Abstract
After traumatic brain injury, extracellular K + in brain can dramatically increase. We studied the effects of increased K + on the isolated pressurized rat middle cerebral artery (MCA). MCAs (200–250 μm OD) were isolated, cannulated with glass micropipettes, and pressurized. K + was increased in the extraluminal bath using three paradigms: (1) isotonic K + (K iso) where increases in K + were offset by decreases in Na +, (2) hypertonic K + (K hyper) where K + was increased without a concomitant adjustment of Na +, and (3) K suc, a solution using K iso but with the addition of sucrose to obtain a hypertonic solution. Increases in K + in the extraluminal bath produced significant dilations (approximately 20%) at 21 mM K + in all three groups (K iso, K hyper, and K suc). With the K hyper and K suc groups, the magnitude of the dilation diminished with further increases in K +. l-NAME (10 −5 M), an inhibitor of nitric oxide synthase, had no effect on the response of the K hyper and K suc groups at 21 mM but significantly enhanced constrictions of the MCAs above 40 mM K + compared to the control. The K iso group was not affected by l-NAME at any K + concentration and showed profound constrictions above 40 mM K +. We conclude that changes in the K + concentration and osmolality of the extracellular fluid may have profound effects on the cerebral vasculature.
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