Surgical Science, 2010, 1, 31-39
doi:10.4236/ss.2010.12007 Published Online October 2010 (
Copyright © 2010 SciRes. SS
Basic Experimental Pancreatitis Models for Beginners
Baris D. Yildiz1, Erhan Hamaloglu2
1Ankara Numune Teaching Hospital 6th General Surgery, Ankara,Turkey
2Hacettepe University Faculty of Medicine General Surgery Department, Sihhiye, Turkey
Received July 6, 2010; revised August 3, 2010; accepted August 10, 2010
Efforts to find an ideal model for pancreatitis date back to 1960’s. Many models are suggested since then.
Every model has its own advantages and disadvantages. Some of these models test etiology while others
simulate the complications of pancreatitis. An ideal model which by itself demonstrates all aspects of pan-
creatitis including systemic changes is yet to be described. In this review we tried to gather the basic, easy to
construct models.
Keywords: Pancreatitis, Experimental Models, Closed Duodenal Loop, Arginine Induced, Ex Vivo Perfusion
Model, Duct Obstruction, Taurocholate Injection, Vascular Induced
1. Introduction
Acute pancreatitis (AP) is inflammation of pancreatic
tissue which can present in a wide spectrum ranging
from edema of the organ to necrosis and hemorrhage.
Acute pancreatitis is a multi-etiology disease with con-
troversial physiopathology. Thus, it has an unpredictable
course without a targeted treatment [1] which results in
high morbidity and mortality.
In the clinical setting gallstone obstruction is the most
common cause (30%-50%) of AP. Alcoholism is the
second most common cause and recurrent alcoholic AP
leads to chronic pancreatitis. Infection, autoimmune re-
sponse, trauma, hyperlipidemia, hyperparathyroidism
account for nearly 10% of AP cases [2].
There are many experimental studies which try to ide-
ntify the pathogenesis and treatment options for pan-
creatitis. In this review we tried to evaluate the differ-
ences between models and the particular methodologies
of each experimental model with outline of evolution of
each technique.
2. Closed Duodenal Loop (CDL) Induced
In physiological conditions there is a pressure difference
between pancreatic duct (PD), sphincter of Oddi and
duodenum. This prevents duodenopancreatic reflux.
CDL, by violating this normal state, increases intraduo-
denal luminal pressure causing reflux of duodenal fluid
to PD causing pancreatitis. Closed loop is constructed
with duodenum surrounding the opening of the PD.
This model was first described by Seidel and popular-
ized later by Pfeffer [1]. The first species used were dogs
but rats were used later on. In dogs, duodenum is re-
sected distal to pylorus and opening of PD then double
layer sutured. The continuity of the gastrointestinal tract
is maintained by gastrojejunostomy and common bile
duct is obliterated with sutures [3].
Mc Cutcheon and Race injected barium sulphate in to
the loop and retrieved it inside the PD intraoperatively
[4]. The same authors after severing the mucosal valvu-
lae of Oddi found that under physiologic intraduodenal
pressures reflux into PD occured [5]. In this model if PD
is sutured pancreas atrophies. Byme and Joison’s modi-
fication enables easy suturing of distended PD after in-
jection of secretin [6].
Contributions to this method were made by Chetty et al.
via either filling the duodenum with Proteus and E coli
infected human bile [2] or filling duodenum with auto-
claved human bile [7].
This model also explains the hyperamylasemia and
duodenopancreatic reflux in afferent loop obstruction
after Billroth 2 gastrectomy [8].
The histopathological changes in pancreas after this
method are studied in detail by Rao et al.
Mild to moderate pancreatitis is seen in six hours and
hemorrhagic pancreatitis becomes widespread after 18
hours. Although changes similar to human pancreatitis is
encountered, this could also be the result of systemic
Copyright © 2010 SciRes. SS
response to duodenal surgery [9].
