[The alteration of inflammatory cytokine during acute pancreatitis].

Objective: To observe the alteration of both inflammatory and anti-inflammatory cytokines during acute pancreatitis, and to investigate the effect of somatostatin on modulation of inflammatory and anti-inflammatory cytokines in experimental acute pancreatitis.

Methods: SD male rats were divided into 3 groups: group 1. the normal rats as control (n = 6); group 2, the rats with acute pancreatitis induced by transabdominal injection of 5% sodium cholate sulfur (at the volume of 1.0 ml/kg) into the parcreatic duct and not given drug treatment; group 3, the rats injected with stilamin 20 micrograms/kg, intravenously, 30 minutes after the successful induction of acute pancreatitis. The animals in groups 2 and 3 were killed at 2, 6 and 24 hours after operation. The blood samples were taken for measurement of IL-1, TNF alpha, IL-6 (by Bioassay) and IL-10, TNF-beta (by ELISA). The wet weight of pancreatic tissue and amylase were also determined.

Results: Serum IL-1, TNF alpha, IL-6, IL-10 and TGF-beta in control group were 0.56 +/- 0.06 ng/ml, 23.50 +/- 1.87 IU/ml, 69.0 +/- 6.40 IU/ml, 32.05 +/- 14.87 pg/ml and 66.4 +/- 13.20 pg/ml, respectively. After acute pancreatitis was induced, the serum level of these inflammation-concerned cytokines increased significantly in group 2 (P < 0.05). Serum IL-1, TNF alpha, IL-6, IL-10 and TGF-beta in group 2 at 24 hours after pancreatitis were 1.15 +/- 0.13 ng/ml, 55.33 +/- 12.79 IU/ml. 127.17 +/- 13.91 IU/ml, 68.13 +/- 19.90 pg/ml, and 103.77 +/- 28.95 pg/ml, respectively. After administration of somatostatin, the inflammation-concerned cytokines in group 3 were remarkably decreased (P < 0.05). Serum IL-1, TNF alpha, IL-6, IL-10 and TGF-beta in group 3 were 0.83 +/- 0.12 ng/ml, 33.00 +/- 7.40 IU/ml. 71.83 +/- 6.34 IU/ml, 42.2 +/- 14.55 pg/ml, and 45.98 +/- 18.10 pg/ml, respectively. The indeies of the severity of pancreatitis, such as amylase and the weight of pancreas alse improved in group 3.

Conclusion: Both inflammatory and antiinflammatory cytokines increased remarkably in the rats with acute pancreatitis. This result indicates that there is a potential tendency of inflammatory response syndrome and compensatory anti-inflammatory response syndrome in the course of acute pancreatitis. Somatostatin can modulate the derangement of these cytokines in acute pancreatitis.