Secretagogue (Caerulein) induced pancreatitis in rodents

Acute pancreatitis is one of the most common diseases in gastroenterology. The incidence of acute pancreatitis per 100,000 population ranges from 10 to 46 per year. Two percent of all patients admitted to hospital are diagnosed with acute pancreatitis. Nevertheless even in the 21 century neither the etiology nor the pathophysiology of the disease are fully understood and causal treatment options are not available. This fact has prompted numerous researchers to study the initial triggering events of acute pancreatitis in order to develop new treatment strategies. Much of our current knowledge regarding the onset of pancreatitis was not gained from studies involving the human pancreas or patients with pancreatitis but from animal or isolated cell models. There are several reasons why these models have been used: 1) the pancreas is a rather inaccessible organ because of its anatomical location in the retroperitoneal space. Unlike the colon or stomach, biopsies of human pancreas are difficult to obtain for ethical and medical reasons. 2) Patients who are admitted to hospital with acute pancreatitis have usually passed through the initial stages of the disease where the triggering early events could have been studied. Particularly the autodigestive process that characterizes this disease has remained a significant impediment for investigations that address initiating pathophysiological events. Therefore, the pathophysiological trigger mechanisms have mostly been studied in animal models of the disease, before randomized placebo controlled trials to evaluate new therapeutic concepts in humans could be initiated. Experimental models are now irreplaceable tools in studying etiological factors, pathophysiology, new diagnostic tools as well as treatment options in acute pancreatitis. The advantages of animal models are the possibility to isolate specific aspects of a complex and varying disease course, the high degree of standardization and reproducibility, and the reduction of the required sample size eliminating variability in the study population.