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[清醒大鼠肾血流量的自身调节与血压变异性]

[Autoregulation of renal blood flow and blood pressure variability in the conscious rat].

作者信息

Pires S L, Barrès C, Sassard J, Julien C

机构信息

CNRS UMR 5014, IFR 39, université Claude-Bernard, 8, av. Rockefeller, 69373 Lyon.

出版信息

Arch Mal Coeur Vaiss. 2001 Aug;94(8):818-21.

Abstract

It is often proposed that autoregulatory mechanisms prevent acute changes in systemic blood pressure (BP) from being transmitted to the glomerular capillary circulation. However, it is not known whether renal blood flow (RBF) is still autoregulated when the kidney is exposed to exaggerated BP fluctuations, in particular hypertensive episodes. The aim of the present study was therefore to evaluate the efficacy of renal autoregulatory responses in an animal model of BP lability, the sinoaortic denervated (SAD) rat. BP and RBF were simultaneously recorded in 8 SAD (2 wks before study) and 8 baroreceptor intact (INT) Sprague-Dawley rats during approximately 3 h of spontaneous activity. The left kidney used for RBF recordings was denervated to prevent the interference of changes in renal sympathetic tone with autoregulatory responses. The SAD procedure modified neither the mean BP nor the mean RBF levels (111 +/- 1 mmHg and 11.3 +/- 1.3 mL/min in INT rats: 113 +/- 6 mmHg and 11.1 +/- 0.9 mL/min in SAD rats). However, SAD strongly increased the BP variability (coefficient of variation: 5.9 +/- 0.2% and 18.2 +/- 1.1% in INT and SAD rats, respectively). In spite of this marked BP lability, RBF variability was not significantly affected by the SAD procedure (9.1 +/- 0.8% and 12.4 +/- 1.6% in INT and SAD rats, respectively). In SAD rats, spontaneous hypertensive episodes (top 1% of BP values: 174 +/- 10 mmHg) did not induce increases in RBF (10.5 +/- 1.0 ml/min). Fast Fourier transform analysis revealed that in SAD rats, autoregulatory mechanisms attenuated approximately 80% of BP fluctuations in the 0.0015-0.01 Hz frequency range, suggesting a major involvement of the tubuloglomerular feedback. In conclusion, autoregulatory mechanisms have an ample capacity to protect the kidney against spontaneous BP fluctuations in the conscious rat. Consequently, BP variability per se is probably not detrimental to the kidney, as long as autoregulatory mechanisms are normally functioning.

摘要

人们常提出,自身调节机制可防止全身血压(BP)的急性变化传导至肾小球毛细血管循环。然而,当肾脏暴露于过度的血压波动,尤其是高血压发作时,肾血流量(RBF)是否仍受自身调节尚不清楚。因此,本研究的目的是评估在血压不稳定的动物模型——去窦弓神经(SAD)大鼠中,肾脏自身调节反应的效能。在8只SAD大鼠(研究前2周)和8只压力感受器完整(INT)的Sprague-Dawley大鼠自发活动约3小时期间,同时记录血压和肾血流量。用于记录肾血流量的左肾去神经支配,以防止肾交感神经张力变化对自身调节反应的干扰。SAD手术既未改变平均血压水平,也未改变平均肾血流量水平(INT大鼠分别为111±1 mmHg和11.3±1.3 mL/min;SAD大鼠分别为113±6 mmHg和11.1±0.9 mL/min)。然而,SAD显著增加了血压变异性(变异系数:INT大鼠和SAD大鼠分别为5.9±0.2%和18.2±1.1%)。尽管存在这种明显的血压不稳定,但SAD手术并未显著影响肾血流量变异性(INT大鼠和SAD大鼠分别为9.1±0.8%和12.4±1.6%)。在SAD大鼠中,自发性高血压发作(血压值最高的1%:174±10 mmHg)并未引起肾血流量增加(10.5±1.0 ml/min)。快速傅里叶变换分析显示,在SAD大鼠中,自身调节机制在0.0015 - 0.01 Hz频率范围内减弱了约80%的血压波动,提示管球反馈起主要作用。总之,自身调节机制有足够能力保护清醒大鼠的肾脏免受自发性血压波动影响。因此,只要自身调节机制正常运作,血压变异性本身可能对肾脏无害。

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