异丙基肾上腺素致大鼠心肌损伤的超微结构及体视学研究

实验用Ｗｉｓｔａｒ大鼠３５只，体重２１０ｇ。异丙肾（ＩＳＰ）组２８只，皮下注射ＩＳＰ５．０ｍｇ／ｋｇ，注射后４、１２、２４和４８小时分别处死７只大鼠，随同处死对照组７只。光镜观察心肌坏死部位和程度；电镜观察心肌超微结构变化；用体视学方法定量分析心肌线粒体形态变化。结果表明：心肌线粒体Ｖｖ和Ｖ值升高，与对照组比较差异显著（Ｐ＜０．０１），ＮＡ和Ｎｖ值变化与对照组比较无显著差异（Ｐ＞０．０５）。实验表明线粒体Ｖｖ和Ｖ植升高主要与线粒体肿胀有关，与线粒体的集聚和增生无关；线粒体的损伤破坏与心肌坏死程度密切相关；并提示注射ＩＳＰ后４８小时是制作大鼠心肌坏死模型的最佳时间。     

风湿性心脏病心肌免疫组织化学及超微结构的观察

风湿性心脏病心肌免疫组织化学及超微结构的观察郑毅，刘振华，蔡凯华本文采用免疫组化及透射电镜方法对风湿性心脏病（风心病）心肌进行研究，试图了解心肌病变与疾病发展及预后的关系。一、材料和方法１．材料来源：临床确诊的风心病患者５１例，在换瓣术中取左室后乳头...     

慢性镉中毒小鼠肾脏的超微结构观察

透射电镜下观察10只慢性镉中毒小鼠肾脏的超微结构变化，结果表明肾小体和近曲小管上皮细胞的超微结构均受损伤，肾小体，毛细血管内皮细胞肿胀，增厚，血管系膜增生，血管球基膜增厚或分裂成层，基膜和内皮细胞之间或基膜的分裂之间有电子致密物沉积，近曲小管上皮细胞，胞核变形，固缩，线粒体肿胀，嵴断裂，脱落，细胞游离面微绒毛肿胀，变形，排列紊乱，细胞基底面质膜内褶减少或消失，这些超微结构的改变与某些类型肾小球肾炎的病理特征相似。     

强心甙中毒的心肌超微结构变化和甘露醇的保护作用

ⅳ羟自由基清除剂甘露醇,1.1mol/L 2g/kg和3 g/kg可分别使哇巴因致豚鼠LD_(100)由298.54±33.30 μg/kg增高至367.44±44.58μg/kg(P<0.05)和398.49±35.39 μg/kg(P<0.01)。甘露醇略可提高哇巴因致心律失常发生的阈值,但无统计学意义。取哇巴因致心脏出现室性早搏、室性心动过速、室性纤维性颤动和心跳停止时的左室游离壁心肌,用透射电子显微镜观察心肌超微结构的改变,结果表明心肌细胞膜结构发生明显的破坏,并随中毒的加重,心肌结构的破坏亦更严重。     

实验性糖尿病大鼠心肌超微结构观察

实验性糖尿病大鼠心肌超微结构观察南京军区南京总医院（南京２１０００２）施志明钱晓明周晓军章俐陈云吴振国糖尿病心肌病是糖尿病主要并发症，也是糖尿病致死的原因之一。本实验对链脲佐菌素（ｓｔｒｅｐｔｏｚｏｔｏｃｉｎ，ＳＴＺ）诱导的实验性糖尿病大鼠心肌超微...     

