The authors describe a reverse end-to-side neurorrhaphy model in which the proximal end of a donor nerve is sutured to an epineurial window in the side of a recipient nerve. If effective, this technique would have useful applications in nerve reconstructive surgery. Female Sprague-Dawley rats were divided into three groups (n = 9). In Group A, the peroneal nerve was transected and directly repaired in standard end-to-end fashion. In Group B, the tibial nerve was transected and the proximal end was sutured to the side of the intact peroneal nerve through an epineurial window. In Group C, the tibial nerve was also transected and the proximal end sutured to the side of the intact peroneal nerve, but the peroneal nerve was then cut proximally. After 12 weeks, contractile forces of the extensor digitorum communis (EDC) were measured, following stimulation of the proximal sciatic nerve on all experimental (and normal) hind limbs. For Group B, the peroneal nerve was transected proximal to the repair site just prior to stimulation. Group B animals did not demonstrate any measurable contractions. No statistically significant differences were found between Groups A and C. This demonstrated the successful neurotization of a denervated muscle using a reverse end-to-side neurorrhaphy model.

No abstract

This study examined the effects of 1400W, an inhibitor of inducible nitric oxide (iNOS), on contractile function and iNOS expression in reperfused skeletal muscle. The right extensor digitorum longus (EDL) muscle of 104 rats underwent a sham operation or 3-h ischemia followed by 3-h or 24-h reperfusion (I/R). Rats received 3 mg/kg 1400W, 10 mg/kg 1400W, or water subcutaneously. Results showed that EDL contractile function in both 1400W-treated groups significantly outperformed the controls at 24-h but not at 3-h reperfusion. Although iNOS expression increased in all three I/R groups during reperfusion, a significantly smaller increase was found in 1400W-treated muscles after 3-h reperfusion, and more dramatically so after 24-h reperfusion. Our results indicate that inhibition of iNOS preserved the contractile function in reperfused skeletal muscle, perhaps via downregulating iNOS expression. Protection by 1400W at 24-h reperfusion suggests that the role of iNOS in exaggerating reperfusion injury is more prominent in the later stages of injury.

This study investigated the effects of inhibition of NF-kappaB activation on microcirculation and inducible NOS expression in reperfused rat cremaster muscle. The muscle from 16 rats underwent 5-h ischemia and 90-min reperfusion. Each rat received NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC, 150 mg/kg) or phosphate-buffered saline 15 min before reperfusion. Results showed that PDTC treatment had a significant overall increase in muscle blood flow during reperfusion. Blood flow more rapidly recovered to and over baseline in the PDTC-treated group than in controls, with a significant difference at 10-30 min and 70-90 min. Expression of iNOS mRNA had a 167-fold increase from normal in controls, but was significantly (P < 0.05) reduced to a 63-fold increase in PDTC-treated muscles. In addition, PDTC treatment significantly (P < 0.05) decreased a reperfusion-induced increase in activated NF-kappaB p65 and nuclear p65 protein. Our results suggest that NF-kappaB is involved in I/R injury and that inhibition of NF-kappaB p65 activation affords protection against I/R injury, perhaps via downregulating expression of iNOS transcription.