四类降压药物两两联合治疗肾血管性高血压大鼠左室重构研究

目的:通过两两药物联合应用治疗高血压,对比药物联合治疗的降压效果,并探讨其对左室重构的作用。方法:用两肾一夹法建立高血压大鼠模型,65只SD大鼠随机分为:假手术组(n=10);高血压组(n=11);β-B+血管紧张素转化酶抑制剂(ACEI)组(n=11)予以比索洛尔5mg·kg-1·d-1及贝那普利5mg·kg-1·d-1灌胃;β-B+血管紧张素Ⅱ受体拮抗剂(ARB)组(n=11)予以比索洛尔5mg·kg-1·d-1及替米沙坦10mg·kg-1·d-1灌胃;ACEI+ARB组(n=11)予以贝那普利5mg·kg-1·d-1及替米沙坦10mg·kg-1·d-1灌胃;ACEI+钙拮抗剂(CCB)组(n=11)予以贝那普利5mg·kg-1·d-1及氨氯地平2.5mg·kg-1·d-1灌胃;期间每2周给大鼠测量鼠尾动脉压和超声心动图;20周后采集标本,用免疫组化法检测胶原Ⅲ、胶原Ⅳ及心钠素。结果:各用药组血压降低程度明显,其中ACEI+CCB组(P<0·01),与假手术组相近,且比其他用药组血压降低明显(P<0·05)。β-B+ACEI组和β-B+ARB组胶原Ⅲ、胶原Ⅳ含量较高血压组降低(P<0·05),ACEI+A...     

阿托伐他汀钙对肾血管性高血压大鼠模型左室重构的影响

该文观察了阿托伐他汀钙对肾血管性高血压大鼠左室重构的保护作用。方法：应用经典的两肾一夹方法，备制肾血管性高血压大鼠模型。实验动物随机分对照组（假手术）、高血压组及治疗组，每组各7只。治疗组给予阿托伐他汀钙（立普妥2mg／kg）治疗6周。采用鼠尾测压法测定大鼠血压的变化；放射免疫分析法测定大鼠血管紧张素（Ang）Ⅱ含量和肾素活性；     

阿托伐他汀钙对肾血管性高血压大鼠模型左室重构的影响

目的观察阿托伐他汀钙对肾血管性高血压大鼠左室重构的保护作用。方法应用经典的两肾一夹方法,制备肾血管性高血压大鼠模型。实验动物随机分对照组(假手术)、高血压组及治疗组,每组各7只。治疗组给予阿托伐他汀钙(立普妥2 mg/kg)治疗6周。采用鼠尾测压法测定大鼠血压的变化;放射免疫分析法测定大鼠血浆血管紧张素(Ang)Ⅱ含量和肾素活性;称量法计算各组大鼠心脏重量及左室重量与体重比值。结果高血压大鼠血浆AngⅡ含量和肾素活性分别为(106.4±7.8)ng/L和(20.6±2.4)ng/L,比对照组〔(72.3±5.4)ng/L和(12.5±3.7)ng/L〕明显增高(P<0.01);心脏重量为(1.46±0.09)g,左室重量与体重比值为(3.54±0.19)×10-3,比对照组〔(0.98±0.07)g和(2.28±0.06)×10-3〕显著增大(P<0.01)。给予小剂量阿托伐他汀钙治疗6周后,AngⅡ含量〔(68.3±6.9)ng/L〕和肾素活性〔(8.7±2.3)ng/L〕明显下降(P<0.01),心脏重量减至(1.05±0.04)g,左室重量与体重比值降至(2.36±0.07)×10-3,与对照组比较差异无统计学意义(P>0.05)。结论阿托伐他汀钙能明显降低高血压大鼠心脏重量及左室重量与体重比值,对高血压大鼠病理性左室重构具有保护作用。     

肾血管性高血压大鼠左室Ⅰ,Ⅲ型胶原变化及卡托普利治疗的影响

目的采用两肾一夹肾血管性高血压大鼠（２Ｋ１Ｃ－ＲＨＲ）模型，探讨Ⅰ、Ⅲ型胶原在心肌纤维化形成过程及卡托普利治疗时的变化。方法建立２Ｋ１Ｃ－ＲＨＲ模型并随机分组，高血压６周组探讨模型６周时心肌胶原纤维的变化，高血压１２周探讨１２周时情况，卡托普利组治疗组６周组胶原纤维的改变。对照组为相应的假手术组。ＶａｎＧｉｅｓｏｎ染色和计算机图象分析作心肌胶原总定量测定。免疫组化作Ⅰ、Ⅲ型胶原半定量分析。结果高血压６周组和１２周组胶原总量增加，６周组以Ⅰ型胶原为主，１２周Ⅲ型胶原亦增加。治疗６周组Ⅰ型胶原减少，总胶原量亦减少，Ⅲ型胶原无显著变化。结论高血压组以Ⅰ型胶原增加为主，Ⅲ型胶原出现在后几周。卡托普利治疗６周有减少Ⅰ型胶原形成作用，但对Ⅲ型胶原作用不明显。     