单甲氧基聚乙二醇—超氧化物歧化酶减轻低氧对兔心肌超微结构损伤

用雄性日本大耳兔（２．５￣３ｋｇ）每组５￣１２只，除常氧对照组外，其余各组分别模拟海拔高度５０００ｍ低压性低氧２４ｈ，左右心室肌超微结构损伤明显，主要表现为线粒体膜破损，嵴部分消的。肌丝间隙增大，肌原纤维断裂。溶酶体增多，糖原颗粒减少，氏氧前由股静脉注入单甲氧基聚乙二醇－超氧化物歧化酶的兔，肌原纤维排列整齐。线粒体含量丰富嵴密集，与肌原纤维基本呈平行。另测定低氧不同时间左右心室肌超氧化物歧化酶活性     

台盼蓝对大鼠胚胎心肌发育分化影响的组织学和组织化学观察

本实验在 SD 大鼠妊娠第7、8、9天腹腔注射1.5%台盼蓝溶液1ml 后,观察了妊娠11至20天鼠胚心肌细胞发育分化的形态结构和组织化学反应的变化。组织学结果表明,实验组心肌细胞光镜下呈空泡状改变,电镜下有肌浆溶解现象,肌原纤维含量减少,线粒体变性肿胀,以及闰盘发育延迟。组化反应显示实验组 PAS 反应减弱,SDH 和 G-6-PDH 活性增强。上述结果表明,台盼蓝干扰了胚胎心肌细胞重要结构的发育分化以及葡萄糖和有氧氧化的代谢。     

高血压合并糖尿病大鼠心肌毛细血管内皮细胞超微结构及eNOS的变化

目的:探讨高血压合并糖尿病(DM)对心肌毛细血管内皮细胞超微结构及内皮型一氧化氮合酶(eNOS)表达的影响。方法:自发性高血压大鼠(SHR)及SD大鼠腹腔注射链脲佐菌素(STZ)结合高能量饲料诱导DM模型。分为4组:正常SD大鼠组(SD组)、SHR组、单纯DM组(DM组)与自发性高血压合并DM大鼠组(SHDM组)。电镜观察各组心肌毛细血管内皮细胞超微结构,免疫组化法测定各组eNOS在毛细血管内皮细胞的表达。结果:SHR、DM和SHDM组心肌毛细血管超微结构明显改变,包括内皮细胞水肿,细胞膜向管腔内呈指状突起,管腔狭窄、不规则等,这些现象在DM组与SHDM组更明显。与SD组比较,SHR组基底膜稍有增厚,但无显著性差异(31.31±4.19nmvs28.64±3.62nm,P>0.05),而DM组(46.58±5.32nm)和SHDM(51.50±4.62nm)组基底膜显著增厚(与SD及SHR组比较,均P<0.01)。SHDM组心肌组织eNOS表达显著低于SHR组及DM组。结论:高血压与DM共存时对心肌毛细血管内皮细胞超微结构及功能有协同损害作用。     

L-精氨酸对糖尿病大鼠心肌自由基损伤的保护作用

探讨L 精氨酸 NO(L Arg NO)在糖尿病大鼠心肌自由基损伤中可能的保护作用。用健康Wistar大鼠 ,应用链脲佐菌素 (STZ)制备糖尿病模型。随机分为糖尿病模型组、左旋精氨酸 (L Arg)组、N 左旋硝基精氨酸 (L NNA)组及正常对照组。第八周末处死动物 ,检测外周血及心肌组织的NO、NOS、SOD活性和MDA含量 ,以及心肌组织Na+-K+ ATPase、Ca2 + ATPase活性。L Arg与糖尿病模型组及其他各组比 ,血清中NO水平及NOS活性明显增加 (P <0 0 5 ) ,心肌组织中的Na+ -K+ ATPase及Ca2 + ATPase和SOD活性增加 (P <0 0 5 ) ,MDA含量减少 (P <0 0 5 )。糖尿病大鼠心肌组织存在着脂质过氧化损伤 ,L 精氨酸可通过L Arg NO通路改善心肌供血 ,提高心肌组织SOD活性 ,降低脂质过氧化反应 ,从而增强心肌组织抗自由基损伤的作用 ,适当补充外源性L 精氨酸对防治糖尿病心血管系统的并发症具有重要意义     

庚型病毒性肝炎肝的超微结构及免疫组织化学观察

庚型病毒性肝炎是一种新型病毒性肝炎，由庚型肝炎病毒（ＨＧＶ）感染引起。近年来，国内外学者相继作了报道，并对ＨＧＶ的分子生物学和庚型肝炎的临床特征进行研究分析，但对庚型肝炎肝的超微结构变化尚缺乏报道。我们对近２年来收治的血清学检查显示单纯ＨＧＶＲＮＡ...     

