Compromised Cerebrovascular Regulation and Cerebral Oxygenation in Pulmonary Arterial Hypertension.
Compromised Cerebrovascular Regulation and Cerebral Oxygenation in Pulmonary Arterial Hypertension.
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DOI：
10.1161/jaha.117.006126
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发表时间：
2017-10-12
影响因子：
5.4
通讯作者：
Provencher S
中科院分区：
文献类型：
--
作者：
Malenfant S;Brassard P;Paquette M;Le Blanc O;Chouinard A;Nadeau V;Allan PD;Tzeng YC;Simard S;Bonnet S;Provencher S
功能脑血管调节机制对于维持健康个体的恒定脑血流和氧供应很重要，但在心力衰竭中发生改变。我们的目的是研究肺动脉高压（PAH）是否与脑血管调节异常和脑氧合降低有关，以及它们的生理和临床后果。大脑中动脉静息平均血流速度（MCAvmean）；对11名PAH患者和11名匹配的健康对照者进行了经颅多普勒（transcranial Doppler）、脑压-血流关系（在休息和蹲位-站立时评估；使用传递函数分析）、脑血管对二氧化碳的反应性和中枢化学反射的评估。两组都完成了渐进式斜坡运动方案，直到精疲力竭，在此期间测量了MCAvmean，平均动脉压，心输出量（光容积描记术），CO 2的潮末分压和脑氧合（近红外光谱）。患者的特点是静息时MCAvmean显著降低（P<0.01），静息时和蹲立时传递函数增益较高（P< 0.05）。PAH患者脑血管对CO2的反应性降低（P=0.03），而中枢化学受体敏感性升高（P<0.01），后者与运动时患者静息通气量增加（r2 =0.47， P<0.05）和运动时通气/CO2产生斜率（斜率；r2 =0.62， P<0.05）相关。运动诱导的MCAvmean升高在PAH中受到限制（P<0.05）。MCAvmean降低导致脑氧输送和脑氧合受损（均P<0.05），后者与PAH患者的运动能力相关（r2 =0.52； P=0.01）。这些发现为PAH脑血流动力学调节和氧合的生理和临床相关损伤提供了全面的证据。
Functional cerebrovascular regulatory mechanisms are important for maintaining constant cerebral blood flow and oxygen supply in heathy individuals and are altered in heart failure. We aim to examine whether pulmonary arterial hypertension (PAH) is associated with abnormal cerebrovascular regulation and lower cerebral oxygenation and their physiological and clinical consequences. Resting mean flow velocity in the middle cerebral artery mean flow velocity in the middle cerebral artery (MCAvmean); transcranial Doppler), cerebral pressure‐flow relationship (assessed at rest and during squat‐stand maneuvers; analyzed using transfer function analysis), cerebrovascular reactivity to CO 2, and central chemoreflex were assessed in 11 patients with PAH and 11 matched healthy controls. Both groups also completed an incremental ramp exercise protocol until exhaustion, during which MCAvmean, mean arterial pressure, cardiac output (photoplethysmography), end‐tidal partial pressure of CO 2, and cerebral oxygenation (near‐infrared spectroscopy) were measured. Patients were characterized by a significant decrease in resting MCAvmean (P<0.01) and higher transfer function gain at rest and during squat‐stand maneuvers (both P<0.05). Cerebrovascular reactivity to CO 2 was reduced (P=0.03), whereas central chemoreceptor sensitivity was increased in PAH (P<0.01), the latter correlating with increased resting ventilation (R 2=0.47; P<0.05) and the exercise ventilation/CO2 production slope ( slope; R 2=0.62; P<0.05) during exercise for patients. Exercise‐induced increases in MCAvmean were limited in PAH (P<0.05). Reduced MCAvmean contributed to impaired cerebral oxygen delivery and oxygenation (both P<0.05), the latter correlating with exercise capacity in patients with PAH (R 2=0.52; P=0.01). These findings provide comprehensive evidence for physiologically and clinically relevant impairments in cerebral hemodynamic regulation and oxygenation in PAH.