不同抗高血压药物对自发性高血压大鼠左心室肥厚及心钠素mRNA表达的影响

探讨抗高血压药物对自发性高血压大鼠（ＳＨＲ）左心室肥厚与心钠素（ＡＮＰ）ｍＲＮＡ表达的影响。方法成年（１６周龄）雄性ＳＨＲ测定收缩压后随机分为３组，分别给予卡托普利（１００ｍｇ／ｋｇ·ｄ－１），双氢克尿塞（１００ｍｇ／ｋｇ·ｄ－１），普萘洛尔（４０ｍｇ／ｋｇ·ｄ－１）治疗，共１２周，年龄、性别及数量配对的正常血压的ＷＫＹ及未治疗ＳＨＲ作为对照组。治疗结束时测体重、收缩压。动物断头处死，取左心室称重后，采用异硫氰酸胍一步法提取组织总ＲＮＡ，Ｎｏｒｔｈｅｒｎ杂交法检测ＡＮＰｍＲＮＡ相对表达量。结果治疗组动物收缩压及左心室重／体重比均明显低于未治疗ＳＨＲ组。卡托普利与普萘洛尔明显抑制心钠素基因的表达，双氢克尿塞对心钠素基因的表达影响较小。结论不同抗高血压治疗在降低血压和逆转左心室肥厚的同时也不同程度地抑制左心室心钠素基因的表达，利尿剂对心钠素表达的影响较小。     

心钠素对肾血管性高血压的临床作用

肾血管性高血压有复杂的病理生理特点,适于全面评价心钠素的生理、药理作用。给7例患者静脉滴注心钠素0.025μg·kg~(-1)/min×60min,引起肾素—血管紧张素—醛固酮系统及交感神经系统的抑制,血浆加压素浓度的降低,产生了利尿、利钠效应并伴有红细胞压积和肌酐清除率的增加,血压轻度平续的下降。一些因素参与了肾血管性高血压的形成和维持。本研究提示,心钠素对这些因素均有一定作用     

血压平逆转肾性高血压大鼠左室重构的作用及机制

目的　探讨复方中药制剂血压平逆转二肾一夹 (2K1C)肾性高血压大鼠左室重构的作用及机制。方法　采用 2K1C法 ,建立肾性高血压大鼠 (RHR)模型 ,术后 8周将造模成功的 40只RHR随机分为 5组 ,每组 8只 ,采用放免法检测血清Ⅲ型前胶原(PCⅢ ) ,测量心肌细胞面积、周长、平均直径、长径和短径。SP免疫组化测量原癌基因C -myc和C -fos表达阳性细胞的平均光密度值。结果　①血压平有降低血压、左室重量 (LVW )、左室重量指数 (LVW /BW )、心肌细胞体积的作用 ;②血压平可降低血清PCⅢ含量 ,抑制原癌基因C -myc和C -fos的表达 ;③血压平的降压和逆转左室重构的药理作用有量效关系。结论　血压平具有逆转RHR左室重构的作用 ,其降低血压、降低血清PCⅢ含量、抑制Ⅲ型胶原合成、防治心肌纤维化及降低原癌基因C -myc和C -fos的表达、抑制心肌细胞肥大、减轻左心室肥厚 ,是其逆转2K1CRHR左室重构的部分机制。     

卡托普利逆转高血压左室重构的实验研究

１４周龄的自发性高血压大鼠（ＳＨＲ）已形成左室肥厚（ＬＶＨ），心肌胶原浓度及心肌Ｃａ￣（２＋）增加，左室顺应性下降，经卡托普利治疗５０ｍｇ／ｋｇ·ｄ１４周后，ＬＶＨ消退。心肌胶原及Ｃａ￣（２＋）消退，左室舒张期弹性硬度改善，表明卡托普利治疗高血压能逆转左室肥厚及心肌胶原重构，并改善心功能。     

