Subarachnoid Hemorrhage, Spreading Depolarizations and Impaired Neurovascular Coupling

Figure 3

Schematic model liking SAH to inversion of neurovascular coupling. In control animals, EFS causes elevated cytoplasmic Ca²⁺ in astrocytes leading to increased BK channel activity and modest (<20 mM) increases in perivascular K⁺, promoting vasodilation. SAH increases the magnitude of spontaneous astrocytic Ca²⁺ oscillations and basal activity of BK channels, elevating K⁺ in restricted perivascular space. The summation of increased basal perivascular K⁺ and “normal” nerve-evoked astrocyte BK channel activity results in extracellular K⁺ concentrations that exceed the dilation-constriction threshold (~20 mM), inducing vasoconstriction. BK: large conductance Ca²⁺-activated K⁺ channel, CBF: cerebral blood flow, EFS: electrical field stimulation, Glu: glutamate, K_ir: inward rectifier K⁺ channel, mGluR: metabotropic glutamate receptor, VDCC: voltage-dependent Ca²⁺ channel (modified from Koide et al. [21]).