Heine Martin, Subudhi Andrew W, Roach Robert C
Altitude Research Center, University of Colorado, Denver, CO, United States.
Respir Physiol Neurobiol. 2009 Apr 30;166(2):125-8. doi: 10.1016/j.resp.2009.02.013. Epub 2009 Mar 5.
We tested hypothesis that cerebral deoxygenation near maximal exercise intensity is mediated by hyperventilation, via hypocapnia-induced reductions in cerebral blood flow, by utilizing canonical correlation analysis (CCA) to determine the relative influence of cardiopulmonary changes on cerebral oxygenation, as assessed by near infrared spectroscopy (NIRS). Twenty-three subjects performed incremental exercise tests under normoxic and hypoxic conditions. Changes in ventilation (V (E)) were strongly correlated with end-tidal CO(2) (P(ET)(CO)(2)) and NIRS after the respiratory compensation point (RCP) (r(2)>0.97). However, in contrast to our expectations, CBF velocity (CBFv) shared the least amount of variance with NIRS measurements (r(2)<0.56) and the reduction in CBFv was not accompanied by a reduction in cerebral blood volume. These results demonstrate that while cerebral deoxygenation was associated with hyperventilation, it was not solely explained by hypocapnia-induced reductions in CBFv. CCA revealed that a relative increase in the venous contribution to NIRS explained a larger amount of variation in cerebral oxygenation than reductions CBFv.
我们通过利用典型相关分析(CCA)来确定心肺变化对脑氧合的相对影响(通过近红外光谱法(NIRS)评估),检验了以下假设:接近最大运动强度时的脑脱氧是由过度通气介导的,通过低碳酸血症引起的脑血流量减少来实现。23名受试者在常氧和低氧条件下进行递增运动测试。呼吸补偿点(RCP)后,通气变化(V(E))与呼气末二氧化碳(P(ET)(CO)(2))和NIRS密切相关(r(2)>0.97)。然而,与我们的预期相反,脑血流速度(CBFv)与NIRS测量值的方差共享量最少(r(2)<0.56),并且CBFv的降低并未伴随着脑血容量的减少。这些结果表明,虽然脑脱氧与过度通气有关,但它不能仅由低碳酸血症引起的CBFv降低来解释。CCA显示,静脉对NIRS贡献的相对增加比CBFv降低能解释更多的脑氧合变化。