Ultrastructural morphometric study on the rat heart after chronic ethanol feeding

Summary Male Wistar rats were fed with ethanol for 33 weeks. Ethanol was administered in a liquid diet containing 33% of the calories as ethanol. In the control group ethanol was isocalorically replaced by glucose. Light and electron microscopic investigation of the hearts did not indicate significant structural abnormalities, in contrast to the results of some other groups. Nevertheless, morphometric analysis revealed considerable quantitative changes. The number of mitochondria was remarkably reduced and the volume of an average single mitochondrion nearly doubled, whereas the volume fractions of mitochondria and myofibrils were unaltered. The analysis of the mitochondrial subcompartments indicated a slight decrease of the surface area of inner mitochondrial membranes per unit volume of mitochondria and a slight increase of the volume fraction of the mitochondrial matrix space. Myocardial cell hypertrophy or atrophy were not observed. We believe that the mitochondrial changes are the expression of an impaired biogenesis of these organelles.The increased number of capillaries in the ethanol-fed group is possibly caused by functional ethanol effects which may be partly similar to effects of chronic hypoxia.Ethanol- or acetaldehyde-induced damage of heart mitochondria may play an important role in the pathogenesis of alcoholic cardiomyopathy.Dedicated to Prof. Dr. G. Ule on the occasion of his 60^th birthdayMore detailed discussion in T. Mattfeldt: Inauguraldissertation (in prep.)Supported by grants of the Deutsche Forschungsgemeinschaft VO 272/3     

Morphometric observations on the rat heart after high-dose treatment with cortisol

Summary Male Wistar rats were treated with high cortisol doses for 1 week. The dose administered daily was 15 mg per animal in group 1 (7 animals) and 30 mg in group 2 (7 animals). 7 rats served as control group. After cortisol treatment the body weights decreased due to skeletal muscle catabolism and the heart weights increased. Morphometric analysis of the left ventricular posterior papillary muscles gave evidence that the increased heart weights resulted from an increased number of mitochondria and an increased volume of the cytoplasm, whereas the myofibrillar mass was not affected. The surface area of inner mitochondrial membranes (+cristae mitochondriales) per myofibrillar unit volume increased from 15.7 ²/³ to 21.3 ²/³ in group 1 and 21.4 ²/³ in group 2. Ultrastructural changes indicating myocardial cell damage were absent. Similar quantitative results have been reported to occur in the early phase of cardiac overload. For elucidating the hemodynamic effects of glucocorticoid a second experiment was performed: 7 Wistar rats were treated with cortisol in the same way as group 1, 7 others of the same body weight served as control. The systolic arterial pressure was significantly elevated in the cortisol group. Though myocardial tissue is known to be able to accumulate large quantities of glucocorticoids our results indicate that the application of high cortisol doses for a short time does not produce myocardial cell damage and does not suppress the myocardial adaption to the glucocorticoid-induced hypertension, i.e. hypertrophy. On the contrary, it seems to be possible that the adaption process is itself facilitated or accelerated by the presence of high cortisol concentrations in the heart. This thesis is supported by the considerably higher relative heart weights in the cortisol groups and is in agreement with observations reported by other authors.Dedicated to Professor Dr. W. Doerr on the occasion of his 65th birthdayThe results have been partially reported in 1977 (cf. G. Mall and H. Reinhard, Verh. Dtsch. Ges. Path. 61, 445)This investigation was supported by the Sonderforschungsbereich 90 of the Deutsche Forschungsgemeinschaft.     

