Objective   To observe the role of IL-1β in regulating calcium sensitivity in superior mesenteric artery (SMA) by changing the PKC and Rho kinase activity in rabbits with endotoxic shock.    Methods  

Ninety-six adult rabbits were divided into endotoxic shock group (including normal control subgroup

and 30 min

1 h

2 h and 4 h LPS subgroups) and IL-1β group (including 0 ng/ml

  50 ng/ml

and 100 ng/ml IL-1β subgroups)

12 rabbits in each subgroup. Rabbits were given LPS at 1mg/kg (O

111

∶B

4

) via marginal ear vein to induce endotoxic shock. Before or 30 min

and 1

2

and 4 h after LPS was given

SMA was collected from rabbits for measuring PKC and Rho kinase activity

and their correlation to vascular calcium sensitivity was evaluated. Effects of IL-1β at different concentrations (0

50 and 100 ng/ml) on PKC and Rho kinase activity in SMA were observed

and their correlation to calcium sensitivity was evaluated.    Results   An endotoxic shock model was successfully established at 30 min-1 h after LPS was administrated. The PKC and Rho kinase activity in SMA was significantly higher in IL-1β group than in control group at 30 min-1 h after LPS was given and significantly lower in IL-1β group than in control group at 2 h and 4 h after LPS was given (P0.01). The changes of PKC and Rho kinase activity were positively correlated with the calcium sensitivity in SMA(r=0.912 and 0.968

P0.05). The PKC and Rho kinase activity in SMA in vitro was reduced much more in the 100 ng/ml IL-1β subgroup than in the 0 ng/ml IL-1β subgroup (P0.05). The changes of PKC and Rho kinase activity were positively correlated with the calcium sensitivity in SMA of the 0

50 and 100 ng/ml IL-1β subgroups(r=0.922 and 0.934

P0.05).     Conclusion    IL-1β may regulate the calcium sensitivity in SMA of rabbits with endotoxic shock by changing the PKC and Rho kinase activity.