Betaxolol HCl

2 years -80 in solvent

Administered via i.p.

Dissociated rat cortical cells

2.5 mg/kg

6 uM [1], 6 uM [1], 6 uM [1], 6 uM [1], 6 uM [1], 6 uM [1]

When Betaxolol is injected i.p. into the rats before ischaemia and on the days of reperfusion the changes to the calretinin and ChAT immunoreactivities are reduced and the reduction of the b-wave is prevented. Inclusion of betaxolol partially prevents the changes caused by NMDA and lack of oxygen/glucose. [5]

Dissociated cortical cells from 16–18-day-old fetal rats are grown, in 35 mm dishes, in DMEM supplemented with L-glutamine (4 mM), glucose (6 g/L), penicillin (100 U/mL), streptomycin (100 ug/mL) and 10% hormonal supplemented medium consisting of transferrin (1 mg/mL), insulin (250 ug/mL) putrescine (600 uM), sodium selenite (0.3 uM), progesterone (0.2 uM) and estradiol (0.1 pM) for 7 days in an atmosphere of 5% CO2/95% O2 at 37 C. The cultures are then transferred to a culture medium which lacks the hormonal supplemented medium. L-glutamate is added to the medium and incubated for a further 4 hours under normoxic conditions. Betaxolol are added to the cultures at the same time as L-glutamate. In other experiments the cultures are subjected to anoxic conditions, 95% N2/5% CO2, for 5 hours at 37 C. Betaxolol is added prior to anoxia. Reoxygenation is then achieved by replacing the cells in normoxic conditions (95% O2/5% CO2) for 3 hours. Cellular injury is assessed by measuring lactate dehydrogenase (LDH) rease into the cell culture supernatant after hypoxia/reoxygenation or glutamate exposure. LDH activity is assayed spectrophotometrically by following NADH metabolism for 2 minutes at 340 nm.

Betaxolol (SL 75212) is a β1 adrenergic receptor blocker with IC50 of 6 μM.