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- W2109452102 abstract "Transmitter-gated ion channel opening may be less relevant for ischemic damage in cerebral white matter (WM) than in gray matter (GM). Rather, neuroactive substances [γ-aminobutyric acid (GABA), adenosine] have been discussed to ameliorate WM damage. In α-chloralose anesthetized cats, we studied simultaneously blood flow by hydrogen clearance, direct current (DC) potential, and multiple ion and transmitter alterations by ion-selective electrodes and microdialysis in GM and WM regions during 120 min of global ischemia. Arterial occlusion stopped blood flow in both regions. Changes in DC potential and extracellular sodium, potassium, and calcium concentrations ([Na+]o, [K+]o and [Ca2+]o) were immediate, the magnitude of change being smaller and the speed slower in WM. Most prominently, [Ca2+]o (preischemic controls ∼1.2 mM) immediately decreased in GM and reached ∼0.3 mM 10 min after occlusion, whereas in WM the [Ca2+]o first increased (∼1.6mM) and decreased only after about 30 min finally reaching ∼0.35 mM. Persistent GABA (and glutamate) increases were immediate in GM but delayed by about 60 min in WM. Adenosine increased transiently, peaking after ∼10 min in GM and after ∼30 min in WM. In conclusion, delayed and smaller shifts of ions and neuroactive substances may explain the longer-lasting ischemic tolerance of WM." @default.
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- W2109452102 date "2001-01-01" @default.
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- W2109452102 title "Pathophysiological Consequences of White Matter Compared to Gray Matter Ischemia" @default.
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- W2109452102 doi "https://doi.org/10.1007/978-4-431-67899-1_24" @default.
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