肾血管性高血压大鼠心肌纤维化发展过程的实验研究

采用二肾一夹肾血管性高血压（２Ｋ１Ｃ－ＲＨＴ）大鼠为模型，观察在反应性和修复性纤维化阶段心肌胶原形态和生化的改变。方法建立２Ｋ１Ｃ－ＲＨＴ模型，将大鼠随机分为４组：术后４，１２周高血压组和对照组。苦味酸天狼星红染色观察胶原形态，图像分析系统测量胶原容积分数（ＣＶＦ）和血管周围胶原面积（ＰＶＣＡ），羟脯氨酸法测定心肌胶原浓度（Ｃｏｌ）。结果在反应性纤维化阶段，心肌胶原从血管周围向邻近间质短距离延伸，同时ＣＶＦ、ＰＶＣＡ和Ｃｏｌ显著增高；在修复性纤维化阶段，胶原在间质中长距离延伸，出现取代缺失心肌细胞的疤痕灶，同时ＣＶＦ、ＰＶＣＡ和Ｃｏｌ进一步升高。结论提示２Ｋ１Ｃ－ＲＨＴ大鼠心肌纤维化呈进行性发展。     

减阻剂改善自发性高血压大鼠左心室重塑

目的探讨静脉应用减阻剂(DRP)对自发性高血压大鼠(SHR)左心室重塑的影响。方法 24只8周龄雄性SHR随机分为3组:生理盐水组(SHR+NS),减阻剂浓度10 ppm组(SHR+10)和减阻剂浓度20 ppm组(SHR+20),隔日予静脉注射DRP或NS,8只年龄匹配的雄性Wistar(WR+NS)大鼠作为对照组予静脉注射NS。静脉给药60 d后,超声心动图评估四组大鼠心功能改变与左心室后壁厚度。分离大鼠左心室心肌,石蜡包埋,HE染色评估左心室心肌肥厚,masson染色评估心肌纤维化,免疫化学检测左室心肌内皮素(ET)-1表达。结果超声心动图显示4组大鼠左心室射血分数无统计学差异,SHR+10组和SHR+20组较SHR+NS组左室收缩末期后壁厚度显著减小;SHR+20组较SHR+NS组左室舒张末期后壁厚度显著减小。左心室心肌HE染色示SHR+20组心肌细胞横截面积较SHR+NS组显著减小。左心室心肌masson染色示SHR+10和SHR+20组较SHR+NS组心肌胶原纤维百分比显著减少。左心室心肌免疫组化显示,静脉应用DRP后,SHR+10、SHR+20组左心室心肌ET-1蛋白表达较SHR+NS组显著降低。结论静脉应用DRP可改善SHR左心室重塑,其机制可能与DRP增加血液剪切应力抑制ET1表达有关。     

Characteristics of the hypertrophied left ventricular myocardium in Goldblatt rats

Summary In Goldblatt rats (GV) 4–24 weeks after coarctation of one renal artery the following characteristics were registered as compared to controls (CV) of the same age: Arterial blood pressure increased to 190–200 mmHg in comparison to 105–110 mmHg in controls. This pressure overload induced an increase in ventricular weights (34%–54%). Noteworthy differences in myocardial water, total protein, and nonprotein substance contents were found. Hydroxyproline concentration in GV did not increase significantly until 24 weeks after onset of pressure overload. No significant alterations were detected in the relationship of myocardial, sarcoplasmic, and stromal protein fractions. However, greater changes could be registered in the concentration of the myofibrillar protein fraction and its single components. Furthermore, a correlative depression in specific actomyosin ATPase activity and in maximum shortening velocity of the unloaded cardiac muscle (2,3) was observed.

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Eigenschaften des hypertrophierten linken Ventrikels in Goldblatt-Ratten

Zusammenfassung Bei Goldblatt-Ratten (GV) wurden 4–24 Wochen nach der Stenosierung einer Renalarterie folgende Veränderungen registriert, verglichen mit gleichaltrigen Kontrollen (CV): Der systolische Blutdruck war auf 190–200 mmHg erhöht (Kontrollwerte: 105–110 mmHg). Als Folge des Druckanstiegs nahm das Gewicht des linken Ventrikels um 34%–54% zu. Bezüglich des myokardialen Wasser-, Gesamtprotein- und Nichtproteinanteils wurden keine nennenswerten Änderungen gefunden. Erst 24 Wochen nach der Operation wurde ein signifikanter Anstieg in Hydroxyprolinkonzentration, in hypertrophierten Ventrikeln festgestellt. Während die Relationen des Myokards nicht signifikant verändert waren, konnte man bezüglich der Konzentration der myofibrillären Proteinfraktion und ihrer einzelnen Komponenten eine interessante Dynamik registrieren. Darüber hinaus wurde eine progressive Abnahme der spezifischen Aktivität der Aktomyosin-ATPase beobachtet, der ein Rückgang der maximalen lastfreien Verkürzungsgeschwindigkeit des Herzmuskels entspricht.