Dickson et al. assessed the applicability of CDL on
humans [7]. Their criticism was as follows:
- Generally mild pancreatitis occurs
- Infected duodenal fluid flows into PD and causes
bacterial infiltration of pancreas while this is not the
usual case in human pancreatitis
- Transmural duodenal necrosis and cholangitis kill the
- Peritoneal sepsis and bacteremia accompanies the
pancreatitis at all times in CDL whereas
This is not a common finding in human pancreatitis
3. Diet Induced Pancreatitis
The relationship between feeding with ethionine and
acute pancreatitis is well known [11].
Ethionine is toxic to pancreatic acinar cells [12]. It
inhibits phospholipid metabolism intracellularly [13,14].
Lombardi et al induced acute hemorrhagic pancreatitis
in female mice with 0.5% ethionine enriched diet [15].
Widespread intra-abdominal fatty necrosis follows pan-
creatitis. If feeding is limited to 24 hours mortality is
55-60%. If fed ad libidum this diet is 100% lethal in 5
days [16]. Histopathologic and gross examination of
pancreas between 48-72 hours after 24 hours feed did
not show any pancreatic damage [17]. When animals are
fed with choline, pancreatitis does not develop [18].
Choline takes up the ethyl groups liberated during
breakdown of ethionine. Female sex steroids seem to
promote development of pancreatitis so either young
female mice or oestrogen treated male mice are pre-
ferred [19].
Diet without choline exerts synergistic effect to ethi-
onine causing intraparanchymal activation of zymogens
leading to massive hemorrhagic necrosis. The subcellu-
lar mechanism underlying this is the inhibition of mem-
brane lipid synthesis resulting in breakdown of endo-
plasmic reticulum and release of autophagic vacuoles.
The end result is autolysis [20-22].
The diet model appears to be a good approximation of
severe necrotizing human pancreatitis. Both the gross
and histological appearance of the pancreatic and peri-
pancreatic inflammation as well as the clinical and bio-
chemical course of diet-induced pancreatitis resemble
human disease. Ascites, acidosis, hypoxia and hypo-
volemia occur in this model like in human pancreatitis.
The time course of the morphological and biochemical
alterations have extensively been studied and are thus
well defined in this model. However, small size of the
animals used is a limitation for evaluation of surgical
procedures and new diagnostic tools [23].
4. Arginine Induced Pancreatitis
Apart from ethionine, other amino acids like arginine can
also induce pancreatitis. High dose intraperitoneal injec-
tion of 500 mg/100 gr arginine can cause acute necrotiz-
ing pancreatitis in rats, rabbits and mice [24-28].
The possible mechanisms underlying the effect of ar-
ginine is via excessive nitric oxide production, lipid per-
oxidation and inhibition of protein synthesis [29-31].
Dose and exposure of arginine determines the severity
of pancreatitis in this model. The changes range between
interstitial edema, inflammatory infiltration, acinar de-
granulation to massive necrosis after 250 mg/kg and 450
mg/100 kg of injections respectively [32,33].
In addition to ease in controlling the destruction, argi-
nine exerts minimal effect on other tissues which makes
this model a plausible non invasive method for experi-
mental pancreatitis [34].
The only drawback is its weak clinical relevance which
made this method get replaced by other models.
5. Secretagogue Induced Pancreatitis
Cerulein is a decapeptide analogue of cholecystokinin
(CCK) derived from the skin of the amphibian Hyra
caerula. When given either 1-5 ng/kg intravenous (iv)
bolus or 0.25-1 ng/kg/min iv infusion or 50-100 ng/kg
subcutaneously this substance increases pancreatic secre-
tions [22]. If administered in supramaximal doses it
causes edematous pancreatitis by increasing pancreatic
protein secretions [35].
Cerulein interferes with packaging of zymogens and
lysosomal hydrolases after synthesis in endoplasmic re-
ticulum leading to intracellular activation of trypsinogen
[36]. In 48 hours after infusion zymogen granules start
fusion with lysosomes resulting in inflammation and
acute pancreatitis [37,38].
The usual way of administration is by a catheter in-
serted in internal jugular vein of the rat at a rate of 1-2
ml/hour [39,40]. Cerulein can be diluted in normal saline
and infused iv in 3-5 hours [41,42].
