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Fundamental Change in Neurovascular Coupling after Subarachnoid Hemorrhage
Author(s) -
Koide Masayo,
Bonev Adrian D,
Nelson Mark T,
Wellman George C
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1021.9
Subject(s) - constriction , medicine , subarachnoid hemorrhage , vasodilation , neurovascular bundle , parenchyma , anatomy , cardiology , anesthesia , pathology
Subarachnoid hemorrhage (SAH) following cerebral aneurysm rupture is associated with substantial morbidity and mortality against which existing therapeutic options have limited efficacy. The impact of SAH on neurovascular coupling, reflecting the coordinated communication between neurons, astrocytes and parenchymal arterioles, is unknown. Using a combination of two‐photon and infrared‐differential interference contrast microscopy, arteriolar diameter and astrocyte endfoot Ca 2+ were simultaneously measured in brain slices from un‐operated, sham‐operated and SAH model of rats. Increased neuronal activity caused by electrical field stimulation (EFS) elicited the predicted elevation in endfoot Ca 2+ and vasodilation in brain slices from control animals (Filosa JA et al , 2006). EFS induced a similar increase in endfoot Ca 2+ , but in marked contrast caused parenchymal arteriolar constriction in brain slices from SAH model animals. Further, elevating endfoot Ca 2+ via two‐photon photolysis of caged Ca 2+ in the range of 200–500 nM caused parenchymal arteriolar dilation in brain slices from control animals and constriction in brain slices from SAH animals. These data demonstrate that SAH causes a fundamental switch from vasodilation to constriction in response to moderate increases in astrocyte endfoot Ca 2+ . (Supported by NIH P01 HL095488, R01 HL078983, R01 HL44455, & Totman Medical Research Trust).