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Paper, presented at the Erwin Riesch Symposium, Tübingen, September 26–29, 1976

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With 1 figure and 2 tables

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Supported by the Deutsche Forschungsgemeinschaft.     

Analysis of myocardial action potential in left ventricular hypertrophy of Goldblatt rats

Summary Action potentials were measured in hypertrophied rat myocardium by means of glass microelectrodes. Left ventricular hypertrophy was induced by experimental chronic coarctation of one renal artery without contralateral nephrectomy. The action potentials of the hypertrophied myocardium exhibit a marked prolongation without any significant changes in the transmembrane resting potential, in the amplitude, or in the maximum upstroke velocity of the action potential. The increase in the half-width of the action potential for the 6-week stage after the surgical procedure is 235%, for the 12-week stage 281%, and for the 24-week stage 314%. The prolongation of the action potentials was more marked when the degree of hypertrophy was more severe.After depression of the fast Na⁺ inward current either by tetrodotoxin, by augmentation of the extracellular K⁺ concentration, or by reduction of the extracellular Na⁺ concentration, action potentials with similar marked broadening were still obtained in hypertrophied myocardium. The results under variation of the extracellular Ca⁺⁺ concentration and simultaneous inactivation of the fast Na⁺ channels suggest that the slow transmembrane inward current is primarily carried by Ca⁺⁺ ions.The prolongation of the action potentials could be one cause of the significant increase in the time to peak force as well as the augmentation of isometric force found in this model of hypertrophied myocardium.

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Analyse des myokardialen Aktionspotentials bei linksventrikulärer Hypertrophie von Goldblatt-Ratten

Zusammenfassung Aktionspotentiale wurden mit Hilfe von Glasmikroelektroden an hypertrophierten linksventrikulären Rattenherzmuskeln abgeleitet. Die Hypertrophie wurde operativ durch die Einengung einer Arteria renalis ohne kontralaterale Nephrektomie erzeugt. Die Aktionspotentiale der hypertrophierten Myokardzelle sind gegenüber den Kontrollherzen durch eine ausgeprägte verbreiterung gekennzeichnet, bei nichtsignifikanten geringfügigen Änderungen im Ruhepotential, in der Amplitude sowie in der maximalen Aufstrichgeschwindigkeit. Sechs Wochen post operationem beträgt die Zunahme der Aktionspotentialhalbwertsbreite 235%, nach 12 Wochen ist der Anstieg 281%, und nach 24 Wochen beläuft sich der Zuwachs auf 314%. Die Verbreiterung der Aktionspotentiale ist im Mittel um so ausgeprägter, je stärker das Ausmaß der Hypertrophie ist.Nach Blockade des schnellen Na⁺-Einwärtsstroms durch die Gabe von Tetrodotoxin, durch Erhöhung des extrazellulären K⁺-Konzentration oder durch Reduktion der extrazellulären Na⁺-Konzentration resultieren im Falle der Hypertrophie gleichfalls stark verlängerte Aktionspotentiale. Die Ergebnisse unter Variation der extrazelluären Ca⁺⁺-Konzentration bei gleichzeitiger Inaktivierung der Na⁺-Kanäle lassen vermuten, daß der langsame transmembranäre Einwärtsstrom primär von Ca⁺⁺-Ionen getragen wird.Die Verbreiterung der Aktionspotentiale kann sicherlich für die signifikante Verlängerung der isometrischen Gipfelzeit sowie die Zunahme der isometrischen Gipfelkraft miverantwortlich gemacht werden, wie sie für das hypertrophierte Myokard der Goldblattratte beschrieben werden.

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With 7 figures and 1 table

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A preliminary report has been presented at the 49^th meeting of the German Physiological Society in Göttingen, March, 1978.

