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Coronary dilatation reserve in experimental hypertension and chronic heart failure: effects of blockade of the Renin-Angiotensin system.

机译:实验性高血压和慢性心力衰竭的冠状动脉扩张储备:肾素-血管紧张素系统的阻断作用。

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摘要

1. The aim of the present study was to investigate left and right ventricular (LV and RV, respectively) coronary vasodilatation reserve (CVR; fluorescent microsphere technique) in rats with hypertension (spontaneously hypertensive rats (SHR)) or congestive heart failure (CHF) and the effects of early and chronic renin-angiotensin system (RAS) blockade thereupon. 2. In adult SHR, both LV and RV CVR were impaired, especially in the non-hypertrophied RV, the main factor involved being coronary vascular remodelling. Blockade of the RAS normalized both LV and RV CVR, mainly through the prevention of hypertension and suppression of the resulting pericoronary fibrosis. 3. In postischaemic CHF rats, there was an early and severe degradation of LV and RV CVR that developed before any significant vascular remodelling and appeared to be linked to the deterioration of cardiac hypertrophy and haemodynamics. This degradation in CVR further worsened over the longer term due to late-developing pericoronary fibrosis and endothelial dysfunction. Blockade of the RAS had no early effects on LV and RV CVR, but improved RV CVR over the long term, mainly by limiting RV hypertrophy and by preventing the development of pericoronary fibrosis and coronary endothelial dysfunction. 4. In kallikrein-kinin system-deficient mice, CVR was not different from that of wild-type mice, suggesting that this system is not implicated in normal CVR regulation.
机译:1.本研究的目的是研究高血压(自发性高血压大鼠(SHR))或充血性心力衰竭(CHF)大鼠的左心室和右心室(分别为LV和RV)冠状动脉舒张储备(CVR;荧光微球技术) )及其对早期和慢性肾素-血管紧张素系统(RAS)的影响。 2.在成人SHR中,LV和RV CVR均受损,特别是在非肥厚性RV中,主要因素是冠状动脉重塑。 RAS的阻滞主要通过预防高血压和抑制冠状动脉周围纤维化来使LV和RV CVR正常化。 3.在缺血后的CHF大鼠中,LV和RV CVR出现了早期严重的退化,该退化在任何重大的血管重塑之前就已经出现,并且似乎与心脏肥大和血流动力学的恶化有关。由于晚期冠状动脉纤维化和内皮功能障碍,CVR的这种降解在长期内还会进一步恶化。 RAS的阻断对LV和RV CVR没有早期影响,但从长远来看改善了RV CVR,主要是通过限制RV肥大和预防冠状动脉纤维化和冠状动脉内皮功能障碍。 4.在激肽释放酶激肽系统缺陷的小鼠中,CVR与野生型小鼠无差异,这表明该系统与正常的CVR调节无关。

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