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Effect of hemoglobin on sympathetic neurovascular transmission in the porcine cerebral circulation.

Subarachnoid hemorrhage (SAH) exposes the adventitia of the cerebral blood vessels to erythrocytes which lyse to release hemoglobin (Hb). Both SAH and Hb have been demonstrated to deplete adrenergic innervation and alter neurogenic responses in these vessels. We examined the effect of Hb on sympathetic adrenergic transmission in isolated pig cerebral arteries. The results indicate that Hb blocks neuronal [3H]norepinephrine ([3H]NE) uptake into anterior cerebral, internal carotid, and middle cerebral arteries in a dose-dependent manner. Gel-filtration experiments suggest that the mechanism underlying the [3H]NE uptake blockade involves binding of NE to Hb, rather than a specific blockade of the uptake pump. Although Hb blocked [3H]NE uptake, it did not influence electrically stimulated, tetrodotoxin (TTX)-sensitive [3H]NE release from cerebral arteries. These findings indicate that the presence of Hb in the subarachnoid space may alter cerebrovascular sympathetic transmission by preventing NE uptake. The altered neurogenic responses observed in the presence of Hb may be influenced by the affinity of NE for this protein but also may involve release of a substance other than NE from the sympathetic terminals.