/dt_max显著低于对照组(P<0.05)。第6周+dT/dt_max、-dT/dt_max、舒张1/2间期与对照组差异显著(P<0.05、P<0.05、P<0.01)。第8周张力增量、+dT/dt_max、-dT/dt_max、+t-dT/dt_max及舒张1/2间期两组比较均有显著差异(P<0.01、P<0.01、P<0.01、P<0.01和P<0.05)。结论: 糖尿病大鼠右心室乳头肌收缩功能从第4周开始下降, 至第8周最明显。     

糖尿病大鼠不同阶段心肌电学的改变

目的:探讨糖尿病(DM)易出现心律失常的可能机制。方法:SD雄性大鼠尾静脉注射四氧嘧啶(alloxan,50mg·kg^-1以生理盐水稀释)复制糖尿病模型,选择以年龄相匹配健康成年SD雄性大鼠尾静脉注射相同剂量的生理盐水作为对照组。分别观察2、4、6和8周4个不同时段。记录大鼠右心室乳头肌跨膜电位。结果:在糖尿病成模后第2周起,右室乳头肌动作电位时程(APD)复极化各水平均不同程度地长于正常大鼠(P<0.01),8周时较2周时更明显(P<0.05)。而去极化最大速率(V_max)超射值(OS)和动作电位幅度(APA)以及静息膜电位(RP)水平均无明显变化。结论:糖尿病大鼠右室乳头肌动作电位时程明显延长,而动作电位的过度延长可能是糖尿病易导致心律失常以及心源性猝死的主要原因,尤其是糖尿病晚期阶段。     

不同浓度腺苷对肥胖症大鼠离体空肠平滑肌活动及肠系膜微循环的影响

目的:探讨腺苷对肥胖症大鼠离体空肠平滑肌活动及肠系膜微循环的影响。方法:实验分为普通饲料喂养大鼠组(A组)和高能量饲料喂养肥胖大鼠模型组(B组)。检测腺苷干预时肥胖症大鼠脂肪/体重比(L/W)?血清甘油三酯(TG)和总胆固醇(TC)水平?空肠平滑肌活动幅度(-dT)?主动张力最大舒张速率(-dT/dt-max)、Lee′s指数以及肠系膜微循环指标的变化。结果:(1)B组大鼠体重?L/W?Lee′s指数?TG、TC及腺苷浓度在200μmol/L时-dT/dtmax均高于A组(P<0.05～0.01)。(2)B组大鼠空肠平滑肌-dT低于A组(P<0.05)。(3)B组大鼠腺苷干预前微血管口径大于A组(P<0.05);血流速度小于A组(P<0.01),腺苷干预(浓度200μmol/L)后血流速度明显大于腺苷干预前(P<0.01),血液流态改善为线流。结论:腺苷可明显改善肥胖症大鼠空肠平滑肌活动和肠系膜微循环。     

糖尿病大鼠心肌电学的改变及环维黄杨星D对其电生理的影响

目的：观察糖尿病大鼠心肌电学变化特点，探讨环维黄杨星D(CVB-D)对糖尿病心肌电生理的影响。 方法： 以SD雄性大鼠尾静脉注射四氧嘧啶(alloxan,50 mg·kg^-1)复制糖尿病模型，选择以年龄相匹配的SD雄性大鼠作为对照组。2周后，记录大鼠体表心电图和右心室乳头肌跨膜电位，观察CVB-D对跨膜电位的影响。 结果： 糖尿病造模后第2周时，心率明显减慢于对照组，体表心电图QT间期和右室乳头肌动作电位时程（APD）各水平均明显长于对照组大鼠（P<0.01）,而静息膜电位（RP）、动作电位幅度(APA)和 超射值（OS）以及0期去极化最大速率（Vmax）均无明显变化。CVB-D具有剂量依赖效应，在13.3-63.3 μmol·L^-1范围内呈剂量依赖性地延长糖尿病大鼠和对照组大鼠APD30、APD50、APD70和APD90，对糖尿病大鼠APD延长作用更大。在33.3-63.3 μmol·L^-1浓度范围内，CVB-D呈剂量依赖性抑制糖尿病大鼠和对照组大鼠的静息电位(RP)、动作电位幅值（APA）和0期最大去极化速度（Vmax），但对糖尿病组抑制更大。研究结果还显示，CVB-D还具有时间依赖效应，当20 μmol·L^-1灌流心室肌10 min后开始出现作用，对照组到40 min左右作用达高峰，而糖尿病组40 min后仍继续延长。 结论： 糖尿病大鼠右室乳头肌动作电位时程和QT间期明显延长。CVB-D可进一步延长糖尿病大鼠的APD，抑制其RP、APA、OS以及Vmax，作用较对照组明显。     

