Objective: To investigate the role of glutamine on splanchnic blood flow, apoptosis of pancreatic acinar and the underlying mechanism in rats with severe acute pancreatitis.
Methods: Forty-eight rats were randomized into two groups: the glutamine group (n = 24) and the severe acute pancreatitis group (n = 24). Jejunotomy was performed in all rats: the glutamine group also received glutamine, and the severe acute pancreatitis group received normal saline. Each group was then subdivided into three subgroups of eight rats each, with the rats be killed at 12, 24 and 36 h after the operation, respectively. A control group underwent sham operation (n = 8). The regional pancreatic microvascular blood flow was measured by Doppler ultrasound. The blood flow of the portal vein, splenic artery and superior mesenteric artery were also recorded. Apoptosis of pancreatic acinar cells was evaluated by TUNEL method.
Results: The regional pancreatic microvascular blood flow (KHz) decreased significantly in the severe acute pancreatitis group (P < 0.01), and continued to decrease after 24 h (vs. 12 h, P < 0.01). The blood flow of the portal vein, splenic artery and superior mesenteric artery also decreased in the severe acute pancreatitis group. The glutamine group showed increased regional pancreatic microvascular blood flows, as well as increased blood flow of the portal vein, splenic artery and superior mesenteric artery (vs. the severe acute pancreatitis group, P < 0.01). The apoptotic index of pancreatic acinar in the glutamine group was higher than in the severe acute pancreatitis group (P < 0.01), and both were much higher than that in the control group (P < 0.01).
Conclusions: Enteral administration of glutamine increased the splanchnic blood flow in severe acute pancreatitis rats. The apoptotic index of pancreatic acinar was negatively correlated with the severity of the disease. The interrelation between glutamine and apoptosis in severe acute pancreatitis is worthy of further investigation.