Impaired cerebral CO2 vasoreactivity: association with endothelial dysfunction
Impaired cerebral CO2 vasoreactivity: association with endothelial dysfunction
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DOI：
10.1152/ajpheart.00014.2006
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发表时间：
2006-10-01
影响因子：
4.8
通讯作者：
Jacob, Giris
中科院分区：
文献类型：
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作者：
Lavi, Shahar;Gaitini, Diana;Jacob, Giris
关于一氧化氮(NO)在脑血流(CBF)自动调节中的作用，存在相互矛盾的数据。以前涉及人和动物的研究似乎表明，NO的参与仅限于二氧化碳依赖的机制(化学调节)，而不是压力依赖的自动调节(机械调节)。与健康对照组相比，我们在内皮功能受损的患者中测试了这一假说。对16例糖尿病和/或高血压患者的血压、心率、呼气末二氧化碳分压、脑血流速度(CBFV)、前臂血流量和反应性充血进行检测，并与12例年龄和性别匹配的健康对照组进行比较。压力依赖的自动调节是通过增加苯肾上腺素剂量来确定的。二氧化碳血管反应性指数是从正常二氧化碳、过度换气和吸入二氧化碳时平均CBFV的个体斜率推断出来的。硝普钠输注后重复测量。血管内皮功能指标，前臂血流(FBF)变化的最大值和曲线下面积(AUC)显著受损(最大血流量：488±/-75比297+/-31%；P=0.01；AUC Delta FBF：173+/-17比127+/-11；P=0.03)。患者和对照组在血压挑战期间脑血管阻力的变化相似(斜率相同)。二氧化碳血管反应性受损：1.19±-0.1vs.1.54+/-0.1 cm(.)S(-1)mm Hg(-1)，P=0.04。没有供体(硝普钠)可以抵消这种差异。这些结果表明，内皮功能障碍的患者二氧化碳血管反应性受损，并保留了压力依赖的自我调节。这支持了我们的假设，即NO单独参与了二氧化碳依赖的CBF调节。因此，CBFV化学调节可作为局部脑内皮细胞功能的替代。
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 CO2-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 PCO2, 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. CO2 vasoreactivity index was extrapolated from individual slopes of mean CBFV during normocapnia, hyperventilation, and CO2 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 Delta FBF: 173 +/- 17 vs. 127 +/- 11; P = 0.03). Patients and controls showed similar changes in cerebrovascular resistance during blood pressure challenges ( identical slopes). CO2 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 CO2 vasoreactivity and preserved pressure-dependent autoregulation. This supports our hypothesis that NO is involved in CO2-dependent CBF regulation alone. CBFV chemoregulation could therefore be a surrogate of local cerebral endothelial function.