尿皮素对高血压大鼠离体心肌的正性肌力效应

目的：研究尿皮素（urocortin）对自发性高血压大鼠离体心肌的影响。方法:采用Wistar及自发性高血压大鼠离体右心房肌、左心房肌和右心室肌标本，观察尿皮素对心肌收缩力及心率的影响。结果:　尿皮素1-10 nmol·L-1浓度依赖性地增强Wistar及高血压大鼠右心房心肌收缩力，尿皮素 3和10 nmol·L-1使自发性高血压大鼠右心房肌收缩力分别增加（31.1±14.9）％和（65.7±22.4）％，明显强于Wistar大鼠的正性肌力作用（P<0.01）。尿皮素 1-10 nmol·L-1浓度依赖性地增强Wistar及自发性高血压大鼠左心房心肌收缩力，但对2种动物的作用无明显差别。尿皮素不影响Wistar及自发性高血压大鼠离体右心房的心率和右心室肌条的收缩力；去甲肾上腺素对上述标本则产生明显的正性频率作用和正性肌力作用。结论:尿皮素对自发性高血压大鼠离体心房的正性肌力作用明显强于对Wistar大鼠的作用，提示尿皮素相关性心脏功能的改变，对高血压病可能具有重要的病理学意义。     

肾性高血压大鼠血浆ET、CGRP、AngⅡ水平变化及缬沙坦、贝那普利干预的影响

目的:研究肾性高血压大鼠血浆内皮素(ET)、降钙素基因相关肽(CGRP)、血管紧张素Ⅱ(AngⅡ)等血管活性物质的变化及降压药物缬沙坦、贝那普利干预对收缩压和ET、CGRP、AngⅡ的影响。方法:采用两肾一夹方法复制肾性高血压大鼠模型,成模大鼠随机分为缬沙坦组(30mg/kg/天,n=8)、贝那普利组(10mg/kg/天,n=8)、肾性高血压模型组(n=8);假造模大鼠作为假手术组(n=10),前两组以缬沙坦和贝那普利溶液、后两组以等量生理盐水每日灌胃。分别于术前及术后每周末测定各组大鼠收缩压变化,并在灌药治疗8周后用放免法测定各组血浆ET、CGRP、AngⅡ含量变化。结果:两肾一夹术后4周可形成稳定肾性高血压大鼠模型。缬沙坦组、贝那普利组大鼠经灌胃治疗8周后血压明显下降(P<0.01)。肾性高血压模型组ET、CGRP、AngⅡ血浆浓度均高于假手术组(P<0.05或P<0.01);缬沙坦组、贝那普利组CGRP浓度高于肾性高血压模型组(P<0.05),贝那普利组AngⅡ浓度低于肾性高血压模型组和缬沙坦组(P<0.05);肾性高血压模型组血浆ET与AngⅡ浓度呈正相关(r=0.62,P<0.05)。结论:肾性高血压大鼠血浆ET、CGRP、AngⅡ浓度增高,缬沙坦、贝那普利可能通过调节血管活性物质水平而降低收缩压。     

血府逐瘀汤对大鼠糖尿病性心肌病的影响

目的: 观察2型糖尿病心肌病大鼠心肌组织的病理改变以及血府逐瘀汤对于糖尿病性心肌病的治疗作用,探讨心肌病发生的病理机制。方法: 雄性Wistar大鼠42只,采用高脂高热量饮食诱导出胰岛素抵抗,加单次中等剂量(50 mg/kg)链脲佐菌素腹腔注射建立糖尿病动物模型。8周后采用心电图及超声心动图评价心肌受损情况;取血检测血糖、胆固醇、甘油三酯含量;心肌组织Masson染色定量左室心肌胶原纤维;TUNEL凋亡试剂盒检测心肌细胞凋亡,光镜和电镜观察心肌细胞结构破坏程度。结果: 与相同时点正常组比较,模型组血糖、甘油三酯、胆固醇含量升高(P<0.05),第11、14周左室收缩末期内径明显增厚(P<0.01),第14周左室舒张末期内径增厚(P<0.05),心肌组织结构破坏严重,胶原纤维含量增多(P<0.01),细胞凋亡增多;与相同时点模型组相比,血府逐瘀汤组大鼠血糖、胆固醇、甘油三酯明显降低(P<0.05),第11周左室收缩末期内径、第14周左室舒张末期内径增厚减低(P<0.05),第14周左室重量明显变轻(P<0.01),心肌组织破坏程度较轻,胶原纤维含量显著减少(P<0.01),心肌细胞亚细胞结构破坏程度较轻,细胞凋亡减少。结论: 糖尿病性心肌病时,血糖、胆固醇和甘油三酯含量升高,心肌增厚,心肌组织内胶原纤维含量增多,结构破坏严重,细胞凋亡增多;血府逐瘀汤能够降低糖尿病心肌病时血糖、胆固醇和甘油三酯水平,减轻心肌纤维化的病理改变程度,延缓糖尿病导致的心肌病进程。     