心肌肽素对大鼠心脏缺血-再灌注损伤的治疗作用

目的:研究多肽类物质心肌肽素对大鼠心脏缺血-再灌注损伤的治疗作用。方法:在大鼠冠脉结扎致心肌缺血-再灌注损伤模型上,观察心肌肽素治疗性给药对缺血大鼠血浆中肌酸磷酸激酶(CPK)、乳酸脱氢酶(LDH)活性及脂质过氧化终产物(MDA)含量的影响。结果:心肌肽素治疗性给药能明显降低血浆CPK、LDH的活性与MDA含量,其作用具有明显的量效关系。结论:心肌肽素对心脏缺血-再灌注损伤有治疗作用,提示可能与其抗脂质过氧化和影响心肌酶的活性有关。     

鱼腥草注射液抗内毒素性心肌损伤作用的实验研究

目的:揭示鱼腥草注射液抗内毒素诱导的心肌损伤作用的机制。方法:取SD雄性大鼠24只随机分成正常对照组(NC组,n=6),内毒素组(ET组,n=6),鱼腥草注射液+内毒素组(HHI+ET组,n=6)和单纯鱼腥草注射液组(HHI组,n=6),在Langendorff装置上用Krebs-Henseleit(KH)液对大鼠离体心脏行主动脉逆灌。在相应时点以HR、LVSP、LVEDP、LVDP、+dp/dt_max、-dp/dt_max等6项参数为指标,测定冠脉流出液中的超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及心肌组织一氧化氮(NO)含量、琥珀酸脱氢酶(SDH)活性。结果:与ET组相比,HHI+ET组在相应时点,左心室压差与心率乘积(LVSP-LVEDP)×HR、LVDP、+dp/dt_max恢复百分率明显改善,对内毒素诱导的心肌SOD、SDH活性的降低和MDA、NO含量的升高有明显抑制作用。结论:鱼腥草注射液具有明显的抗内毒素心肌损伤作用,通过降低心肌中NO的量,增强心肌的抗氧化能力,稳定心肌酶活性和膜相结构等途径,提高心肌对内毒素性损伤的抵抗力。     

大鼠缺血性急性肾损伤对肺脏超微结构的影响

目的　观察大鼠缺血性急性肾损伤对肺脏细胞超微结构的影响。 方法　应用光学显微镜和透射电子显微镜技术以及立体计量学方法观察急性肾缺血60 min再灌注24 h后的肺脏。 结果　部分肺泡I型上皮细胞发生了肿胀性坏死,II型上皮细胞也出现了肿胀性坏死,细胞内大量空泡出现。嗜锇性板层小体消失,肺泡内皮细胞出现了凋亡的表现。肺内组织出现了中性粒细胞浸润。 结论　大鼠肾脏急性肾缺血损伤可引起肺细胞坏死与凋亡,其中坏死损伤为多见。此外,炎性细胞浸润也是不可忽略的症候。     

体外反搏对心肌缺血犬心肌超微结构的影响

目的探讨体外反搏对心肌缺血犬心肌超微结构的影响。方法19只健康杂种犬随机分为对照组、缺血组和反搏组,采用透射电镜观察缺血区心肌组织的超微结构变化,并通过图像分析系统对线粒体进行形态定量分析。结果形态学观察发现反搏组犬心肌肌小节、肌丝、线粒体和血管内皮细胞损伤比缺血组明显减轻。定量分析发现反搏组犬心肌线粒体数密度和比表面均明显高于缺血组,而线粒体体积和平均表面积均小于缺血组(P<0.05)。结论体外反搏可减轻心肌缺血犬的心肌超微结构损伤。     

在培养的心肌细胞中锌的抗氧自由基损伤作用的观察

本文通过向培养基中加入黄嘌呤和黄(?)呤氧化酶系统成分造成培养的心肌细胞受氧自由基伤害,以电生理的改变和BaCL_2引起心肌细胞停搏的闭浓度为指标,观察了微量元素Zn的抗氧化损伤作用。结果示:XOD组与对照组比较,动作电位APA、OS、MDP、TP、Vmax及APD_(50)各电参数明显减小。BaCl_2引起心肌细胞停搏的阈浓度亦减低。而加Zn组与对照组比较,以上结果除TP值偏低P<0.05外,其它参数则无显著性改变。加Zn组与XOD组相比,动作电位各电参数明显增大,BaCl_2引起心肌细胞停搏的阈浓度亦增高。提示Zn对培养的心肌细胞氧自由基所致的损伤具有保护作用。     

