The fastigial nucleus (FN) plays an important role in regulating cardiovascular, respiratory, and visceral activities. We investigated the effect and mechanism of FN stimulation (FNS) on the prevention of oxidative damage in wistar rats undergoing surgically induced acute myocardial infarction (AMI). The FN lesion (FNL) group was subjected to bilateral FN lesioning before the nucleus was electrically stimulated and AMI was induced. FN of AMI rats were electrically stimulated as the FNS and AMI group. Sham-stimulated and sham-operated rats were randomly selected in one group as control. We measured lactic dehydrogenase (LDH) and creatine phosphokinase (CK) activity, as well as myocardial infarction (MI) size. Malondialdehyde (MDA) content, total anti-oxidative capability (TAOC) and superoxide dismutese (SOD) activity in myocardium were also measured. FNS lowered the activities of LDH and CK in comparison to the AMI group. Infarct size was less in FNS-treated rats. The AMI group had elevated MDA levels compared with sham-treated animals. TAOC and SOD activities were decreased in the AMI group; there was attenuation of MDA and increases of TAOC and SOD activities in the FNS group (p<0.01). We conclude that FNS can reduce damage during MI. The mechanism of the protective effect might be partially related to its antioxidative role.
2008 by The Pharmaceutical Society of Japan