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.

Figure 1

Compartmentalized neurovascular coupling relationship. Neurovascular cells are grouped into three compartments: neurons (N), supporting cells that are potential transmission sites of vasoactive signals (T), and vascular cells (V). The vasoactive signals that are released accompanying neural processing are transferred to the vascular cells directly or indirectly via the supporting cells and help coordinate local cerebral blood flow (CBF) (F). A sequential relationship is depicted (A). Each transfer function represents cortical neural processing (f_n), vasoactive signal transmission (g_t), and vascular reactivity (h_v), which are functions of time (t) and space (r). Hemodynamic response, a final output of neurovascular function, is expressed by the convolution of these transfer functions. (B) Linear and nonlinear relationships have been observed between neural (f_n) and vascular (h_v) signal changes. However, their relationships to transmission function (g_t) remain uncertain.

Figure 2

Summary of the effects of anesthesia on neurovascular coupling. The effects of anesthetics involve systemic physiology (i), neural processing (ii), vasoactive signal transmission (iii), and vascular responses (iv). Depending on the type and dose of anesthetic, the anesthesia differentially modifies the individual transfer functions of neural processing (f'_n), vasoactive signal transmission (g'_t), and vascular reactivity (h'_v). CBF, cerebral blood flow.