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首页> 外文期刊>American Journal of Physiology >Early experimental hypertension preserves the myocardial microvasculature but aggravates cardiac injury distal to chronic coronary artery obstruction.
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Early experimental hypertension preserves the myocardial microvasculature but aggravates cardiac injury distal to chronic coronary artery obstruction.

机译：早期的实验性高血压可以保留心肌的微脉管系统，但会加重慢性冠状动脉阻塞远端的心脏损伤。

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Coronary artery disease is a leading cause of death. Hypertension (HT) increases the incidence of cardiac events, but its effect on cardiac adaptation to coexisting coronary artery stenosis (CAS) is unclear. We hypothesized that concurrent HT modulates microvascular function in chronic CAS and aggravates microvascular remodeling and myocardial injury. Four groups of pigs (n=6 each) were studied: normal, CAS, HT, and CAS+HT. CAS and HT were induced by placing local irritant coils in the left circumflex coronary artery and renal artery, respectively. Six weeks later multidetector computerized tomography (CT) was used to assess systolic and diastolic function, microvascular permeability, myocardial perfusion, and responses to adenosine in the "area at risk." Microvascular architecture, inflammation, and fibrosis were then explored in cardiac tissue. Basal myocardial perfusion was similarly decreased in CAS and CAS+HT, but its response to adenosine was significantly more attenuated in CAS. Microvascular permeability in CAS+HT was greater than in CAS and was accompanied by amplified myocardial inflammation, fibrosis, and microvascular remodeling, as well as cardiac systolic and diastolic dysfunction. On the other hand, compared with normal, micro-CT-derived microvascular (20-200 mum) transmural density decreased in CAS but not in HT or CAS+HT. We conclude that the coexistence of early renovascular HT exacerbated myocardial fibrosis and vascular remodeling distal to CAS. These changes were not mediated by loss of myocardial microvessels, which were relatively preserved, but possibly by exacerbated myocardial inflammation and fibrosis. HT modulates cardiac adaptive responses to CAS and bears cardiac functional consequences.
机译：冠状动脉疾病是死亡的主要原因。高血压（HT）会增加心脏事件的发生率，但尚不清楚其对心脏适应并存冠状动脉狭窄（CAS）的影响。我们假设并发HT调节慢性CAS中的微血管功能并加重微血管重塑和心肌损伤。研究了四组猪（每组n = 6）：正常，CAS，HT和CAS + HT。通过在左旋支冠状动脉和肾动脉中分别放置局部刺激线圈来诱导CAS和HT。六周后，使用多探测器计算机断层扫描（CT）评估“危险区域”的收缩和舒张功能，微血管通透性，心肌灌注以及对腺苷的反应。然后在心脏组织中探索微血管结构，炎症和纤维化。在CAS和CAS + HT中，基础心肌的灌注同样降低，但是在CAS中，其对腺苷的反应明显减弱。 CAS + HT的微血管通透性高于CAS，并伴有放大的心肌炎症，纤维化和微血管重塑，以及心脏收缩和舒张功能障碍。另一方面，与正常相比，CAS中微CT来源的微血管（20-200 mum）的透壁密度降低，而HT或CAS + HT则没有。我们得出的结论是，早期肾血管性肝炎的并存加剧了CAS远端的心肌纤维化和血管重构。这些变化不是由相对保留的心肌微血管丧失所介导，而是可能由加剧的心肌炎症和纤维化所介导。 HT调节心脏对CAS的适应性反应并承担心脏功能后果。

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