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首页> 外文期刊>The Internet Journal of Orthopedic Surgery >Left Ventricular Hypertrophy, Cardiac Myocyte Adaptation, and Collagen/Parenchymal Distribution in Response to Subpressor and Pressor Doses of Angiotensin II in Sprague-Dawley Rats
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Left Ventricular Hypertrophy, Cardiac Myocyte Adaptation, and Collagen/Parenchymal Distribution in Response to Subpressor and Pressor Doses of Angiotensin II in Sprague-Dawley Rats

机译：Sprague-Dawley大鼠对降压和升压剂量血管紧张素II的反应左心室肥大，心肌细胞适应和胶原/实质分布

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The alteration of cardiovascular myocytes is an important compensatory response to hypertension; however the pressor effect of angiotensin-II (A-II) on the correlation of myocyte morphological adaptation and collagen/parenchyma distribution in the ventricles has not been determined. Previous observations that the AII peptide is involved in the etiology of hypertension, suggested that ventricular collagen remodeling and associated pathophysiological alterations may be induced by a dysfunctional renin-angiotensin system. The objectives of this study were to 1) determine the contribution and distribution of collagen and parenchyma remodeling in the left ventricles after chronic exposure to subpressor (Sd) or pressor doses (Pd) of angiotensin II (A-Il); and 2) correlate the morphological adaptations of cardiomyocytes to weight changes of the entire heart after A-Il. The increase was 0.03 to 0.11 in the Pd-treated rats which was accompanied by a higher level of hypertrophic response than with the Sd treatment. Left-ventricular cell lengths (CL) of Pd-treated rats increased by 13%, while the heart weight to body weight ratio (HW/BW) increased by 22%. The myocardial interstitium response to the hypertrophic stimulation by A-Il included disproportionate collagen/parenchyma distribution to myocyte enlargement that is more pronounced with larger doses of A-Il and level of hypertrophy. This suggests that the A-II peptide is involved in the etiology of hypertension and a local increase is a primary factor of sustained myocardial remodeling. Introduction Cardiovascular function integrally involves the renin angiotensin system (RAS). Classically, endogenous angiotensin II (A-Il), the central product of the RAS, is well known to produce potent vasoconstrictive responses resulting in increases in arterial blood pressure. A growing body of evidence on A-lI’s actions, from several labs, supports the conclusion that the peptide is involved in the etiology of hypertension, as well as the pathophysiology of cardiac hypertrophy and remodeling, heart failure, vascular thickening, atherosclerosis and glomerulosclerosis (Yamamoto et. al., 2007, Ahmad et. al., 2008, Uechi et al., 2008,). Several studies have shown that A-Il stimulates myocardial protein synthesis, while more recent reports have emphasized a difference between the systemic vs. the local generation of A-Il (Abrahamsen et. al., 2002, Schnee and Hsueh, 2000). The myocardial component of the heart wall consists of myocytes, non-myocyte cells and a coronary microcirculation, which are supported and surrounded by a fibrous network within the interstitial space. Within this network, the major structural protein is collagen. Studies have shown differential effects of A-II on supportive cells than on cardiomyocytes and on fibrillar collagen (Pope et. al., 2008). An accumulation of connective tissue in general and fibrillar collagen in particular is present in patients with cardiocyte necrosis and myocardial infarction (Nian et. al., 2004, Weber et. al., 2004). Evidence has also accumulated to indicate that the structural protein matrix of the interstitium is also an active participant in the hypertrophic process that accompanies left ventricular pressure overload and in patients with end stage cardiomyopathy (Wilke et. al., 1996, Elliot 2007, Deschamps and Spinale, 2005). Based on the heterogeneity of the myocardial structure it has been put forward that there are several different cellular responses that occur during the progression of cardiovascular disease. These include non-myocyte cell growth without myocyte hypertrophy; myocyte hypertrophy without non-myocyte growth; and concomitant equal or disproportionate growth of all cells. Furthermore, the A-II may also be related to calcium intracellular availability as has been suggested for several years now (Bird et. al., 1995, McDonald et. al., 1995). It has previously been established that a single intracardiac administration of retroviral vect
机译：心血管肌细胞的改变是对高血压的重要补偿反应。然而，尚未确定血管紧张素II（A-II）对心室中肌细胞形态适应和胶原/薄壁组织分布的相关性的加压作用。先前关于AII肽参与高血压病因的观察表明，功能障碍的肾素-血管紧张素系统可能诱发心室胶原重塑和相关的病理生理改变。这项研究的目的是：1）确定长期暴露于降压素（Sd）或升压剂量（Pd）的血管紧张素II（A-11）后左心室中胶原蛋白和实质重构的贡献和分布;和2）将心肌细胞的形态适应性与A-11后整个心脏的体重变化相关。在Pd处理的大鼠中，增加幅度为0.03至0.11，与Sd处理相比，伴有更高水平的肥大性反应。 Pd处理的大鼠的左心室细胞长度（CL）增加了13％，而心脏重量与体重之比（HW / BW）增加了22％。心肌间质对A-11的肥大刺激的反应包括不均衡的胶原/实质分布到心肌细胞增大，这在较大剂量的A-11和肥大水平下更为明显。这表明A-II肽与高血压的病因有关，局部升高是持续心肌重塑的主要因素。简介心血管功能整体涉及肾素血管紧张素系统（RAS）。经典地，众所周知，内源性血管紧张素II（A-II）是RAS的主要产物，可产生有效的血管收缩反应，从而导致动脉血压升高。来自多个实验室的有关A-II作用的越来越多的证据支持这一结论，即该肽与高血压的病因，心脏肥大和重塑，心力衰竭，血管增厚，动脉粥样硬化和肾小球硬化的病理生理有关（ Yamamoto等，2007; Ahmad等，2008; Uechi等，2008，）。几项研究表明，A-II刺激心肌蛋白的合成，而最近的报道则强调了全身性和局部生成的A-I1之间的差异（Abrahamsen等，2002; Schnee和Hsueh，2000）。心脏壁的心肌部分由心肌细胞，非心肌细胞和冠状动脉微循环组成，它们由间隙空间内的纤维网络支撑和包围。在这个网络中，主要的结构蛋白是胶原蛋白。研究表明，A-II对支持细胞的作用不同于对心肌细胞和对原纤维胶原的作用（Pope等，2008）。在患有心肌细胞坏死和心肌梗塞的患者中，通常存在结缔组织的积累，尤其是原纤维胶原蛋白的积累（Nian等，2004; Weber等，2004）。也有证据表明间质的结构蛋白基质也是左室压力超负荷和患有终末型心肌病的肥厚过程的积极参与者（Wilke等，1996; Elliot 2007; Deschamps和Spinale，2005年）。基于心肌结构的异质性，已经提出在心血管疾病的进展过程中会发生几种不同的细胞反应。这些包括无心肌细胞肥大的非心肌细胞生长;肌细胞肥大，无非肌细胞生长;并伴随所有细胞均等或不成比例的生长。此外，正如几年来已经提出的那样，A-II也可能与钙的细胞内可用性有关（Bird等，1995，McDonald等，1995）。先前已确定逆转录病毒vect的单次心脏内给药

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