Cerulein can also be administered intraperitoneally [43-
45]. Multiple injections can be done in one hour intervals
with 5-200 g/kg doses.
Subcutaneous delivery can be achieved in multiple in-
jections with 25-50 g/kg dose [46,47].
In order to increase the degree of pancreatitis more
than one model can be used. Schmidt et al. combined iv
cerulein (5 g/kg/hr) with low pressure intraductal gly-
codeoxycholic acid infusion [48]. They observed that
edema, acinar necrosis, inflammation and hemorrhage
were profound.
Schoenberg et al. infused cerulein (5 micrograms/kg
per hour) for 30 minutes, 3.5 hours, and 12 hours in rats.
Copyright © 2010 SciRes. SS
No damage was seen after 30 minutes whereas after 3.5
hours interstitial edema, intravascular migration of gran-
ulocytes, zymogen degranulation and acinar cell necrosis
was seen. After 12 hours, histological evaluation showed
pronounced zymogen degranulation, extensive tissue
necrosis, and migration of granulocytes into the tissue.
Amylase and lipase activities increased 15 and 35-fold
respectively during this time [49].
6. Duct Obstruction Induced Pancreatitis
This model mimics benign and malignant partial or com-
plete obstruction of PD. The model reflects tumors, gall-
stone disease, trauma in the clinical setting. The surgical
manipulation is simple, requiring either ligation of the
common biliopancreatic duct or obstruction of the pan-
creatic duct by vertical cannulation or insertion of a bal-
loon-tipped catheter. The point of obstruction is close to
the entry to duodenum, much like gallstone obstruction
at the ampulla of Vater [50,51].
Duct obstruction leads to acinar atrophy without caus-
ing pancreatitis. The physiological mechanism of this
model is thought to be similar to that of the CDL tech-
nique. It is postulated that bile reflux by triggering intra-
pancreatic digestive enzyme activation accounts for the
major pathological factor in this model. Duct obstruction
induced pancreatitis can be complicated with other
stimulations and surgical manipulations.
For example, caerulein or secretin can be administered
to the animal together with duct ligation to exaggerate
the pancreatic secretions [52-54].
The severity of pancreatitis produced by the duct ob-
struction model varies depending on the animal species
used for experiment. In dogs physiological pressure in
PD is 30 cmH2O [55]. When PD is ligated pressure rises
to 40-80 cmH2O in 6-12 hours. Fluid accumulation in PD
starts in 10-30 hours and continues up to 40 hours [56,
After 24 hours the equilibrium between secretion and
PD obstrucion is maintained which stops further PD
pressure rise and parenchymal water content [55,56]. One
week after PD ligation acinar cell zymogen content was
found to be decreased, rough endoplasmic reticulum is
fragmented, golgi apparatus function is lost, autophagic
vacuoles appear and exocrine pancreas is replaced with
fibrous tissue [57]. These changes occur faster in rats than
dogs. In rats, main bile duct passes through pancreas and
many small pancreatic ducts join with it. In order to pre-
vent flow of only pancreatic secretions, duodenum is
separated from transverse colon and a polyethylene tube
inserted in to the proximal part of main bile duct [58].
In rabbits PD obstruction does not lead to the mor-
phological changes of pancreatic trauma or inflammation
but exocrine pancreas atrophies. PD is directly cannu-
lated and located in vertical direction in rabbits. This is
thought to mimic obstructive biliary pancreatitis in hu-
mans [59]. This technique had been also utilized for as-
sessment of effect of pancreatic enzymes on small intes-
tine brush border enzyme activity [60].
Oppossums were also used for this model. Oppos-
sum’s bile structure closely resembles human biliary
system. Bile tract has a single terminal end combining
with PD 2-3 cm before opening into duodenum.
Occlusion of the common bilipancreatic duct causes
acute hemorrhagic pancreatitis and results in 100% mor-
tality in 14 days [61].