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This work has been supported by grants from the Deutsche Forschungsgemeinschaft     

Effect of Xinjikang on left ventricular hypertrophy remodeling in hypertensive rats

ObjectiveTo investigate the effects of Xinjikang on the left ventricular hypertrophy remodeling and myocardial activity in hypertension.MethodsSixty Wistar rats were randomly divided into four groups. The pressure-loaded left ventricular hypertrophy model was established with abdominal aorta ligation method. Rats in A and B groups were intragastrically administered with physiological saline, while C and D groups were administered with Xinjikang and metoprolol, respectively. The changes in blood pressure, E/A ratio, myocardial pathological morphology, myocardial lipoperoxides and superoxide dismustase activity in four groups were observed and compared before and after treatment.ResultsThere were statistically significant differences in E/A ratio between C group after treatment and model group (P<0.05), while no difference was observed between A and D groups (P>0.05); after treatment the myocardial lipoperoxides and superoxide dismustase contents in C and D groups were improved significantly compared with model group (P<0.05).ConclusionsXinjikang can improve myocardial injury, restore myocardial parenchyma and myocardial interstitial remodeling functions in hypertensive rats with the left ventricular hypertrophy.     

Atorvastatin prevents left ventricular remodeling in spontaneously hypertensive rats

Statins improve left ventricular (LV) remodeling in spontaneously hypertensive rats (SHRs). This study was designed to investigate the effects of atorvastatin administered in the early stage on LV remodeling in SHRs, and to explore the underlying mechanisms.Sixteen male 8-week-old SHRs were randomized to receive distilled water (SHR-DW) or atorvastatin (SHR-ATV) for 12 weeks. Age-matched male Wistar-Kyoto (WKY) rats gavaged with distilled water served as controls. LV remodeling was evaluated, myocardial CTGF expression levels were detected using Western blotting, and cardiomyocyte apoptosis was detected with the TUNEL method.Compared with WKY and SHR-DW, atorvastatin treatment significantly decreased systolic blood pressure in SHRs; atorvastatin significantly inhibited LV remodeling, as indicated by the reduced LV weight/body weight ratio (SHR-ATV: 4.0 ± 0.4 versus SHR-DW: 4.7 ± 0.4 mg/g, P < 0.05), cardiomyocyte diameter (SHR-ATV: 16.2 ± 2.8 versus SHR-DW: 19.0 ± 1.0 μm, P < 0.05), and interstitial fibrosis (SHR-ATV: 3.3 ± 2.1 versus SHR-DW: 4.5 ± 1.8%, P < 0.05). Compared with WKY, myocardial CTGF expression was significantly increased and cardiomyocyte apoptosis decreased in SHRs. Compared with the SHR-DW group, atorvastatin treatment significantly inhibited myocardial CTGF expression (SHR-ATV: 0.69 ± 0.21 versus SHR-DW: 1.12 ± 0.27, P < 0.05) and induced cardiomyocyte apoptosis in SHRs (SHR-ATV: 5.2 ± 0.6 versus SHR-DW: 1.9 ± 0.3%, P < 0.05).The results indicate that early-stage administration of atorvastatin effectively prevented LV remodeling in SHRs, and that inhibition of myocardial CTGF expression and induction of cardiomyocyte apoptosis may be the underlying mechanisms.     

Reconstituted high-density lipoprotein attenuates postinfarction left ventricular remodeling in rats

Since little is known about the effects of reconstituted high-density lipoprotein (rHDL) in left ventricular (LV) remodeling, these effects were examined in rats after acute myocardial infraction (MI). Sixteen male Wistar rats were randomly divided into three groups: Sham-operated (n=6), and MI rats that received a permanent ligation around the proximal left coronary artery and infusions of placebo (MI group, n=5) or rHDL (containing as apolipoproteinA-I 6mg/kg) administered intravenously (MI+rHDL group, n=5). rHDL was infused once a week for 4 weeks. In addition, in vitro assays were performed to examine the effect of rHDL. The MI+rHDL group showed a significant increase in LV ejection fraction (EF) between weeks 1 and 4, a decrease in LV end-systolic diameter, compared with the progressive deterioration of LV size and function in the MI group. In addition, the MI+rHDL group showed a significant decrease in fibrotic area of MI in LV compared to that in the MI group, while there were no significant increases in capillary density or cell size in LV in the MI+rHDL group. Interestingly, the MI+rHDL group showed a significant activation of retinoblastoma and ERK (extracellular-signal-regulated kinase) but not cleaved caspase-3, p38 MAPK or Jun N-terminal kinase. rHDL suppressed H(2)O(2)-induced arrest of cell growth in myocytes. This effect was blocked by PD98059, an ERK inhibitor. In conclusions, rHDL-promoted cell survival has beneficial morphological effects that help to prevent LV remodeling and improve function after MI, and may prevent arrest of cell growth through ERK pathway in myocytes.     

