【Abstract】Objective To study the change of pancreatic microcirculation in the early phase of acute pancreatitis. MethodsLiteratures on acute pancreatitis and microcirculation were collected and reviewed.ResultsPancreatic microcirculation has changed in the early phase of acute pancreatitis, including contraction of interlobular arteriole, slowing of blood fluid, increasing of pancreatic vascular permeability, leukocyte adherence in postcapillary venules, and decreasing of pancreatic perfusion.Conclusion Impairment of pancreatic microcirculation in the early phase of acute pancreatitis may play a key role in the progression of this disease.
Objective To observe the blood circulation compensation in the involved area of the liver following ligation of the third grade branches of hepatic artery and portal vein and bile duct enclosed in Glisson’s capsule. Methods Ligation of the third grade branches of these ducts was carried out in 7 pigs. Uptake of 99mTc-EHIDA in the liver was scanned with SPECT pre-and post-operatively. Liver angiography of hepatic artery and portal vein were taken at regular interval. Corrosion casts of these ducts were made with ABS following extirpation of the liver at the end of experiment. The histological specimens were examined with electronic microscope. Results Compensatory circulation occurred between involved and noninvolved part of the liver through the sinusoids in 30-60 minutes after ligation. In the 6 weeks following the procedure, there was also blood supply in the affected region of liver, and collateral developed through hepatic aterioles and capillaries. Conclusion Liver has an ability to establish compensatory blood supply on the condition of ischema in a local region of liver.
ObjectiveTo establish a mouse model of acute necrotizing pancreatitis.MethodsThirty-six male ICR mice were randomly divided into control group (n=6) and experimental group (n=30). Each of the animals in the experimental group received 7 intraperitoneal injections of caerulein (50 μg/kg body weight) in 0.9% NaCl at hourly intervals over 6 hours. The animals in the experimental group were killed at 9,18,24,48 and 72 hours respectively after the first caerulein injection. The control animals received the same volume of 0.9% NaCl without caerulein. The animals in the control group were killed at the 18th hour after the first intraperitoneal injection. The severity of acute necrotizing pancreatitis was evaluated in terms of amylase level, pancreatic weight/body weight and the histological changes. Variance analysis was employed in the processing of these data. ResultsBoth amylase level and pancreatic weight elevated 9 hours after the first caerulein injection, and correlated with the course of pancreatitis. The maximums of both alterations were observed at the same time point (18 hours after the first injection of caerulein). Prominent interstitial inflammation and acinar cell necrosis occurred at the 18th hour, and the histological score for pancreatitis reached a maximum （P＜0.05）. Conclusion Intraperitoneal injection of a large dosage of caerulein can induce acute necrotizing pancreatitis in ICR mice. This method is simple and noninvasive, and the model established thus is stable and reproducible.