Table 1.
Physiological and pharmacological modulators of the cerebral hemodynamic response to spreading depression
| Hemodynamic Component | Augmented By | Attenuated By |
|---|---|---|
| Initial hypoperfusion/constriction (component I) | Elevated [K+]o | Preceding SD |
| Reduced NO availability | ||
| Voltage-gated Na+ channel inhibition | ||
| High resting CBF | ||
| Hypotension | ||
| Peak hyperemia/dilation (component II) | 5-HT1D/1B activation | CGRP inhibition |
| KATP inhibition | NO inhibition | |
| Voltage-gated Na+ channel inhibition | Muscarinic inhibition | |
| Adenosine A1 receptor inhibition | 5-HT2A/2C inhibition | |
| Cyclooxygenase inhibition | Sensory perivascular nerve inhibition | |
| Lipoxygenase inhibition | Parasympathetic perivascular nerve inhibition | |
| mPTP inhibition | Hypotension | |
| Low resting CBF | ||
| Hyperglycemia | ||
| Post-SD oligemia/constriction (component IV) | Voltage-gated Na+ channel inhibition | 20-HETE inhibition |
| Hyperglycemia | Cyclooxygenase inhibition | |
| L-type Ca2+ channel inhibition | ||
| NO activation | ||
| Preceding SD | ||
| mPTP inhibition | ||
| Calcineurin inhibition |
SD, spreading depression; [K+]o, extracellular K+ concentration; CBF, cerebral blood flow; NO, nitric oxide; CGRP, calcitonin gene-related peptide; mPTP, mitochondrial permeability transition pore; 5-HT, serotonin.