Subarachnoid blood converts neurally evoked vasodilation to vasoconstriction in rat brain cortex.

The matching of blood flow to regional brain function, called functional hyperemia or neurovascular coupling, involves the coordinated activity of neurons, astrocytes, and parenchymal arterioles. Under physiological conditions, localized neuronal activation leads to elevated astrocyte endfoot Ca(2+) and vasodilation, resulting in an increase in cerebral blood flow. In this study, we examined the impact of subarachnoid hemorrhage (SAH) on neurovascular coupling. SAH model rats received two injections of autologous blood into the cisterna magna 24 h apart. Cortical brain slices from SAH model animals were prepared 4 days after the initial blood injection. Arteriolar diameter and astrocyte endfoot Ca(2+) were simultaneously measured using two-photon microscopy. As expected, neuronal activity evoked by electrical field stimulation (EFS) caused an elevation in endfoot Ca(2+) and vasodilation in brain slices from control animals. However, in brain slices from SAH animals, EFS induced a similar increase in astrocyte endfoot Ca(2+) that caused arteriolar constriction rather than vasodilation. Vasoconstriction was observed in approximately 90% of brain slices from SAH animals in response to EFS, with 40% exhibiting a sustained vasoconstriction, 30% exhibiting a transient vasoconstriction -(diameter restored within 1 min after EFS), and 20% responded with a biphasic response (brief vasodilation followed by -vasoconstriction). This inversion of neurovascular coupling may play a role in the development of neurological deficits following SAH.