Does hypercapnia-induced impairment of cerebral autoregulation affect neurovascular coupling? A functional TCD study

• Published in: Journal of applied physiology (1985) 2013-08, Vol.115 (4), p.491-497
• Main Authors: Maggio, Paola, Salinet, Angela S M, Panerai, Ronney B, Robinson, Thompson G
• Format: Article
• Language: English
• Subjects: Aged; Blood; Blood Circulation Time; Blood Flow Velocity - physiology; Blood pressure; Blood Pressure - physiology; Carbon dioxide; Carbon Dioxide - metabolism; Cerebral Cortex - blood supply; Cerebral Cortex - metabolism; Cerebral Cortex - physiology; Cerebrovascular Circulation - physiology; Female; Heart Rate - physiology; Homeostasis - physiology; Humans; Hypercapnia - metabolism; Hypercapnia - physiopathology; Ischemia; Male; Mental depression; Middle Aged; Middle Cerebral Artery - metabolism; Middle Cerebral Artery - physiology; Stroke - physiopathology; Vascular Resistance - physiology
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00327.2013

Neurovascular coupling (NVC) and dynamic cerebral autoregulation (dCA) are both impaired in the acute phase of ischemic stroke, but their reciprocal interactions are difficult to predict. To clarify these aspects, the present study explored NVC in a healthy volunteer population during a surrogate state of impaired dCA induced by hypercapnia. This study aimed to test whether hypercapnia leads to a depression of NVC through an impairment of dCA. Continuous recordings of middle cerebral arteries cerebral blood flow velocity (CBFv), blood pressure (BP), heart rate, and end-tidal CO2 were performed in 19 right-handed subjects (aged >45 yr) before, during, and after 60 s of a passive paradigm during normocapnia and hypercapnia. The CBFv response was broken down into subcomponents describing the relative contributions of BP (VBP), critical closing pressure (VCrCP), and resistance area product (VRAP). VRAP reflects myogenic activity in response to BP changes, whereas VCrCP is more indicative of metabolic control. The results revealed that hypercapnia significantly affected NVC, with significant reductions in the relative contribution of VCrCP to the paradigm-induced increase in CBFv. The present study suggests that hypercapnia impairs both dCA and NVC, probably acting through an impairment of the metabolic component of CBF control.