糖尿病性勃起功能障碍大鼠模型的建立

目的探讨理想糖尿病性勃起功能障碍(ED)大鼠模型的制备方法。方法90只SD大鼠,随机分为Ⅰ、Ⅱ、Ⅲ组,每组再分为正常组(CN)和糖尿病组(DM),每组各15只,糖尿病组腹腔注射链脲佐菌素(STZ,65 mg/kg)诱导糖尿病大鼠模型,成模8、12及16周注射阿朴吗啡(APO,80μg/kg)观察大鼠阴茎勃起情况,制备糖尿病性ED大鼠模型。结果DM组在8、12、16周注射阿朴吗啡后勃起次数分别为1.0±0.0、1.0±0.0、1.0±0.0,勃起率分别为33.3%、21.4%、14.3%,ED发生率分别为66.7%、78.6%、85.7%,CN组勃起次数分别为2.2±0.8、2.3±0.8、2.0±0.7,勃起率均为100%,ED发生率为0。组间差异有统计学意义(P0.01)。结论采用STZ 65 mg/kg腹腔注射建立糖尿病大鼠模型方法安全有效,颈部皮下注射APO 80μg/kg筛选糖尿病ED大鼠可行可靠。     

益景汤对糖尿病大鼠心脏血流动力学指标和心肌细胞凋亡的影响

目的:观察益景汤对糖尿病(DM)大鼠心脏血流动力学、心肌肥大和心肌细胞凋亡的影响。方法:采用链脲佐菌素(STZ)成功诱导DM大鼠模型,将成模大鼠分为益景汤治疗组(每天汤药灌胃3ml,相当于生药10.71g/kg)、贝那普利治疗组(每天腹腔注射10μg/kg)、模型组(每天给予3ml生理盐水灌胃),每组20只,另选20只为正常组(每天灌胃3ml生理盐水)。连续12周后采用动脉插管测定心脏血流动力学指标左室压力(LVP)、左室内压最大上升/下降速率(+dp/dtmax和-dp/dtmax)及左室舒张末压(LVEDP)。之后称取大鼠体重(BW),并取各组大鼠心脏称重(HW),再取左室称重(LVH),计算心脏质量指数(HMI)和左室质量指数(LVMI);切取部分左室制备心肌组织切片,采用TUNEL法检测心肌细胞凋亡。结果:方差分析显示,各组大鼠心脏血流动力学指标及HMI和LVMI均有统计学差异(P均0.01)。两两比较表明,DM各组LVP、+dp/dtmax及-dp/dtmax均低于正常组,且模型组益景汤治疗组贝那普利治疗组,差异均有统计学意义(P均0.01);DM各组LVEDP均高于正常组,且模型组益景汤治疗组贝那普利治疗组,差异也有统计学意义(P均0.01);DM各组HMI和LVMI均明显高于正常组(P0.01),但益景汤治疗组与模型组之间无统计学差异(P0.05);DM大鼠治疗组较模型组心肌细胞的凋亡程度轻,差异具有统计学意义(P0.05)。结论:DM大鼠在第12周已经出现心肌凋亡,益景汤能改善DM大鼠心脏血流动力学,抑制心肌细胞凋亡。     