When it is sutured adjacent to duodenum, pancreatic
edema forms in 6 hours and peaks in 12 hours. At this
stage fatty necrosis and parenchymal hemorrhage start to
appear and infiltration by inflammatory cells occurs [61-
Another variant of this techique is partial obstruction
of the pancreatic duct studied on cats. After exposure of
the PD it is partially sutured proximally. PD is cannu-
lated from the tail and secretions are collected. The se-
cretion is increased with secretin and CCK. It was found
that changes in pancreas depend on the degree of ob-
struction. If it exceeds 75%, acinar atrophy and decrease
in response to secretin and CCK stimulation occurs.
Lesser degrees of obstruction only impairs enzymatic
secretions. Three months after recovery from obstruction
neither enzyme nor bicarbonate secretions return to nor-
mal and tissue regeneration does not occur [64]. The
disadvantage of this technique is difficulty in determin-
ing the degree of obstruction which is assessed by in-
stilling vinyl chloride in retrograde fashion in to PD and
examining it under microscope.
The duct obstruction model has high clinical relevance
in that it simulates obstruction induced AP. Moreover,
this induction method is quick and does not require so-
phisticated surgical techniques. These advantages have
made this model a favorite for investigating the patho-
physiology, as well as the therapeutic treatment of ob-
struction induced pancreatitis. It does not require ad-
ministration of systemically active substances. Although
not used as frequently as it had been, it should be kept in
mind when experimenting chronic obstructive pancreati-
tis as acinar cell loss and fibrosis is encountered in long
term ductal obstruction.
7. Ex Vivo Perfusion Model
This model was first described by Saharia et al. in 1977.
It enables experimentation of different etiologies of pan-
creatitis [65].
The technical details are as follows: Pancreas of the
dog is mobilized with the duodenal segment adjacent to
it. Splenic artery and superior mesenteric artery distal to
Copyright © 2010 SciRes. SS
inferior pancreaticoduodenal artery is cannulated. Portal
vein is cannulated and incoming venous blood is col-
lected in a reservoir. A 16 G polyethylene catheter is
placed in PD via a small duodenotomy. The circulation
in this model is first started with 200ml of autologous
blood. Human serum albumin (2.5 g), glucose (500 mg)
and sodium bicarbonate (20 ml) is added to the perfused
blood. During the experiment pH should be kept at 7.40.
Blood glucose level is fixed at 100 mg/dl [65,66].
After the pancreas is harvested it is stored on a plexi-
glass surface in a humid environment. The blood in ve-
nous reservoir is passed through 95% oxygen and 5%
carbondioxide suppyling oxygenator. Another pump pu-
shes back the blood via the splenic and superior mesen-
teric arteries. The index for blood flow is either 20-30
ml/min or 1 ml/min/6 gr of tissue [67]. Temperature of
the perfusate is adjusted to 37°C. Partial obstruction can
be added to the model by inserting 25 G catheter in to
pancreas [68]. Increasing the blood flow results is edema
[65]. Albumin added previously decreases edema and
hemorrhage of the pancreas [69].
Alcoholic pancreatitis can be induced by adding free
fatty acids or acetaldehyde in to perfusate [65,70-73].
Different etiologies can be studied by changing the flow
rate, oxygen content, delaying perfusion or adding ceru-
lein [71,74,75].
Although expensive, ex vivo perfusion model is a
plausible model as the organ is isolated from body pre-
venting systemic factors intervening. A complex equip-
ment which has a propensity for breakdown in about 4
hours made this model remain inpopular.
8. Duct Infusion Pancreatitis
Cannulation of the pancreatic duct provides another way
of inducing an experimental AP model. Once the cannula
has been implanted, an exogenous substance can be in-
fused into the pancreas via the pancreatic ductal system.
Several substances have been used as inducers of pan-
creatitis in this method. These have included stimulating
factors and toxic substances such as bile acids (tauro-
cholate or glycodeoxycholic acid), ethyl alcohol, perace-
tate and tert-butyl hydroperoxide. The most common of
all these substances are bile acids [76-78].
