The Cellular and Biophysical Origins of Microvascular Vasomotion: A Scoping Review.

内容摘要

Microvascular vasomotion involves spontaneous rhythmic changes in arteriolar diameter that contribute to local perfusion and oxygen delivery. Although this phenomenon has long been recognized, the mechanisms underlying the initiation and coordination of these oscillations remain incompletely defined. A focused synthesis of recent mechanistic studies helps to better elucidate how vasomotion is initiated and regulated across vascular beds. Our objective was to review and integrate current evidence on the cellular, molecular, and biophysical mechanisms underlying microvascular vasomotion, with a focus on intrinsic smooth muscle oscillatory behavior and the factors that influence its expression. A scoping review was conducted using Web of Science, PubMed, Embase, and Ovid MEDLINE. English language studies published from 2005 onward were considered, and earlier foundational reports were included when directly relevant to mechanistic interpretation. Experimental, clinical, and modeling studies addressing the origins or regulation of vasomotion in microvessels were eligible. From 958 retrieved records, duplicates were removed, and titles and abstracts were screened. Full-text assessment identified 30 studies for inclusion in the data synthesis. Considering a range of experimental models and vascular regions, the results suggested a common mechanistic theme. Oscillatory intracellular calcium activity within arteriolar smooth muscle cells was most consistently associated with the generation of vasomotor rhythms and periodic shifts in vascular tone. Electrophysiologic studies indicated that membrane potential behavior, ion channel function, and intercellular coupling were important in determining the timing and coordination of these oscillations. Signals arising from endothelial and astrocytic pathways were repeatedly shown to modulate oscillation amplitude and regional responsiveness, whereas neural and sympathetic inputs altered oscillatory strength in response to changing physiological demands. Mechanical influences, including shear forces and network geometry, contributed to the organization and propagation of oscillations through the microvascular network. Under hypoxic or ischemic stress, vasomotor activity often intensified, and altered patterns were described in conditions such as peripheral arterial disease and cerebrovascular dysfunction. It is concluded that the existing evidence supports a model in which microvascular vasomotion originates primarily from intrinsic oscillatory behavior of arteriolar smooth muscle cells, with endothelial, neural, metabolic, and mechanical factors shaping amplitude, synchronization, and spatial expression. The variability in study design, measurement approaches, and frequency band definitions remains a challenge to cross-study comparison. Future investigations that incorporate standardized analytical methods and in vivo approaches to link cellular oscillations to network-level flow dynamics may help clarify the physiological and clinical significance of vasomotion.