神经型一氧化氮合酶在1型糖尿病大鼠肾皮质中的表达

目的观察1型糖尿病大鼠肾皮质内神经型一氧化氮合酶(nNOS)的表达变化。方法采用一次性腹腔注射大量链脲佐菌素(STZ)的方法建立1型糖尿病大鼠模型。分别在成模后的第1,2,4周3个时间点处死动物,采用亚硝酸还原酶法检测一氧化氮(NO)的含量;采用免组织化学染色法观察nNOS在肾皮质的表达;采用Western blot方法测定nNOS在肾皮质含量的变化。结果1周病程时糖尿病模型组大鼠肾皮质NO表达水平低于对照组(P<0.05),2周病程时高于对照组(P<0.05),4周病程时显著高于对照组(P<0.01)。nNOS在肾皮质中的表达部位主要在致密斑,在肾小管中也有少量的表达。糖尿病模型组大鼠肾皮质nNOS含量在1周病程时低于正常对照组,2周病程时与正常对照组无显著性差异,4周病程时高于正常对照组。结论在1型糖尿病大鼠肾脏病变的早期,肾皮质内NO的减少主要是由于nNOS合成减少造成的。     

Polyol pathway-mediated changes in cardiac muscle contractile properties: studies in streptozotocin-diabetic and galactose-fed rats.

Contractile properties of left ventricular papillary muscles and atria from streptozotocin-diabetic and from non-diabetic rats fed a 40% galactose diet were measured in vitro. There was a characteristic slowing of twitch responses for both tissues and both treatments (P < 0.05). Time to peak contraction was prolonged by 18-33% and maximum rate of contraction was reduced by 10-17%. Relaxation was also affected, with a 13-37% increase in half-relaxation time and a 7-25% reduction in the maximum rate of relaxation. There were treatment differences between papillary muscles and left atrium, diabetes having a more marked effect on the former, whereas galactosaemia caused more pronounced changes in the latter. The resting beat rate of the right atrium was 22% reduced in diabetic and galactosaemic rats (P < 0.01). When maximally stimulated with isoprenaline, beat rate did not rise to the level of stimulated controls (P < 0.01). Papillary muscle speed-related contractile properties also showed a reduced response to isoprenaline in diabetic and galactosaemic groups compared to normal controls. The greatest deficit was found for maximum rate of relaxation where responsiveness was 41 and 34% less for diabetic and galactosaemic groups respectively (P < 0.01). Polyol pathway metabolites in diabetic ventricles were increased 8-fold. In galactosaemic rats galactitol accumulation led to a 530-fold increase in polyols. The data suggest that polyol pathway activity may be an important factor in the aetiology of contractile and chronotropic changes in diabetic and galactosaemic cardiomyopathy.     

Cardiovascular adaptive responses in rats submitted to moderate resistance training

The present study investigated the effects of 8 week of resistance training (RT) on hemodynamic and ventricular function on cardiac myosin ATPase activity, and on contractility of papillary muscles of rats. Groups: control (CO), electrically stimulated (ES), trained at 60% (TR 60%) and 75% of one repetition maximum (1RM) (TR 75%). Exercise protocol: 5 sets of 12 repetitions at 60 and 75% of 1RM, 5 times per week. The CO and ES groups had similar values for parameters analyzed (P > 0.05). Blood pressure (BP), heart rate (13%), left ventricle systolic pressure (LVSP 13%) decreased and cardiac myosin ATPase activity increased in the TR 75% group (90%, P < 0.05). The contractile performance of papillary muscles increased in trained rats (P < 0.05). Eight weeks of RT was associated with lowering of resting BP, heart rate and LVSP, improvements in contractility of the papillary muscle and an increase of cardiac myosin ATPase activity in rats.     

右心收缩时间间期在测定右心舒缩性能中的应用——附56例慢阻肺和肺心病病人右心导管资料分析

本文依据56例慢性阻塞性肺病和肺心病人的右心导管资料,分析了右心收缩时间间期(RSTI)指标RICT、RPEP、RVET、RPEP/RVET与右心舒缩能中dp/dtmax、t-dp/dtmax,VCE_(10)、Vmax,-dp/dtmax诸参数的关系,结果显示了二者之间有一定的相关性。还探讨了使用无创性方法可以检测的RSTI来定量反映不易广泛开展的右心舒缩性能指标的可行性。用多元逐步回归分析方法建立了五个计算右心舒缩性能指标的方程式,经F检验,其dp/dtmax、t-dp/dtmax、-dp/dtmax三个方程式有显著意义(P<0.05)。     

