首页> 外文期刊>Journal of vascular research >New insight into abnormal muscle vasodilatory responses in aged hypertensive rats by in vivo nuclear magnetic resonance imaging of perfusion.
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New insight into abnormal muscle vasodilatory responses in aged hypertensive rats by in vivo nuclear magnetic resonance imaging of perfusion.

机译:通过灌注的体内核磁共振成像对老年高血压大鼠的异常血管舒张反应的新见解。

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摘要

OBJECTIVE: Increased peripheral arterial resistances and decreased maximum vasodilation are characteristic features of chronic hypertension. However, little data are available in the literature regarding the possible alterations in the temporal patterns of vasodilatory responses elicited by various stimuli. DESIGN: This question was addressed by measuring skeletal muscle perfusion using nuclear magnetic resonance imaging combined with arterial spin labeling. METHODS: Ninety-week-old male spontaneously hypertensive (SHR; n = 7) and normotensive Wistar Kyoto (WKY; n = 8) rats were studied, and calf muscle perfusion was measured at rest and during reactive hyperemia following total ischemia of 5 and 30 min duration. RESULTS: Reactive hyperemia profiles differed according to duration of ischemia. In WKY rats, 5 min of ischemia induced a short peak of hyperemia lasting no more than 63 s, while 30 min of ischemia were followed by a prolonged hyperemic response of 261 s. In SHRs, after 5 min of ischemia, peakmuscle arterial conductance was decreased to 0.5 +/- 0.3 versus 0.9 +/- 0.3 ml.min(-1).100 g(-1).mm Hg(-1) in the WKY rats (p < 0.05), as expected. After 30 min of ischemia, there was, in addition, a shortening of the hyperemic response duration. Time to post-ischemic half normalization of arterial conductance was 38 +/- 24 s in the SHRs versus 149 +/- 58 s in the WKY rats (p < 0.001). CONCLUSION: In vivo perfusion measurement not only confirmed the existence of a reduced maximum peripheral vasodilation in chronically hypertensive rats, it revealed a blunted hyperemic response after prolonged ischemia in the SHRs, which might be an important contributing factor to the increased sensitivity to ischemia in hypertension.
机译:目的:增加外周动脉阻力和减少最大血管舒张是慢性高血压的特征。然而,关于各种刺激引起的血管舒张反应的时间模式可能发生变化的文献资料很少。设计:这个问题是通过使用核磁共振成像结合动脉自旋标记测量骨骼肌灌注来解决的。方法:研究了九十周大的雄性自发性高血压(SHR; n = 7)和血压正常的Wistar Kyoto(WKY; n = 8)大鼠,在总缺血5和5次后的静止和反应性充血期间测量了小腿肌肉的灌注。持续时间30分钟。结果:根据缺血持续时间,反应性充血情况有所不同。在WKY大鼠中,缺血5分钟诱导了充血的短峰,持续时间不超过63 s,而缺血30 min则持续了261 s的充血反应。在SHRs中,缺血5分钟后,峰值肌肉动脉电导降低至0.5 +/- 0.3相对于WKY中的0.9 +/- 0.3 ml.min(-1).100 g(-1).mm Hg(-1)如预期的那样(p <0.05)。缺血30分钟后,此外,充血反应持续时间缩短。 SHRs缺血后达到动脉电导半正常化的时间为38 +/- 24 s,而WKY大鼠为149 +/- 58 s(p <0.001)。结论:体内灌注测量不仅证实了慢性高血压大鼠最大外周血管舒张功能的降低,而且还显示了SHRs长时间缺血后充血性充血反应减弱,这可能是导致高血压对缺血性敏感性增加的重要因素。

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