Maryam Dastan

Infrasound, a low-frequency physical stimulus from environmental and anthropogenic sources, is assumed to impact microvascular regulation, though the mechanism is not fully understood. This study examines the effects of bipolar infrasound exposure (1 Hz, 100 dB) on the sublingual microcirculation in mice, with a single 4-hour exposure and repeated 4-hour daily exposures for 14 days. Control mice were placed in the same chamber without infrasound exposure. Using sidestream dark-field (SDF) videomicroscopy and laser Doppler flowmetry (LDF), we assessed microvascular diameter oscillations (vasomotion) and flow changes (flowmotion), respectively. A single exposure significantly increased vasomotion oscillation amplitude in the low-frequency band, while changes in the very-low- and high-frequency bands were not significant. Flowmotion measured by LDF significantly increased in the very-low-frequency band after a single exposure, while the other frequency bands remained unchanged. In contrast, repeated exposure significantly increased vasomotion oscillation amplitude within the very-low-, low-, and high-frequency bands, while LDF-derived flowmotion did not change significantly. The findings suggest that repeated exposure to infrasound may induce irregular microvascular oscillations, primarily affecting vessel diameter rather than overall perfusion, warranting further exploration into related mechanisms.

Infrasound, physically defined as sound at frequencies below 20 Hertz, can travel long distances with minimal attenuation and permeate biological tissues due to its marked particle displacement and deep penetration. Generated by both natural phenomena and human-made systems, infrasound has drawn increasing scientific and public attention regarding its potential physiological and psychological effects. Experimental studies demonstrate that infrasound can modulate mechanosensitive structures at the cellular level, particularly pressure-sensitive ion channels such as PIEZO1 and TRPV4, leading to intracellular calcium influx, oxidative stress, altered intercellular communication, and in some settings, apoptosis. These responses vary according to sound pressure levels, frequencies, exposure duration, and tissue type. In the cardiovascular system, higher sound pressures have been associated with mitochondrial injury and fibrosis, whereas low sound pressures may exert context-dependent protective effects. In animal models, prolonged or intense exposure to infrasound has been shown to induce neuroinflammatory responses and memory impairment. Short-term studies in humans at moderate intensities have reported minimal physiological changes, with psychological and contextual factors influencing symptom perception. Occupational environments such as factories and agricultural settings may contain elevated levels of infrasound, underscoring the importance of systematic measurements and exposure assessments. At the same time, controlled infrasound stimulation has shown potential as an adjunct modality in bone repair and tissue regeneration, highlighting its dual capacity as both a biological stressor and a possible therapeutic tool. Overall, existing data indicate that infrasound may be harmful at chronic exposure depending on intensity and frequency, yet beneficial when precisely regulated. Future research should standardize exposure metrics, refine measurement technologies, and clarify dose–response relationships to better define the health risks and therapeutic applications of infrasound.

Infrasound, physically defined as sound at frequencies below 20 Hertz, can travel long distances with minimal attenuation and permeate biological tissues due to its marked particle displacement and deep penetration. Generated by both natural phenomena and human-made systems, infrasound has drawn increasing scientific and public attention regarding its potential physiological and psychological effects. Experimental studies demonstrate that infrasound can modulate mechanosensitive structures at the cellular level, particularly pressure-sensitive ion channels such as PIEZO1 and TRPV4, leading to intracellular calcium influx, oxidative stress, altered intercellular communication, and in some settings, apoptosis. These responses vary according to sound pressure levels, frequencies, exposure duration and tissue type. In the cardiovascular system, higher sound pressures have been associated with mitochondrial injury and fibrosis, whereas low sound pressures may exert context-dependent protective effects. In animal models, prolonged or intense exposure to infrasound has been shown to induce neuroinflammatory responses and memory impairment. Short-term studies in humans at moderate intensities have reported minimal physiological changes, with psychological and contextual factors influencing symptom perception. Occupational environments such as factories and agricultural settings may contain elevated levels of infrasound, underscoring the importance of systematic measurements and exposure assessments. At the same time, controlled infrasound stimulation has shown potential as an adjunct modality in bone repair and tissue regeneration, highlighting its dual capacity as both a biological stressor and a possible therapeutic tool. Overall, existing data indicate that infrasound may be harmful at chronic exposure depending on intensity and frequency, yet beneficial when precisely regulated. Future research should standardize exposure metrics, refine measurement technologies, and clarify dose–response relationships to better define the health risks and therapeutic applications of infrasound.

Sepsis causes profound microcirculatory dysfunction, where heterogeneous capillary perfusion and abnormal vasomotion contribute to tissue hypoxia and organ failure. Sublingual videomicroscopy is established in large animals and humans to monitor these alterations, but this approach has not been applied in murine models. We developed a method to assess sublingual perfusion and vasomotion in mice using sidestream dark field (SDF) videomicroscopy. Male C57BL/6 mice were anesthetized, and sublingual vessels were imaged for 90 min. Perfusion and vasomotion parameters were assessed, and a Fast Fourier Transform was performed on vasomotion data to characterize the frequency components of rhythmic microvessel diameter changes. Another group of animals was administered lipopolysaccharide (LPS) intraperitoneally as a model of systemic inflammation in sepsis. LPS-treated mice exhibited a significant decline in the proportion of perfused vessels at 90 min and in the microvascular flow index. Very low-frequency vasomotion (0.005–0.15 Hz) declined in controls but was preserved during endotoxemia, suggesting an active microvascular tone response to inflammatory stress. This study establishes the first murine protocol for sublingual SDF imaging, allowing early detection of perfusion deficits and vasomotor changes in experimental sepsis. The minimal-invasive approach offers a translational platform for mechanistic and therapeutic studies in sepsis.

Sepsis causes profound microcirculatory dysfunction, where heterogeneous capillary perfusion and abnormal vasomotion contribute to tissue hypoxia and organ failure. Sublingual videomicroscopy is established in large animals and humans to monitor these alterations, but this approach has not been applied in murine models. We developed a method to assess sublingual perfusion and vasomotion in mice using sidestream dark field (SDF) videomicroscopy. Male C57BL/6 mice were anesthetized, and sublingual vessels were imaged for 90 minutes. Perfusion and vasomotion parameters were assessed, and a Fast Fourier Transform was performed on vasomotion data to characterize the frequency components of rhythmic microvessel diameter changes. Another group of animals was administered lipopolysaccharide (LPS) intraperitoneally as a model of systemic inflammation in sepsis. LPS-treated mice exhibited a significant decline in the proportion of perfused vessels at 90 minutes and in the microvascular flow index. Very low-frequency vasomotion (0.005–0.15 Hz) declined in controls but was preserved during endotoxemia, suggesting an active microvascular tone response to inflammatory stress. This study establishes the first murine protocol for sublingual SDF imaging, allowing early detection of perfusion deficits and vasomotor changes in experimental sepsis. The minimal-invasive approach offers a translational platform for mechanistic and therapeutic studies in sepsis.