The article by Vera-Portocarrero et al.  1in this issue of Anesthesiology titled “Nociception in persistent pancreatitis in rats: the effects of morphine and neuropeptide alterations” is of clinical interest due to the high prevalence of pancreatic pain. 2However, the presentation of yet another model of pain begs the question, do we need another animal model? I believe the resounding answer to this question should be “Yes!”

There are still numerous clinical scenarios for which we need improved treatments and the pain due to chronic pancreatitis is an excellent example of such a clinical entity. As a course of constant pain with intermittent flares, it has the additional complicating factor that approximately 50% of the subjects who develop it do so because of substance abuse. 2The pain of chronic pancreatitis can often be managed with narcotics, but often the patients can't. The clinician is frequently faced with scenario of a patient who has substituted one addiction (alcohol) for another (narcotics). This does not mean that narcotics are not appropriate and that the pain cannot be managed in this fashion, but this management is often difficult at best and most clinicians would like to have some other options to employ, hence the need for new models.

Models exist that are useful for investigating pain from multiple viscera, 3for example pain due to kidney stones or cystitis, but clinically, chronic pancreatitis does not act like a bladder infection or a kidney stone. As a consequence the extrapolation of pain from one site to another may be of limited value. It should not be expected that the mechanisms of pain generation arising from a structure such as the colon, which is filled with sewer contents, should be identical to structures such as the bladder or pancreas, which have sterile contents.

This does not mean that all pain models are worth the lives of the mice, rats, cats, dogs, monkeys, guinea pigs, and other nonhumans sacrificed to the development of these pain models. If one looks to the literature using the PubMed search engine of the National Library of Medicine and uses the search terms “pain” and “model,” one finds over 5,000 references describing pain models and the use thereof. Buried in these references are roughly 30 animal models that have ever been usefully employed in more than one laboratory. One can predict which models would prove to be of value as they typically have two features in common: one feature is technical simplicity, and the other feature is direct applicability to a clinical situation. The model put forth by Vera-Portocarrero et al.  1has both of these qualities. In their model, a simple intravenous injection of dibutyltin dichloride induces acute or subacute pancreatitis with increased lipase and amylase concentrations and histologic evidence of pancreatic inflammation. This pancreatitis produces “clinical” sensitivity to abdominal palpation and thermal stimuli, which are improved with traditional analgesics. One can argue over use of the term “persistent” in the title when the model is only studied in a 1- to 3-week timeframe. However, the authors have presented an excellent argument that the pain does arise from the pancreas, that the methods are technically simple, and that the findings are clinically relevant. There is hope that this group from Galveston and others will use this new model to test nontraditional methods of treatment, so that clinicians faced with the difficult task of treating pancreatic pain may have some novel tools to employ.

Vera-Portocarrero LP, Lu Y, Westlund KN: Nociception in persistent pancreatitis in rats: the effects of morphine and neuropeptide alterations. A nesthesiology 2002; 98: 474–84
Warshaw AL, Banks PA, Fernandez-Del Castillo C: AGA technical review: treatment of pain in chronic pancreatitis. Gastroenterology 1998; 115: 765–76
Ness TJ: Models of visceral nociception. ILAR Journal 1999; 40: 119–28