In rats biliopancreatic duct is catheterized with 24 G
polyethylene tube and ligated [79]. Main hepatic duct is
clamped under liver and intraductal infusion is started.
Glycodeoxycholic acid prepared in glycylglycine buffer
(pH = 8) is recommended as infusate. Infusion should be
in 1.5 minutes, with 30 mmHg pressure and 0.1-0.5 ml
In dogs trypsin is used along with bile acids [80]. After
duodenectomy accessory pancreatic duct is cannulated
with 1.5 mm tube and bile acids and trypsin in 1:1 ratio,
0.5 ml/kg solution is given with 140-150 mmHg pressure.
Infusion of bile acids is a fast and cheap way of inducing
pancreatitis resembling human pancreatitis. Mortality
can be controlled with changing the quantity of the in-
fusate. Both edematous and hemorrhagic pancreatitis can
be induced. Major disadvantage is different response of
different species to infusion.
Taurodeoxycholate (0.2 ml, 0.025 molar, glycylgly
cine-NaOH, pH: 8.0) is the second most used substance.
In rats it is delivered 0.04 ml/min with an infusion pump
[81]. Schoenberg et al. recommend that the pressure does
not exceed 15 cmH2O during infusion [82]. In 3.5 hours
20% of rats die while in 57% die in 12 hours. After 3.5
hours fulminant hemorrhagic pancreatitis is seen under
light microscope. Zymogen degranulation, 50% cell ne-
crosis, mild tissue edema, inflammatory cell infiltration
is observed. In 12 hours almost all of the acinar cells
undergo necrosis.
In dogs 20 G catheter is placed in pancreatic duct and
1.8 gr sodium taurocholate with 250.000 U benzoyl L-
arginine ethyl ester hydrochloride crystal trypsine in 20
ml sorenson buffer infusion is carried on for 30 minutes
not exceeding a pressure of 30 cmH2O [83]. Intraductal
taurocholate infusion causes severe pancreatitis. Inflam-
mation is not homogenous and mostly on the head of
pancreas [84].
The repeatability and clinical relevance associated
with the duct perfusion induced pancreatitis make it an
excellent experimental model for pancreatitis studies.
However it requires careful monitoring of perfusion
pressure and an invasive surgery. Intraductal infusion of
saline alone has been reported to induce mild pancreatitis
[85]. Findings demonstrated that pancreatic injury is at-
tributable not only to the exogenous substance infused
but the combination of the exogenous substance and the
hydrostatic pressure associated with the infusion. The
presence of exaggerated hydrostatic pressure makes it
less clinically relevant relative to other models like the
duct obstruction model. Despite this drawback, the duct
perfusion model is the most commonly used pancreatitis
model because of its similarity to clinical pancreatitis
The confounding effects of increased ductal pressure
can be ameloriated by antegrade perfusion model which
is first studied by Reber et al. [88]. They used cats for
this purpose. The technique requires removal of spleen
and greater omentum. Two catheters are placed in PD;
one through duodenum and the other from the tail of
pancreas [89]. Perfusion is maintained by a pump at a
rate of 0.2-3.75 ml/hour for two hours. At this rate intra-
ductal pressure does not exceed 20 cmH2O. Reber et al.
recommend use of certain substances (bile, aspirin, hy-
drochloric acid, ethanol, secondary bile acids) to over-
come pancreatic canal barrier and increase permeability.
Copyright © 2010 SciRes. SS
9. Vascular Induced Pancreatitis
Acute pancreatitis is encountered after cardiopulmonary
bypass [90]. Changes in vascular perfusion of pancreas
leads to pancreatitis in many animals including dogs, rats,
cats [91,92].
Vascular perfusion can be changed by altering either
of inflow, outflow or microcirculation of the organ.
In 1962 Pfeffer et al. used 8-20 gr polyetyhlene mi-
crospheres to occlude superior pancreaticoduodenal ar-
teries. With this technique irreversible occlusion of ter-
minal arterioles is achieved impeding microcirculation
[93] causing hemorrhagic pancreatitis in 11 hours. Using
larger particles only result in pancreatic edema.
