抄録
We examined the role of nitric oxide (NO) in the development of muscle damage. A standardized eccentric stretch injury was created to the tibialis anterior (TA) muscle of 40 male Wistar rats (220 to 250 g), using a customized isokinetic test device and electrical stimulation. We evaluated the effects of the nitric oxide synthase inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAME; 85 mg/kg/day) on skeletal muscle damage and repair. The TA muscle was isolated immediately, 1, 3 and 7 days after muscle stretch injury. The animals were divided into two groups: (1) structural muscle damage, without L-NAME infusion (SMD/-L-NAME) (n=5 at each day); (2) structural muscle damage, with L-NAME infusion (SMD/+L-NAME) (n=5 at each day). NO content was greater in the SDM/-L-NAME group at all time points. Additionally, significant differences in NO content were observed on day 0 (p<0.05), and day 3 (p<0.05), SMD/+L-NAME vs. SMD/-L-NAME. The first day following injury, muscle protein degradation, as characterized by m-calpain mRNA levels and calpain activity, was increased in both groups. However, Myo-D and Myogenin mRNA levels were both increased at 3 days in the SMD/-L-NAME group. Our results demonstrate that NO influenced both muscle degradation and regeneration following structural damage in rat skeletal muscle. [Jpn J Physiol 54 Suppl:S118 (2004)]
