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Preparing a Mice Model of Severe Acute Pancreatitis via a Combination of Caerulein and Lipopolysaccharide Intraperitoneal Injection
Published on: May 10, 2024
The lethal toxicity of pancreatic ascites fluid in severe acute necrotizing pancreatitis
Maki Sugimoto1, Tadahiro Takada, Hideki Yasuda
1Department of Surgery, Teikyo University School of Medicine, Ichihara Hospital, 3426-3 Anesaki Ichihara, 299-0111 Chiba, Japan. sugimoto@med.teikyo-u.ac.jp
Background/Aims:
The pathogenesis and the molecular mechanisms of the development and progression of the acute pancreatitis (AP) are not clearly understood. Ascites fluid is known to be important in the clinical progression of AP. We present the lethal toxicity of human pancreatic ascites fluid for experimental pancreatitis, with the therapeutic course of severe necrotizing AP.
Methodology:
The material was in a 33-year-old male admitted with epigastric pain. An abdominal CT revealed that his pancreas was swollen and contained pancreatic fluid collection extending to the pelvic cavity. He had complicated acute renal failure, sepsis, and DIC, and received hemodialysis, and continuous arterial infusion therapy (CAI). The peripancreatic infection was acquired, and percutaneous interventional radiology (IVR) was performed for the abscess drainage. The drained liquid around the pancreas contained high molecular cytokines, protease, and bacterial contamination. To evaluate the toxicity of the ascites fluid, we gave it intraperitoneally to rats in which pancreatitis had been induced and rats that had undergone a sham operation; these rats died immediately. The consistent irrigation and drainage of the abscess was administered and the patient's general condition improved. At this time, we gave the drained material intraperitoneally to other rats with induced pancreatitis and sham operation, but all these rats survived.
Results:
These experimental results suggested that pancreatitis-associated ascites fluid contained a lethal toxicity. For curing this disease, elimination of these potential toxic mediators was essential. Our intensive IVR-based therapy improved the patient's prognosis.
Conclusions:
Downregulating this inflammatory process leads to a decrease in the mortality of severe acute pancreatitis.
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