Cerebral autoregulation in humans: role of the myogenic mechanism

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Myogenic mechanisms have been hypothesized to account in part for cerebral autoregulation. Previous work in rats and more recent work in humans provide equivocal results. The animal data suggests that myogenic mechanisms are active at frequencies below 0.1 Hz. In contrast, the human data suggests that myogenic mechanisms are less important at these frequencies, but this was assessed using lower body negative pressure at levels beyond the threshold for syncope. Therefore, we examined cerebral blood flow responses to augmented arterial pressure oscillations with and without Ca2+ channel blockade (nicardipine) across a range of frequencies (0.03, 0.04, 0.05, 0.06, 0.07, and 0.08 Hz) and with levels of oscillatory lower body negative pressure (OLBNP) well below the threshold for syncope in humans (30 mmHg) in 16 healthy subjects. Ca2+ channel blockade resulted in an increase in mean pressure and heart rate, but decreased cerebral flow. Despite these hemodynamic changes, the transfer function relationship between flow and pressure was not significantly altered (Coherence: 0.514±0.077 vs. 0.512±0.077, Gain: 0.1740±0.0756 versus 0.2341±0.0287 at 0.03 Hz). Our data demonstrate that although myogenic mechanisms may have some role in determining tonic cerebral flow, they have no clear involvement in cerebral autoregulatory blood flow control in humans.