Beneficial effects of adrenomedullin on left ventricular remodeling after myocardial infarction in rats

OBJECTIVE: We previously reported that plasma adrenomedullin (AM) levels increase in patients with acute myocardial infarction (MI) and AM inhibits growth of rat cardiac myocytes and fibroblasts. The aim of this study was to examine the effects of long-term administration of AM on left ventricular (LV) remodeling, hemodynamic and hormonal parameters in a rat model of MI. METHODS: Rats with MI induced by left coronary ligation were intravenously infused with 1.0 microg/h of recombinant human AM or saline by osmotic mini-pump. After infusion for 4 weeks, hemodynamic and hormonal studies were performed, and the myocyte size and collagen volume in non-infarct LV area were quantified morphometrically. RESULTS: When compared with the MI rats infused with saline, continuous infusion of AM reduced the heart weight/body weight (4.4+/-0.2 vs. 3.6+/-0.1 g/kg, P<0.01), myocyte size (922+/-23 vs. 868+/-10 microm(2), P<0.05) and collagen volume fraction of non-infarct LV area (7.6+/-0.8 vs. 4.8+/-0.5%, P<0.05), without affecting the infarct size. The AM infusion had no significant effect on the arterial pressure, but decreased the LV end-diastolic pressure (8.8+/-1.8 vs. 4.4+/-0.5 mmHg, P<0.05) in the MI rats. The plasma level of endogenous rat AM in the MI rats infused with human AM was reduced by 27% (P<0.05), with a slight reduction of plasma atrial natriuretic peptide, compared with the control. CONCLUSIONS: Continuous administration of AM had beneficial effects on LV remodeling and hemodynamics in MI rats, suggesting the possibility that this peptide could be a useful therapeutic tool for acute MI.     

重组人脑利钠肽对大鼠心肌梗死后心室重构及功能的影响

目的 探讨重组人脑利钠肽(rhBNP)对心肌梗死后大鼠心室重构及心功能的影响.方法 建立急性心肌梗死(AMI)雄性SD大鼠模型45只,随机分为AMI对照组、小剂量rhBNP治疗组、大剂最rhBNP治疗组,每组各15只.另设15只作假手术组.rhBNP治疗组经颈静脉输液管输注rhBNP,剂量分别为5μg/ks和15 μg/kg,1次/d,持续4周,假手术组及AMI对照组仅以等体积的生理盐水输注.4周后检测血液动力学及心功能参数,心脏标本检测左室重量及左室重量指数(LVMI)、心肌梗死面积,并检测血浆和心肌血管紧张素Ⅱ(Ang Ⅱ)水平.结果 AMI对照组左室重量、LVMI及心肌AngⅡ水平明显高于假手术组,而收缩压及左室内压最大上升和下降速率(±dp/dt)均明显低于假手术组(均P<0.01).大、小剂量rhBNP治疗组左室重量及LVMI、心肌梗死面积和心肌AngⅡ水平均明显低于AMI对照组[左室重量:分别为(492.6±34.0)mg、(498.8±47.8)mg比(570.0±24.2)mg,P<0.01;LVMI:2.0±0.2、2 0±0.2比2.3±0.1,P<0.01;心肌梗死面积:(25.3±2.9)%、(31.4±3.0)%比(46.4±3.0)%,P<0.01;Ang Ⅱ水平:(881.3±62.7)pg/L、(1186.0±94.5)pg/L比(2436.7±280.3)pg/L,P<0.05],收缩压和±dp/dt也高于AMI对照组(P<0.01或P<0.05).结论 外源性的rhBNP连续应用能限制梗死面积、减轻AMI后心室重构、保护心功能.     

老龄性心室重构过程

老龄是心力衰竭最主要的危险因素之一.与年轻者相比,老龄性心脏重构的分子基础包括心肌细胞凋亡、自噬、更新失效等更明显.细胞凋亡可以通过内在的或者外在的途径进行调节.与这些途经相关的许多因素都随年龄的增长而增加.自噬是心肌细胞生存必不可少的过程.心肌细胞肥大和心肌间质纤维化作为老龄化心脏心肌细胞数量减少的代偿机制,被认为是...