Anesthesia and the Quantitative Evaluation of Neurovascular Coupling

Abstract

Anesthesia has broad actions that include changing neuronal excitability, vascular reactivity, and other baseline physiologies and eventually modifies the neurovascular coupling relationship. Here, we review the effects of anesthesia on the spatial propagation, temporal dynamics, and quantitative relationship between the neural and vascular responses to cortical stimulation. Previous studies have shown that the onset latency of evoked cerebral blood flow (CBF) changes is relatively consistent across anesthesia conditions compared with variations in the time-to-peak. This finding indicates that the mechanism of vasodilation onset is less dependent on anesthesia interference, while vasodilation dynamics are subject to this interference. The quantitative coupling relationship is largely influenced by the type and dosage of anesthesia, including the actions on neural processing, vasoactive signal transmission, and vascular reactivity. The effects of anesthesia on the spatial gap between the neural and vascular response regions are not fully understood and require further attention to elucidate the mechanism of vascular control of CBF supply to the underlying focal and surrounding neural activity. The in-depth understanding of the anesthesia actions on neurovascular elements allows for better decision-making regarding the anesthetics used in specific models for neurovascular experiments and may also help elucidate the signal source issues in hemodynamic-based neuroimaging techniques.

Model of the Transient Neurovascular Response Based on Prompt Arterial Dilation

“…This could be a consequence of anesthesia, which strongly dampens the HRF. 36,38 Also, we show here that stimulusevoked ringing has substantial site-to-site variations in frequency, so the ringing would be masked to spatially averaged measurements such as laser speckle or Doppler flowmetry. 31,39 Regardless, our model is also capable of fitting non-oscillatory flow responses using the overdamped form of the FEW impulse response.…”

A Critical Role for Purinergic Signalling in the Mechanisms Underlying Generation of BOLD fMRI Responses

“…Assuming ␣-chloralose has the same effect, it is possible that astrocytic calcium signaling is affected under the anesthetic conditions used in this study. While anesthesia is known to have an impact on the magnitude of the evoked BOLD responses (Franceschini et al, 2010;Masamoto and Kanno, 2012), neurovascular coupling has been found to be robustly maintained when ␣-chloralose is used to maintain general anesthesia (Ueki et al, 1992;Masamoto and Kanno, 2012). In the present study we demonstrate release of ATP (primary signaling molecule of astrocytes), BOLD fMRI responses and intact cerebrovascular responses to CO 2 in the somatosensory cortex of ␣-chloralose-anesthetized rats allowing study of the fundamental mechanisms underlying the role of astrocytes in the mechanisms of neurovascular coupling.…”

Mitochondrial Calcium Uptake Capacity Modulates Neocortical Excitability

“…36,37 Urethane, another widely used anesthetic, minimally affects cardiovascular, respiratory, and spinal reflexes, providing long-term stability and balanced actions on multiple neurotransmitter receptors. 38 Hence, a-chloralose or urethane was suitably used with urethane preferred for the relatively longer fLDI and fMRI experiments. As similar evoked potentials and neuronal-hemodynamic coupling exist between a-chloralose and urethane anesthesia, 39 there were no major anesthetic confounds affecting the results.…”