Acute protective effect of nimodipine and dimethyl sulfoxide against hypoxic and ischemic damage in brain slices

Nimodipine and dimethyl sulfoxide (DMSO) were tested (alone and in combinat ion) regarding their ability to increase hypoxic tolerance of brain slices under 'hypoxic' (deprivation of oxygen) or 'ischemic' (hypoxia+withdrawal o f glucose) conditions. Direct current (DC) and evoked potentials were recor ded in the CAI region cf hippocampal slices of adult guinea pigs. After ind uction of hypoxia or ischemia, the latency of anoxic terminal negativity (A TN) of the DC potential was determined during superfusion with artificial c erebrospinal fluid alone (aCSF), and during superfusion with aCSF containin g DMSO [0.1% (14.1 mmol/l) and 0.4% (56.3 mmol/l)] with the addition of nim odipine (40 mu mol/l). Latencies of ATN with first hypoxia were 6.7+/-3.7 m in in the control group, 9.3+/-4.2 min in the 0.4% DMSO group and 12.3+/-5. 5 min (P=0.007) in the nimodipine/0.4% DMSO group. Latencies of ATN with fi rst ischemia were 2.9+/-2 min in the control group, 4.1+/-1.6 min in the 0. 1% DMSO group, 7.1+/-3.9 min in the 0.4% DMSO group (P=0.006), 5.3+/-1.5 mi n in the nimodipine/0.1% DMSO group and 7.6+/-3 ruin (P<0.001) in the nimod ipine/0.4% DMSO group. DMSO (0.4%), either alone or in combination with nim odipine, increase the latency of the ATN after acute onset of hypoxia and i schemia. (C) 2000 Elsevier Science B.V. All rights reserved.