Ogoh S, Dalsgaard M K, Secher N H, Raven P B
Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Acta Physiol (Oxf). 2007 Sep;191(1):3-14. doi: 10.1111/j.1748-1716.2007.01708.x. Epub 2007 May 17.
Cardiac failure and ischaemic heart disease patients receive standard of care cardiac beta(1)-adrenergic blockade medication. Such medication reduces cardiac output and cerebral blood flow. It is unknown whether the beta(1)-adrenergic blockade-induced reduction of cardiac output in the presence of an exercise-induced reduction in cardiac-arterial baroreflex gain affects cerebral blood flow variability. This study evaluated the influence of cardiac output variability on beat-to-beat middle cerebral artery mean blood velocity (MCA V(mean)) during exercise with and without cardiac beta(1)-adrenergic blockade.
Eight men (22 +/- 1 years; mean +/- SE) performed 15 min bouts of moderate (105 +/- 11 W) and heavy (162 +/- 8 W) intensity cycling before and after cardio-selective beta(1)-adrenergic blockade (0.15 mg kg(-1) metoprolol). The relationship between changes in cardiac output or mean arterial pressure (MAP) and MCA V(mean) as well as cardiac-arterial baroreflex gain were evaluated using transfer function analysis.
Both exercise intensities decreased the low frequency (LF) transfer function gain between cardiac output and MCA V(mean) (P < 0.05) with no significant influence of beta(1)-blockade. In contrast, the LF transfer function gain between MAP and MCA V(mean) remained stable also with no significant influence of metoprolol (P > 0.05). The LF transfer function gain between MAP and HR, an index of cardiac-arterial baroreflex gain, decreased from rest to heavy exercise with and without beta(1)-blockade (P < 0.05).
These findings suggest that the exercise intensity related reduction in cardiac-arterial baroreflex function at its operating point does not influence the dynamic control of MCA V(mean), even when the ability of exercise-induced increase in cardiac output is reduced by cardiac beta(1)-adrenergic blockade.
心力衰竭和缺血性心脏病患者接受标准治疗的心脏β1-肾上腺素能阻滞剂药物治疗。此类药物会降低心输出量和脑血流量。目前尚不清楚在运动引起心脏-动脉压力反射增益降低的情况下,β1-肾上腺素能阻滞剂引起的心输出量降低是否会影响脑血流变异性。本研究评估了在有和没有心脏β1-肾上腺素能阻滞剂的运动过程中,心输出量变异性对逐搏大脑中动脉平均血流速度(MCA V(mean))的影响。
八名男性(22±1岁;平均值±标准误)在进行心脏选择性β1-肾上腺素能阻滞剂(0.15 mg kg(-1)美托洛尔)治疗前后,分别进行15分钟的中度(105±11 W)和重度(162±8 W)强度的骑行运动。使用传递函数分析评估心输出量或平均动脉压(MAP)变化与MCA V(mean)以及心脏-动脉压力反射增益之间的关系。
两种运动强度均降低了心输出量与MCA V(mean)之间的低频(LF)传递函数增益(P<0.05),β1-阻滞剂对此无显著影响。相比之下,MAP与MCA V(mean)之间的LF传递函数增益也保持稳定,美托洛尔对此同样无显著影响(P>0.05)。MAP与HR之间的LF传递函数增益(心脏-动脉压力反射增益的指标)在有和没有β1-阻滞剂的情况下,从静息状态到剧烈运动均降低(P<0.05)。
这些发现表明,即使运动诱导的心输出量增加能力因心脏β1-肾上腺素能阻滞剂而降低,运动强度相关的心脏-动脉压力反射功能在其工作点的降低也不会影响MCA V(mean)的动态控制。