Morphological changes in the mechanically unloaded myocardial cell

The role of stretch and/or tension in maintaining the structural integrity of the myocardial cell was investigated in 16 cats. Right ventricular papillary muscles were studied 1–28 days after transection of the chordae tendinae and compared to adjacent intact papillary muscles. A progressive atrophy, as shown by decreased mean cell cross-sectional area, occurred; by the 28th day mean cardiocyte area was only 28% of the control value. The earliest ultrastructural changes (one day after surgery) were primarily focal and included disorientation of contractile filaments and loss of Z-line substance. During the first week, vacuolation, loss of contractile filaments, and infiltration of macrophages and fibroblasts were characteristic. By the second week a massive loss of contractile substance, disappearance of the sarcoplasmic reticulum, and a marked increase in connective tissue occurred. Leptomere structures, membrane alterations, and phagocytosis were the most typical changes between the second and fourth week. Hydroxyproline assays on papillary muscles unloaded for three days showed a 38% increase in connective tissue, indicating an early increase in connective tissue/muscle mass associated with mechanical unloading. It is concluded that the cardiocyte is extremely dependent upon mechanical loading, i.e., stretch and/or tension. Mechanical unloading (tenotomy) results in rapid and marked cellular degeneration which exceeds that observed in skeletal muscle following either disuse or denervation.     

Effect of hypoxia on mechanical properties of hyperthyroid cat papillary muscle.

It has been previously established that hyperthyroid myocardium exhibits increased performance under well-oxygenated conditions. To date, it is not known whether hyperthyroid cardiac muscle can maintain this increased performance during hypoxia. The responses of isolated right ventricular papillary muscles from hyperthyroid and euthyroid kittens to hypoxia were compared under isometric conditions at 31 degrees C. Under well-oxygenated conditions, the hyperthyroid cardiac muscle exhibited both an increased contractility and an accelerated rate of relaxation. A similar degree of acute hypoxic stress for 15 min resulted in a greater decrease in contractility in the hyperthyroid compared with the euthyroid papillary muscle as indicated by a greater fall in both peak tension development (2.2 +/- 0.25 from 4.2 +/- 0.2 vs. 0.9 +/- 0.15 from 3.2 +/- 0.4 g/mm2, P less than 0.01) and +dT/dt (12.9 +/- 2.3 from 25 +/- 3 vs. 4.0 +/- 0.6 from 14 +/- 1 g-s-1-mm-2, P less than 0.01). In addition, compared with the euthyroid data, hypoxia resulted in impaired myocardial relaxation in the hyperthyroid cardiac muscle. Thus, the hyperthyroid compared with the euthyroid papillary muscle exhibits both a greater decrease in contractility and an impairment of myocardial relaxation during hypoxia, indicating a greater susceptibility to a given hypoxic stress.     

Rho激酶在失血性休克大鼠心肌收缩功能障碍中的作用

目的:观察Rho激酶对失血性休克大鼠心肌收缩力的影响。方法:利用离体乳头肌张力测定技术和心脏灌流技术,测定失血性休克后不同时间大鼠离体左室乳头肌在K-H液中的等长收缩张力的变化,以及大鼠的血流动力学指标(包括LVSP、±dp/dtm ax),并观察Rho激酶在其中的作用。结果:失血性休克后大鼠离体乳头肌收缩力和离体心脏血流动力学指标随着休克时间延长逐渐降低,在休克1 h、2 h以及4 h时乳头肌对异丙肾上腺素的收缩反应性显著低于正常对照组,同时休克后不同时点心肌组织Rho激酶活性发生明显变化,在休克1 h、2h、4 h Rho激酶活性显著低于正常对照组,Rho激酶活性变化与大鼠离体乳头肌收缩力和离体心脏血流动力学参数变化之间呈明显相关性,Rho激酶激动剂U-46619在浓度为10-8m ol/L预孵育休克2 h离体乳头肌或离体心脏后,离体乳头肌对异丙肾上腺素收缩力明显增加,最大收缩张力显著高于休克2 h组,曲线向左移。U-46619也可明显改善休克离体心脏血流动力学指标,Rho激酶特异性抑制剂Y-27632可明显拮抗由U-46619引起的休克大鼠离体乳头肌收缩反应性和离体心脏的改善作用。结论:Rho激酶在休克心肌收缩功能调节中发挥重要作用。     

Negative inotropic influence of hyperosmotic solutions on cardiac muscle.

