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. © 2001 Elsevier Science Ireland Ltd.
Von Arnim, C. A. F., Timmler, M., Ludolph, A. C., & Riepe, M. W. (2001). Chemical preconditioning in mice is not mediated by upregulation of nitric oxide synthase isoforms. Neuroscience Letters, 299(1–2), 130–134. https://doi.org/10.1016/S0304-3940(00)01762-6