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去窦弓神经大鼠高血压期间脑血管自动调节功能得以保留的机制。

Mechanisms for preserved cerebrovascular autoregulation during hypertension in rats after sinoaortic denervation.

作者信息

Talman W T, Dragon D N

机构信息

Department of Neurology, University of Iowa College of Medicine, Veterans Affairs Medical Center, Iowa City, USA.

出版信息

Clin Exp Pharmacol Physiol Suppl. 1995 Dec;22(1):S77-9. doi: 10.1111/j.1440-1681.1995.tb02978.x.

Abstract
  1. Cerebral blood flow (CBF) and cerebrovascular resistance (CVR) autoregulate to higher levels of arterial pressure (AP) in rats after sinoaortic denervation (SAD) than in intact rats. 2. Potential mechanisms for this phenomenon were studied by monitoring CBF by laser flowmetry while increasing AP in rats after: (i) SAD; (ii) SAD plus bilateral removal of the superior cervical ganglia; (iii) SAD plus interruption of all renal vessels and nerves (renal isolation); (iv) SAD plus sympathectomy and renal isolation; and (v) intravenous treatment with the nitric oxide synthase inhibitor L-nitroarginine (LNA). 3. Compared to intact control rats autoregulation persisted to higher absolute levels of AP in SAD rats with isolation of the kidneys and resistance did not fall significantly below that in rats with SAD alone. 4. Effects of SAD on autoregulation were not altered by combining renal isolation with an interruption of sympathetics. 5. LNA did not affect the baroreflex but blocked a breakthrough of autoregulation even at a maximal mean AP (MAP) of 189 +/- 2 mmHg. 6. Breakthrough occurred in animals pretreated with LNA plus L-arginine but not in animals given LNA plus D-arginine. 7. These data are consistent with a role of the baroreflex in the expression of breakthrough and suggest that breakthrough may result from release of nitric oxide or a nitric oxide donor.
摘要
  1. 与完整大鼠相比,去窦弓神经支配(SAD)的大鼠脑血流量(CBF)和脑血管阻力(CVR)对更高水平的动脉压(AP)进行自动调节。2. 通过激光血流仪监测CBF,同时在以下大鼠中升高AP,研究了这种现象的潜在机制:(i)SAD;(ii)SAD加双侧切除颈上交感神经节;(iii)SAD加切断所有肾血管和神经(肾隔离);(iv)SAD加交感神经切除术和肾隔离;以及(v)用一氧化氮合酶抑制剂L-硝基精氨酸(LNA)进行静脉治疗。3. 与完整对照大鼠相比,肾隔离的SAD大鼠自动调节持续到更高的绝对AP水平,阻力并未显著低于单独SAD大鼠。4. 将肾隔离与交感神经切断相结合,并未改变SAD对自动调节的影响。5. LNA不影响压力反射,但即使在最大平均动脉压(MAP)为189±2 mmHg时也能阻止自动调节的突破。6. 在预先用LNA加L-精氨酸处理的动物中出现突破,但在给予LNA加D-精氨酸的动物中未出现。7. 这些数据与压力反射在突破表达中的作用一致,并表明突破可能是由一氧化氮或一氧化氮供体的释放引起的。

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