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首页> 外文期刊>American Journal of Physiology >Impaired cerebral CO2 vasoreactivity: association with endothelial dysfunction.
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Impaired cerebral CO2 vasoreactivity: association with endothelial dysfunction.

机译：脑CO2血管反应性受损：与内皮功能障碍有关。

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Conflicting data exist on the role of nitric oxide (NO) in cerebral blood flow (CBF) autoregulation. Previous studies involving human and animal subjects seem to indicate that NO involvement is limited to the CO(2)-dependent mechanism (chemoregulation) and not to the pressure-dependent autoregulation (mechanoregulation). We tested this hypothesis in patients with impaired endothelial function compared with healthy controls. Blood pressure, heart rate, end-tidal Pco(2), CBF velocities (CBFV), forearm blood flow, and reactive hyperemia were assessed in 16 patients with diabetes mellitus and/or hypertension and compared with 12 age- and sex-matched healthy controls. Pressure-dependent autoregulation was determined by escalating doses of phenylephrine. CO(2) vasoreactivity index was extrapolated from individual slopes of mean CBFV during normocapnia, hyperventilation, and CO(2) inhalation. Measurements were repeated after sodium nitroprusside infusion. Indexes of endothelial function, maximal and area under the curve (AUC) of forearm blood flow (FBF) changes, were significantly impaired in patients (maximal flow: 488 +/- 75 vs. 297 +/- 31%; P = 0.01, AUC DeltaFBF: 173 +/- 17 vs. 127 +/- 11; P = 0.03). Patients and controls showed similar changes in cerebrovascular resistance during blood pressure challenges (identical slopes). CO(2) vasoreactivity was impaired in patients compared with controls: 1.19 +/- 0.1 vs. 1.54 +/- 0.1 cm.s(-1).mmHg(-1); P = 0.04. NO donor (sodium nitroprusside) offsets this disparity. These results suggest that patients with endothelial dysfunction have impaired CO(2) vasoreactivity and preserved pressure-dependent autoregulation. This supports our hypothesis that NO is involved in CO(2)-dependent CBF regulation alone. CBFV chemoregulation could therefore be a surrogate of local cerebral endothelial function.
机译：关于一氧化氮（NO）在脑血流量（CBF）自动调节中的作用存在矛盾的数据。先前涉及人类和动物受试者的研究似乎表明，NO的参与仅限于CO（2）依赖性机制（化学调节），而不受压力依赖性自动调节（机械调节）的限制。与健康对照组相比，我们在内皮功能受损的患者中检验了这一假设。在16名糖尿病和/或高血压患者中评估了血压，心率，潮气末Pco（2），CBF速度（CBFV），前臂血流量和反应性充血，并与12名年龄和性别相匹配的健康人进行了比较控制。通过增加去氧肾上腺素的剂量来确定压力依赖性自动调节。 CO（2）血管反应性指数是从正常碳酸血症，换气过度和CO（2）吸入期间平均CBFV的各个斜率推断出来的。硝普钠输注后重复测量。患者的内皮功能指标，前臂血流量（FBF）变化的最大和曲线下面积（AUC）明显受损（最大血流量：488 +/- 75 vs. 297 +/- 31％; P = 0.01， AUC DeltaFBF：173 +/- 17与127 +/- 11; P = 0.03）。患者和对照组在血压挑战（相同的斜率）期间显示出类似的脑血管阻力变化。与对照组相比，患者的CO（2）血管反应性受损：1.19 +/- 0.1 vs. 1.54 +/- 0.1 cm.s（-1）.mmHg（-1）; P ＝ 0.04。没有供体（硝普钠）可以弥补这一差距。这些结果表明，具有内皮功能障碍的患者受损的CO（2）血管反应性和保存压力依赖性自动调节。这支持我们的假设，即NO仅参与CO（2）依赖性CBF调节。因此，CBFV化学调节可能是局部脑内皮功能的替代。

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