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 microm 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.
journal_name
Brain Resjournal_title
Brain researchauthors
Golding EM,Steenberg ML,Johnson TD,Bryan RM Jrdoi
10.1016/s0006-8993(00)02793-1subject
Has Abstractpub_date
2000-10-13 00:00:00pages
159-66issue
1-2eissn
0006-8993issn
1872-6240pii
S0006-8993(00)02793-1journal_volume
880pub_type
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