前列腺素E_2对体外培养的新生大鼠心肌细胞的机能及超微结构的影响

本实验观察了PGE_2对体外培养的新生大鼠心肌细胞的机能及超微结构的影响。发现4ng/ml PGE_2可以立即引起细胞搏动频率明显减慢,作用6分钟对心肌细胞及微丝的形态结构没有明显影响;作用6小时,其微丝排列规则而整齐,与正常比较未见异常,但心肌细胞膜出现皱折,微足突变粗短甚至消失,微泡也消失。表明PGE2对心肌细胞的作用具有时间依赖性。     

丹参素对大鼠心肌缺血/再灌注致线粒体变化的影响及其作用机理的探讨

本实验分别以ESR自旋标记法、TBA比色法测定大鼠离体心脏缺血,再灌注时线粒体膜流动性及脂质过氧化物含量。发现心肌线粒体膜深层的流动性在缺血40分钟后有氧再灌注20分钟时(S=0.112±0.006、τ_e=7.13±0.09×10~(-10)sec)明显低于富氧灌注组(S=0.103±0.007、τ_e=6.86±0.20×10~(-10)sec),P<0.05;而脂质过氧化物含量再灌注组(3.02±0.68nmol/mgpr.)则极明显高于富氧灌注组(1.94±0.35nmol/mgpr.),P<0.01。预先给予丹参素,对以上变化有明显的改善作用,上述两项指标与富氧灌注组相比,无明显差别,P>0.05。另外,采用ESR自旋捕集技术发现丹参素对外源性O_2~-·有清除作用。因而推测,丹参素可能作为一种O_2~-·的清除剂保护心肌线粒体免受氧自由基引发的脂质过氧化损害。     

Effects of combined renovascular hypertension and diabetes mellitus on myocardial cells,non-vascular interstitium and capillaries: a stereological study on rat hearts

Summary The effects of combined renovascular hypertension and diabetes mellitus on the rat heart were investigated in order to detect possible synergistic effects of the two conditions. Hypertensive diabetic and hypertensive non-diabetic animals were compared to diabetic and non-diabetic controls. Hypertension was established for 12 weeks by a surgical stenosis of the left renal artery; diabetes mellitus was maintained for 8 weeks by a single intraperitoneal injection of 60 mg/kg streptozotocin. Light microscopic stereology did not reveal significant divergences between diabetic hypertensives and non-diabetic hypertensives. Hypertension induced a focal perivascular and interstitial fibrosis with increased volume densities of non-vascular interstitium and fibrosis (P<0.001). Capillary density (Q_A) was decreased in transverse sections (P<0.01) and increased in longitudinal sections (P<0.01). This indicates a three-dimensional remodelling of the capillary bed with an increased number of obliquely running capillaries. At least the length density (L_V) of capillaries (mm/mm³) tends to be normalized in long-term renovascular hypertension. At the ultrastructural level, a synergism of hypertension and diabetes mellitus was observed: the volume ratio of mitochondria to myofibrils was significantly decreased in hypertensive diabetics, but not in non-diabetic hypertensives or in diabetics. This may enhance the risk of cardiac deterioration. We conclude that the primary target of the synergistic damage in hypertensive diabetic heart muscle disease is the myocardial cell and not the cardiac interstitium.Preliminary results of this study have been published in: Mall G (1991) Morphometric study on the rat heart in combined renovascular hypertension and diabetes mellitus. In: Nagano N, Dhalla NS (eds) The diabetic heart. Raven Press, New York, pp 115–124Dedicated to Prof. Dr. med. G. Seifert on the occasion of his 70th birthday