Chemical preconditioning in mice is not mediated by upregulation of nitric oxide synthase isoforms

Ischemic preconditioning requires increased nitric oxide (NO) production. However, NO may also trigger delayed neuronal death cascades. The goal therefore was to investigate nitric oxide synthase (NOS) isoforms (neuronal NOS: nNOS; endothelial NOS: eNOS; inducible NOS: iNOS) with reverse transcriptase-polymerase chain reaction in hippocampal slices from control mice and slices prepared upon preconditioning in vivo (single intraperitoneal injection of 20 mg/kg body weight 3-nitropropionate (3NP)). One hour after preconditioning nNOS (108+/-34%, mean+/-SD), eNOS (93+/-34%), and iNOS (282+/-261%) remained at control levels. Similarly, nNos, eNOS, and iNOS stayed at control level 12, 24, and 72 h after preconditioning with 3NP. Incubation of slices, however, drastically increased iNOS (1676+/-818, P<0.01). We conclude that chemical preconditioning other than ischemic preconditioning may not increase potentially harmful nitric oxide synthase isoforms.