Sympathetic regulation of the human cerebrovascular response to carbon dioxide.
Sympathetic regulation of the human cerebrovascular response to carbon dioxide.
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人脑血管对二氧化碳反应的交感调节。
DOI：
10.1152/japplphysiol.00614.2012
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发表时间：
2012
影响因子：
3.3
通讯作者：
Y. Tzeng
中科院分区：
文献类型：
--
作者：
K. Peebles;O. G. Ball;B. MacRae;H. Horsman;Y. Tzeng
虽然已知脑血管系统对CO(2)非常敏感，但交感神经系统是否在调节脑血管对动脉CO(2)变化的反应中起作用尚未达成共识。为了解决这个问题，我们调查了健康受试者的人脑血管CO(2)反应性，这些受试者被随机分配到α(1)-肾上腺素受体阻断组（9名受试者；口服哌唑嗪，0.05 mg/kg）或安慰剂对照组（9名受试者）。我们记录了5% CO(2)吸入和自愿过度通气时的平均动脉血压（MAP）、心率（HR）、平均大脑中动脉血流速度（MCA(V mean)）和末潮CO分压(Pet（CO(2)）。在将MAP作为协变量后，将CO(2)反应性量化为连续呼吸中呼吸间Pet（CO(2)）与平均MCAv（平均值）之间线性关系的斜率。哌唑嗪未改变静息HR、Pet（CO(2)）、MAP或MCA（V均值）。与安慰剂（-0.19±0.087 cm·s（-1）·mmHg(-1)）相比，哌唑嗪治疗后低碳一氧化碳(2)反应性的降低（-0.48±0.093 cm·s（-1）·mmHg(-1)）更大；交互作用P < 0.05)。相比之下，哌唑嗪（-0.23 cm·s（-1）·mmHg(-1)）后高碳一氧化碳(2)反应性的变化与安慰剂（-0.31 cm·s（-1）·mmHg(-1)）相似；相互作用P = 0.50)。这些数据表明，交感神经系统通过α(1)-肾上腺素受体参与CO(2)反应性；用哌唑嗪阻断这一途径可降低CO(2)对低碳酸血症的反应性，但不能降低高碳酸血症的反应性。
Although the cerebrovasculature is known to be exquisitely sensitive to CO(2), there is no consensus on whether the sympathetic nervous system plays a role in regulating cerebrovascular responses to changes in arterial CO(2). To address this question, we investigated human cerebrovascular CO(2) reactivity in healthy participants randomly assigned to the α(1)-adrenoreceptor blockade group (9 participants; oral prazosin, 0.05 mg/kg) or the placebo control (9 participants) group. We recorded mean arterial blood pressure (MAP), heart rate (HR), mean middle cerebral artery flow velocity (MCA(V mean)), and partial pressure of end-tidal CO(2) (Pet(CO(2))) during 5% CO(2) inhalation and voluntary hyperventilation. CO(2) reactivity was quantified as the slope of the linear relationship between breath-to-breath Pet(CO(2)) and the average MCAv(mean) within successive breathes after accounting for MAP as a covariate. Prazosin did not alter resting HR, Pet(CO(2)), MAP, or MCA(V mean). The reduction in hypocapnic CO(2) reactivity following prazosin (-0.48 ± 0.093 cm·s(-1) · mmHg(-1)) was greater compared with placebo (-0.19 ± 0.087 cm · s(-1) · mmHg(-1); P < 0.05 for interaction). In contrast, the change in hypercapnic CO(2) reactivity following prazosin (-0.23 cm · s(-1) · mmHg(-1)) was similar to placebo (-0.31 cm · s(-1) · mmHg(-1); P = 0.50 for interaction). These data indicate that the sympathetic nervous system contributes to CO(2) reactivity via α(1)-adrenoreceptors; blocking this pathway with prazosin reduces CO(2) reactivity to hypocapnia but not hypercapnia.
DOI：
10.1152/ajpheart.1999.276.5.h1691
发表时间：
1999-05-01
影响因子：
4.8
作者：
Rudas, L;Crossman, AA;Eckberg, DL
通讯作者：
Eckberg, DL