In cardiac muscle, moderate degrees of hyperosmolality of the type encountered physiologically or clinically (i.e., less than 200 mosM above control) characteristically exert a positive inotropic effect, which presumably is mediated by increased Ca2+ availability for binding to troponin. In contrast, skeletal muscle displays significant contractile depression on exposure to hyperosmotic solutions, even at mild degrees of hypertonicity. To determine whether a similar potential for hyperosmolarity-induced depression also exists in cardiac muscle, right ventricular papillary muscles from cats were exposed to hypertonic solutions of mannitol or sucrose under circumstances in which positive inotropic effects were precluded by prior exposure to a bathing solution of 4.0 mM Ca2+ and paired electrical stimulation to maximize intracellular Ca2+ before addition of the hyperosmotic substances. In contrast to their usual positive inotropic effects, hypertonic solutions under these conditions caused cardiac depression at all osmolarities tested. Developed tension and its maximal rate of development (dT/dt) decreased by 18% at 50 mosM above control, by 30% at 100 mosM, by 36% at 150 mosM, and by 42% at 200 mosM (P less than 0.01 for all). Time to peak tension and resting tension were not changed significantly. When the muscles were returned to control solutions, tension development also returned toward normal. The data are compatible with the hypothesis that, within the range tested, all degrees of hyperosmolarity exert a significant negative inotropic influence on cardiac muscle, as is true in skeletal muscle; manifestation of this effect of increased tonicity normally would be obscured at low degrees of hyperosmolality, however, by an overriding positive influence that is absent in skeletal muscle.     

The influence of streptozotocin diabetes and metformin on erythrocyte volume and on the membrane potential and the contractile characteristics of the extensor digitorum longus and soleus muscles in rats

The effects of streptozotocin (STZ) diabetes and the antihyperglycaemic agent metformin on the contractile characteristics of the limb skeletal muscles and on erythrocyte volume were examined in rats. After 8 weeks of diabetes, the tetanic tension of the extensor digitorum longus (EDL) muscle decreased and the half-relaxation time of the soleus muscle increased. Endurance decreased in both muscles. Metformin treatment of the diabetic rats did not prevent the development of these contractile changes. Diabetes induced depolarisation in the EDL and soleus muscles. Following exposure to insulin, both muscles repolarized. Metformin treatment of control rats induced depolarisation in the EDL and soleus muscles, but in the depolarised EDL and soleus muscles of the diabetic rats metformin treatment caused no further depolarisation. The muscles of metformin-treated control and diabetic rats hyperpolarized in the presence of insulin. Diabetes caused an increase in the volume of the blood erythrocytes. This was prevented by metformin treatment.     

组织蛋白酶B和胱抑素C在糖尿病肾病大鼠肾组织中的表达及意义

目的： 观察糖尿病大鼠肾组织中组织蛋白酶B(CB)和胱抑素C(CC)的表达并探讨其在糖尿病肾病中的可能作用。方法: 将Wistar大鼠分成健康对照组(C组,n=30)和糖尿病组(M组,n=35),糖尿病组给予STZ 55 mg/kg腹腔内注射,72 h后随机血糖>16.7 mmol/L为造模成功。分别在第4、8、16周各处死10只,在处死前留取24 h尿量测24 h尿白蛋白,留取血清标本测血肌酐,留取肾脏标本做免疫组化和实时荧光定量PCR测CC、CB、Ⅳ型胶原(colⅣ)、纤维连接蛋白(FN)的表达情况。结果: C组的各项指标各时点均未见到有显著变化,与第4周相比,第8周M组大鼠内生肌酐清除率(Ccr)和24 h尿白蛋白显著升高(P<0.01),免疫组化和PCR结果显示CB、CC、colⅣ、FN在第8周出现明显上调(P<0.01或P<0.05),CB在16周下调(P<0.01),而CC显著上调(P<0.01)。相关分析显示CB的表达与24 h尿蛋白、colⅣ、FN蛋白表达和mRNA表达呈负相关（P<0.01）。结论: 糖尿病大鼠肾组织存在CB和CC平衡的失调,这可能是引起糖尿病肾病细胞外基质沉积的原因之一。     

Effect of myocardial hypertrophy on the dynamics of restoration of diastolic contractility

The amplitude of extrasystolic contraction of the papillary muscle of rats is always smaller than the amplitude of the regular contraction. In hypertrophy of the heart this rule is disturbed and extrasystolic contraction exceeds regular throughout most of diastole. A similar pattern is found in the normal frog heart muscle. In experiments on the papillary muscles from hypertrophied hearts automatic activity was frequently observed. The amplitude of the contractions was much smaller than the amplitude of the regular contractions evoked by electrical stimulation. This phenomenon was not observed in experiments on papillary muscles from the hearts of control rats. The results evidently reflect disturbances of the process of calcium binding by the sarcoplasmic reticulum in hypertrophy.