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首页> 外文期刊>Journal of cardiac failure >Vascular alterations during the development and progression of experimental heart failure.
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Vascular alterations during the development and progression of experimental heart failure.

机译：实验性心力衰竭的发生和发展过程中的血管改变。

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BACKGROUND: Congestive heart failure (HF) is a multifactorial and progressive condition associated with multiple systemic and vascular alterations. The onset and progression of these alterations and the cause of the condition remain undefined. The main purpose of the present study was to help understand the temporal evolution of vascular alterations and their contribution to the pathogenesis of HF. Vascular reactivity to angiotensin II (Ang II) and norepinephrine (NE), as well as circulating and local angiotensin-converting enzyme (ACE) activity, were assessed in the Syrian cardiomyopathic hamster (SCH) model. METHODS AND RESULTS: We have shown previously that in 2-month-old SCH animals that had not yet developed the clinical manifestations of HF, the contractile response of aortic rings to Ang II was markedly enhanced compared with normal animals. In addition, SCHs showed increased ACE activity in aortic tissue. To assess the relevance of these findings to the development and progression of HF, the temporal evolution of the contractile response of aortic rings to Ang II and NE was evaluated in hamsters at 2, 6, and 11 months of age. Age-matched normal hamsters were used as controls. Within the SCH group, the maximal contraction induced to 10 mumol/L of NE in 2- and 11-month-old animals was similar, but significantly greater than in the age-matched controls (for 2-month-old animals; 1.43 +/- 0.21 g in SCHs v 1.04 +/- 0.15 g in controls; P < .05 and for 11-month-old animals; 1.41 +/- 0.14 g in SCHs v 1.06 +/- 0.07 g in controls; P < .05). The drug concentrations necessary to obtain 50% of the maximal response from the NE concentration-response curves were similar for SCHs and controls at all ages tested. In contrast, the contractility induced by 0.1 mumol/L of Ang II increased progressively in cardiomyopathic animals from 2 to 11 months of age (from 1.3 +/- 0.1 to 1.8 +/- 0.2 g; n = 9; P < .05). In age-matched normal hamsters, the contractile response to Ang II (0.9 +/- 0.1 g) did not vary with age. These findings were observed concomitantly with an increased ACE activity in plasma (18.65 +/- 1.77 nmol/mg x min in controls v 26.5 +/- 1.79 nmol/mg x min in SCHs; P < .05; n = 7) and in heart tissue (0.244 +/- 0.016 nmol/mg x min in controls v 0.563 +/- 0.027 nmol/mg x min in SCHs; P < .05; n = 20) of 11-month-old SCHs. CONCLUSIONS: These results suggest that, in young animals, increased vascular response to elevated levels of NE and hyperreactivity to Ang II could be critical factors in the development and progression of HF. Indeed, Ang II-induced contractility, as well as plasma and heart ACE activity, are good predictors of the progression and severity of HF.
机译：背景：充血性心力衰竭（HF）是与多种系统和血管改变相关的多因素和进行性疾病。这些改变的发作和进展以及病因尚不清楚。本研究的主要目的是帮助了解血管改变的时间演变及其对心衰发病机制的贡献。在叙利亚心肌病仓鼠（SCH）模型中评估了对血管紧张素II（Ang II）和去甲肾上腺素（NE）的血管反应性，以及循环和局部血管紧张素转化酶（ACE）的活性。方法和结果：我们先前已经表明，在2个月大的尚未出现HF临床表现的SCH动物中，与正常动物相比，主动脉环对Ang II的收缩反应明显增强。此外，SCHs在主动脉组织中显示出增加的ACE活性。为了评估这些发现与HF的发生和发展的相关性，在2、6和11个月大的仓鼠中评估了主动脉环对Ang II和NE的收缩反应的时间演变。使用年龄匹配的正常仓鼠作为对照。在SCH组内，在2个月和11个月大的动物中，对NE的10μmol/ L的最大收缩是相似的，但显着大于与年龄匹配的对照组（对于2个月大的动物; 1.43 + /-SCHs中为0.21 g，对照组中为1.04 +/- 0.15 g;对于11个月大的动物，P <.05; SCHs中为1.41 +/- 0.14 g，而对照组中为1.06 +/- 0.07 g; P <。 05）。从NE浓度-响应曲线中获得最大响应的50％所需的药物浓度在所有测试年龄的SCH和对照中均相似。相反，在2至11个月大的心肌病动物中，由0.1μmol/ L Ang II诱导的收缩力逐渐增加（从1.3 +/- 0.1到1.8 +/- 0.2 g; n = 9; P <.05） 。在年龄匹配的正常仓鼠中，对Ang II（0.9 +/- 0.1 g）的收缩反应没有随年龄变化。在血浆中ACE活性增加的情况下观察到了这些发现（对照组中的ACE活性为18.65 +/- 1.77 nmol / mg x min; SCH中的ACE活性为26.5 +/- 1.79 nmol / mg x min; P <0.05; n = 7）。 11个月大的SCHs的心脏组织（对照组中0.244 +/- 0.016 nmol / mg x分钟; SCHs中0.563 +/- 0.027 nmol / mg x分钟; P <.05; n = 20）。结论：这些结果表明，在幼小动物中，对高水平NE和对Ang II反应过度的血管反应增加可能是HF发生和发展的关键因素。实际上，Ang II诱导的收缩力以及血浆和心脏ACE活性是HF进展和严重程度的良好预测指标。

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