Objective: To investigate the effects of cervical chordotomy on systemic inflammatory response and the outcome in rats with endotoxemia induced by lipopolysaccharide (LPS).
Methods: Ninety-two Sprague Dawley (SD) rats were randomly divided into three groups: normal control group (group I, n=8) , endotoxemia group (group II, n=42) and endotoxemia with cervical chordotomy (group III, n=42). Endotoxemia was induced by intra-peritoneal injection of LPS 10 mg/kg. In group III, "cervical chordotomy" was attained by transection of spinal cord at C7 immediately before intra-peritoneal LPS administration. Ten rats of group II and III each were observed for 48-hour survival. The other rats were further divided into four subgroups of 8 animals each, according to the time when the animals were sacrificed . The animals were sacrificed at 3, 6, 12, and 48 hours after intra-peritoneal LPS injection. Heart blood samples were obtained for determination of plasma concentration of norepinephrine [NE, by high performance liquid chromatography (HPLC)] and plasma concentration of interleukin-10 (IL-10) and IL-6 [by enzyme linked immunosorbent assay (ELISA)].
Results: Plasma NE concentration were significantly increased after intra-peritoneal LPS injection in group II and III as compared with group I and were significantly lower in group III than in group II starting from 6 hours after LPS (all P<0.05). Plasma IL-10 concentration was significantly lower at 3 hours and 6 hours while plasma IL-6 concentration was significantly higher after LPS challenge in group II than in group I at all time points (all P<0.05). High transection of spinal cord significantly elevated plasma IL-10 level at 12 hours and 48 hours, lowered IL-6 release at 3, 6, and 12 hours (all P<0.05), and improved 48-hour survival (20% vs. 70%) in group III as compared with group II.
Conclusion: Transection of spinal cord at C7 level can ameliorate the systemic inflammatory response induced by endotoxemia thus improving the outcome through elevation in IL-10 level, decreases in IL-6 release, and improves 48-hour survival. This might be attributable to loss of sympathetic nerve function.