C. O. Tan: Cardiovascular Research Laboratory, SW052, Spaulding Hospital Cambridge, Cambridge, MA 02138, USA.
J Physiol. 2013 Oct 15;591(20):5095-105. doi: 10.1113/jphysiol.2013.259747. Epub 2013 Aug 19.
Although myogenic mechanisms have been hypothesized to play a role in cerebrovascular regulation, previous data from both animals and humans have not provided an unequivocal answer. However, cerebral autoregulation is explicitly non-linear and most prior work relied on simple linear approaches for assessment, potentially missing important changes in autoregulatory characteristics. Therefore, we examined cerebral blood flow responses to augmented arterial pressure oscillations with and without calcium channel blockade (nicardipine) during blood pressure fluctuations (oscillatory lower body negative pressure, OLBNP) across a range of frequencies in 16 healthy subjects. Autoregulation was characterized via a robust non-linear method (projection pursuit regression, PPR). Blockade resulted in significant tachycardia, a modest but significant elevation in mean arterial pressure, and reductions in mean cerebral blood flow and end-tidal CO2 during OLBNP. The reductions in flow were directly related to the reductions in CO2 (r = 0.57). While linear cross-spectral analysis showed that the relationship between pressure-flow fluctuations was preserved after blockade, PPR showed that blockade significantly altered the non-linearity between pressure and flow, particularly at the slowest fluctuations. At 0.03 Hz, blockade reduced the range of pressure fluctuations that can be buffered (7.5 ± 1.0 vs. 3.7 ± 0.8 mmHg) while increasing the autoregulatory slope (0.10 ± 0.05 vs. 0.24 ± 0.08 cm s(-1) mmHg(-1)). Furthermore, the same rate of change in pressure elicited a change in flow more than twice as large as at baseline. Thus, our results show that myogenic mechanisms play a significant role in cerebrovascular regulation but this may not be appreciated without adequately characterizing the non-linearities inherent in cerebrovascular regulation.
虽然肌源性机制被假设在脑血管调节中发挥作用，但来自动物和人类的先前数据并没有给出明确的答案。然而，脑自动调节是明确的非线性的，大多数先前的工作依赖于简单的线性方法进行评估，可能会错过自动调节特征的重要变化。因此，我们在 16 名健康受试者中，在血压波动（振荡下体负压，OLBNP）期间，在一系列频率下检查了增强动脉压振荡时的脑血流反应，同时存在和不存在钙通道阻断（尼卡地平）。通过强大的非线性方法（投影寻踪回归，PPR）来描述自动调节。阻断导致显著的心动过速，平均动脉压适度但显著升高，OLBNP 期间平均脑血流和呼气末 CO2 减少。流量的减少与 CO2 的减少直接相关（r = 0.57）。虽然线性互谱分析表明阻断后压力-流量波动之间的关系保持不变，但 PPR 表明阻断显著改变了压力和流量之间的非线性，特别是在最慢的波动时。在 0.03 Hz 时，阻断降低了可以缓冲的压力波动范围（7.5 ± 1.0 对 3.7 ± 0.8 mmHg），同时增加了自动调节斜率（0.10 ± 0.05 对 0.24 ± 0.08 cm s(-1) mmHg(-1))。此外，相同的压力变化率引起的流量变化比基线时大两倍以上。因此，我们的结果表明，肌源性机制在脑血管调节中起着重要作用，但如果不能充分描述脑血管调节中固有的非线性，则可能无法理解这一点。
