Cerebral vasoreactivity during hypercapnia is reset by augmented sympathetic influence

Area of Science:

• Neuroscience
• Cardiovascular Physiology
• Cerebrovascular Regulation

Background:

• Sympathetic nerve activity plays a role in regulating cerebral blood flow.
• The impact of heightened sympathetic activity on the brain's response to carbon dioxide (CO2) is not fully understood.
• Cerebral vasoreactivity, the ability of cerebral arteries to dilate or constrict in response to CO2 changes, is crucial for maintaining brain function.

Purpose of the Study:

• To investigate whether increased sympathetic nerve activity, induced by lower-body negative pressure (LBNP), impairs cerebral vasoreactivity to hypercapnia (elevated CO2 levels).
• To test the hypothesis that LBNP-stimulated sympathoexcitation restrains cerebral vasodilation during hypercapnia.

Main Methods:

• Nine healthy volunteers underwent rebreathing tests to induce controlled increases in partial pressure of end-tidal CO2 (Pet(CO2)).
• Cerebral hemodynamic responses were measured at rest and during -15 Torr LBNP using transcranial Doppler sonography for middle cerebral artery velocity (MCAV) and near-infrared spectroscopy for regional cerebral tissue oxygenation (ScO2).
• The sensitivity of cerebral vasoreactivity was assessed by the slopes of MCAV/Pet(CO2) and ScO2/Pet(CO2) relationships.

Main Results:

• Pet(CO2) levels were similarly increased during rebreathing at rest and during LBNP.
• The rate of increase in MCAV and ScO2 per unit increase in Pet(CO2) was significantly reduced during LBNP compared to rest.
• Specifically, the MCAV/Pet(CO2) slope decreased from 2.62 to 1.68 cm·s(-1)·mmHg(-1), and the ScO2/Pet(CO2) slope decreased from 0.89 to 0.63%/mmHg.

Conclusions:

• LBNP-induced sympathoexcitation significantly diminishes the brain's vasodilatory capacity in response to elevated CO2.
• The sensitivity of cerebral vasoreactivity to hypercapnia is impaired under conditions of augmented sympathetic nerve activity.
• These findings highlight a mechanism by which sympathetic activation can modulate cerebral blood flow regulation.