Inhibition of nitric oxide synthase does not alter dynamic cerebral autoregulation in humans.
Inhibition of nitric oxide synthase does not alter dynamic cerebral autoregulation in humans.
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一氧化氮合酶的抑制不会改变人类的动态大脑自动调节。
DOI：
10.1152/ajpheart.00373.2003
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Levine,BenjaminD
中科院分区：
文献类型：
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作者：
Zhang,Rong;Wilson,ThadE;Witkowski,Sarah;Cui,Jian;Crandall,GraigG;Levine,BenjaminD
这项研究的目的是确定一氧化氮合酶(NOS)的抑制是否改变了人类动态的脑自动调节。测定了8名健康受试者仰卧位和60°头高位(HUT)时的血压(BP)和脑血流速度(CBF)。静脉注射N-甲基-L-精氨酸(N-甲基-N-甲基-L-精氨酸)抑制NOS。动态脑自动调节通过对BP和CBF速度逐次变化的传递函数分析来量化。比较l-NMMA与苯肾上腺素对脑血流动力学的升压作用。卧位时，平均血压由83±3升至94±3毫米汞柱(P<；0.01)。但CBF血流速度无明显变化。脑血管阻力指数(CVRI)增加15%(P<；0.05)。0.0 7~0.2 0 Hz低频段的BP和CBF速度变异性和传递函数增益不受l-NMMA的影响。在注射苯肾上腺素后，平均血压、CBF血流速度和CVRI也有类似的变化，表明l-NMMA后CVRI的增加是通过动脉压的升高而不是脑血管NOS抑制的直接作用来实现的。基础倾斜时，无1-NMMA时，稳态血压升高，CBF速度降低。低频时BP和CBF速度变异性分别增加277%和217%(P<；0.05)。然而，传递函数增益保持不变。在倾斜过程中，使用l-NMMA的稳态血流动力学、BP和CBF速度变异性以及传输增益和相位的变化与不使用l-NMMA的相似。这些数据表明，抑制NO的紧张性产生似乎不会改变人类大脑的动态自我调节。
The aim of this study was to determine whether inhibition of nitric oxide synthase (NOS) alters dynamic cerebral autoregulation in humans. Beat-to-beat blood pressure (BP) and cerebral blood flow (CBF) velocity (transcranial Doppler) were measured in eight healthy subjects in the supine position and during 60° head-up tilt (HUT). NOS was inhibited by intravenousNG-monomethyl-l-arginine (l-NMMA) infusion. Dynamic cerebral autoregulation was quantified by transfer function analysis of beat-to-beat changes in BP and CBF velocity. Pressor effects ofl-NMMA on cerebral hemodynamics were compared with those of phenylephrine infusion. In the supine position,l-NMMA increased mean BP from 83 ± 3 to 94 ± 3 mmHg (P< 0.01). However, CBF velocity remained unchanged. Consequently, cerebrovascular resistance index (CVRI) increased by 15% (P< 0.05). BP and CBF velocity variability and transfer function gain at the low frequencies of 0.07–0.20 Hz did not change withl-NMMA infusion. Similar changes in mean BP, CBF velocity, and CVRI were observed after phenylephrine infusion, suggesting that increase in CVRI afterl-NMMA was mediated myogenically by increase in arterial pressure rather than a direct effect of cerebrovascular NOS inhibition. During baseline tilt withoutl-NMMA, steady-state BP increased and CBF velocity decreased. BP and CBF velocity variability at low frequencies increased in parallel by 277% and 217%, respectively (P< 0.05). However, transfer function gain remained unchanged. During tilt withl-NMMA, changes in steady-state hemodynamics and BP and CBF velocity variability as well as transfer gain and phase were similar to those withoutl-NMMA. These data suggest that inhibition of tonic production of NO does not appear to alter dynamic cerebral autoregulation in humans.