Ultrafast venous and sagittal sinus constrictions in the brain driven by abdominal pressure.

Nearly all the blood supplying the cortex exits via the bridging veins (BVs) that drain into the superior sagittal sinus (SSS), making these vessels key chokepoints for cerebral blood flow. Using optical imaging in head-fixed mice, we found that the SSS, BVs, and some other pial veins exhibit ultrafast constrictions (<0.1 s) at the onset of locomotion, following whisker stimulation, and upon awakening from sleep. Constrictions of the BVs and the SSS were strongly correlated with abdominal muscle electromyography activity and were tightly correlated with respiration at rest. The rapid decrease in blood volume caused by venous constrictions resulted in spurious increases in fluorescence in mice expressing fluorescent reporter proteins, creating artifacts that could mimic functional signals. Venous constrictions with the same amplitude and dynamics could be generated in anesthetized mice by abdominal pressure application, showing that these constrictions were generated by mechanical coupling with the abdomen. Externally imposed abdominal pressures also drove a rapid but transient increase in blood flow. Unlike the pial and parenchymal microvasculature whose diameters are largely controlled by local signals, the diameters of SSS/BVs are dynamically controlled during behavior in part by abdominal muscle regulation of intracranial pressure, establishing a pathway for regulation of cerebral hemodynamics via mechanical coupling between the central nervous system and the viscera.