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自发性高血压大鼠动脉扩张性与血压低频功率谱之间的关系。

Relationship between arterial distensibility and low-frequency power spectrum of blood pressure in spontaneously hypertensive rats.

作者信息

Dabiré Hubert, Lacolley Patrick, Chaouche-Teyara Kamel, Fournier Berthe, Safar Michel E

机构信息

Institut National de la Santé et de la Recherche Médicale, Paris, France.

出版信息

J Cardiovasc Pharmacol. 2002 Jan;39(1):98-106. doi: 10.1097/00005344-200201000-00011.

Abstract

The aim of this study was to determine in spontaneously hypertensive rats (SHRs) whether a significant association may be observed between the low-frequency component of blood pressure variability (BPV) and arterial distensibility and to evaluate the role of the autonomic nervous system in this relationship. Doxazosin (1 mg/kg/d s.c.), flesinoxan (1 mg/kg/d s.c.), and urapidil (30 mg/kg/d s.c.) were infused over 24 h in SHRs. Blood pressure was recorded in conscious rats and BPV was characterized by spectral analysis. The distensibility-pressure curves for the carotid artery were determined by an ultrasonic echo-tracking device in anesthetized rats. Untreated SHRs had higher mean arterial pressure (MAP) and low-frequency MAP but a lower distensibility than normotensive Wistar-Kyoto rats. In SHRs inhibition of the autonomic nervous system by peripheral blockade of alpha1-adrenoceptors (doxazosin, 1 mg/kg, or urapidil, 30 mg/kg) or centrally mediated reduction of sympathetic tone (flesinoxan, 1 mg/kg) reduced MAP and low-frequency MAP in the conscious state and increased carotid operational distensibility in the anesthetized state. In these SHRs, we observed a negative association between low-frequency MAP and operational distensibility ( r = -0.48, p < 0.01). From multiple regression analysis, MAP and low-frequency MAP, but not drug treatment, influenced arterial distensibility. Our study in SHRs provides evidence for a strong association between increased low-frequency MAP and reduced arterial distensibility, with a common modulation provided by the autonomic nervous system via the alpha 1 -adrenergic receptor component and central nervous system.

摘要

本研究的目的是确定在自发性高血压大鼠(SHR)中,血压变异性(BPV)的低频成分与动脉扩张性之间是否存在显著关联,并评估自主神经系统在这种关系中的作用。将多沙唑嗪(1毫克/千克/天,皮下注射)、氟西诺生(1毫克/千克/天,皮下注射)和乌拉地尔(30毫克/千克/天,皮下注射)在SHR中输注24小时。在清醒大鼠中记录血压,并通过频谱分析对BPV进行特征描述。在麻醉大鼠中,使用超声回声跟踪装置测定颈动脉的扩张性-压力曲线。未治疗的SHR比正常血压的Wistar-Kyoto大鼠具有更高的平均动脉压(MAP)和低频MAP,但扩张性更低。在SHR中,通过外周阻断α1肾上腺素能受体(多沙唑嗪,1毫克/千克,或乌拉地尔,30毫克/千克)或中枢介导的交感神经张力降低(氟西诺生, 1毫克/千克)来抑制自主神经系统,可降低清醒状态下的MAP和低频MAP,并增加麻醉状态下颈动脉的操作扩张性。在这些SHR中,我们观察到低频MAP与操作扩张性之间存在负相关(r = -0.48,p < 0.01)。多元回归分析表明,MAP和低频MAP而非药物治疗会影响动脉扩张性。我们对SHR的研究为低频MAP升高与动脉扩张性降低之间的强关联提供了证据,自主神经系统通过α1肾上腺素能受体成分和中枢神经系统提供了共同调节。

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