Permanent occlusion of the superior pancreaticoduo-
denal artery results in elevated serum pancreatic enzymes
and necrosis. However, the artery occlusion induced pan-
creatitis model has weak clinical correlation because
pancreatitis induced by artery occlusion in humans is
rare [94].
Pancreatic blood flow can also be severed by occlu-
sion of pancreatic veins, either by ligation or injection of
microspheres. Splenic or gastroduodenal vein occlusion
has been shown to lead to elevated serum amylase and
histopathological findings [95].
One of the methods for suppressing the inflow to the
pancreas is to create a low flow state by inducing hypo-
volemic shock. In 1987, Brasilia et al. showed that with-
drawal of 30% to 35% of blood from dogs created hy-
povolemic shock. After 3 hours of hypovolemia canine
pancreases showed a significant weight gain.
Microscopic analysis revealed significant edema, he-
morrhage, acinar cell necrosis, and fat necrosis. Hypo-
volemic shock induced pancreatitis imitates the pan-
creatitis observed after extensive surgery in the clinical
setting [96].
The major disadvantage of vascular induced pancreati-
tis is the effects of intense surgical trauma exerted on the
animals. It neccessitates extensive bleeding, complex
surgical protocol and continuous analgesia. It is usually
applied to large animals like dogs and pigs. In hypo-
volemic shock induced pancreatitis, the damage is not
localized to pancreas but systemic. Venous occlusion and
disturbance of pancreatic microcirculation have low re-
peatability. Thus, the vascular-induced pancreatitis mo-
del has become less popular [97].
10. Intraparenchymal Taurocholate
This model is worth mentioning because it is highly re-
producible any easy to apply.
When injected into tail or body of rat pancreas with 25 G
needle, 1 ml 10% solution of taurocholate causes ne-
crotic lobules, fatty necrosis in and arround pancreas
Paran et al. showed that six hours after injection
plasma activites of amylase, lipase and lactate dehydro-
genase increase and twenty four hours after injection
pancreatic morphological changes with good correlation
to clinical findings and mortality were seen [99].
11. Conclusions
Endoveurs to identify an ideal model for pancreatitis date
back to 1960’s. The models tested are summarized in
Table 1. Each model has its own advantages and draw-
backs. The researcher should choose among the models
depending on what he wants to test in his experiment, the
infrastructure of his laboratory and his surgical skills.
Table 1. Summary of the models reviewed.
Animals Advantages Disadvantages
CDL Rats, dogs Clinical relevence Complex surgical technique
High surgical trauma
Not suitable for small animals
Diet Induced Mice Non invasive, reproducible Weak clinical relevance
Suitable for small animals
Arginine Induced Rats, mice, rabbits Non invasive,easy to control damage, Weak clinical relevance
toxicity limited to pancreas
Secretagogue Induced Mice, rats, rabbits, Non invasive, easy to control damage Weak clinical relevance
dogs,pigs Reproducible
Duct Obstruction Rats, rabbits, opossums Mimics gallstone-obstruction Severe AP only in oppossums
induced pancreatitis
Ex vivo Perfusion Model Dogs,pigs Organ isolated from systemic effectors Expensive, complex surgery
Complex equipment
Duct Infusion Rats, rabbits, dogs, pigs Clinical relevence, wide spectrum of Hydrostatic pressure as
substances to test confounding factor
Vascular Induced Rats, cats, dogs, pigs Assesment of operative and Complex surgical technique
venous thrombosis pancreatitis High surgical trauma, expensive
Low reproducibility
Intraparenchymal Taurocholate Rats Highly reproducible, easy to apply Localized pancreatitis
Copyright © 2010 SciRes. SS
Some models test etiology while others simulate the
complications of pancreatitis. Combination of models
can also be used if single model does not fulfill the needs.
Ideal model which by itself demonstrates all aspects of
pancreatitis including systemic changes is yet to be de-
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