Experimental pancreatitis in the rat. Changes in pulmonary phospholipids during sodium taurocholate-induced acute pancreatitis

Aho, Heikki; Ahola, Raija; Tolvanen, Anna; Nevalainen, Timo J.

doi:10.1007/bf01852290

Cited by 24 publications

(7 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The bile salt-induced acute pancreatitis model was first reported by Aho et al8,9 and has been widely accepted as a representative model of severe acute pancreatitis that shows pancreatic necrosis. This type of acute pancreatitis is induced by first inserting the cannula through the orifice that opens into the duodenum and infusing 0.2 to 0.3 mL of 3% to 5% sodium taurocholate in a retrograde fashion.…”

Section: Experimental Models Of Acute Pancreatitismentioning

confidence: 99%

Experimental Models of Pancreatitis

Hyun

Lee

2014

Clin Endosc

View full text Add to dashboard Cite

Acute pancreatitis is an inflammatory disease characterized by interstitial edema, inflammatory cell infiltration, and acinar cell necrosis, depending on its severity. Regardless of the extent of tissue injury, acute pancreatitis is a completely reversible process with evident normal tissue architecture after recovery. Its pathogenic mechanism has been known to be closely related to intracellular digestive enzyme activation. In contrast to acute pancreatitis, chronic pancreatitis is characterized by irreversible tissue damage such as acinar cell atrophy and pancreatic fibrosis that results in exocrine and endocrine insufficiency. Recently, many studies of chronic pancreatitis have been prompted by the discovery of the pancreatic stellate cell, which has been identified and distinguished as the key effector cell of pancreatic fibrosis. However, investigations into the pathogenesis and treatment of pancreatitis face many obstacles because of its anatomical location and disparate clinical course. Due to these difficulties, most of our knowledge on pancreatitis is based on research conducted using experimental models of pancreatitis. In this review, several experimental models of pancreatitis will be discussed in terms of technique, advantages, and limitations.

show abstract

Section: Experimental Models Of Acute Pancreatitismentioning

confidence: 99%

Experimental Models of Pancreatitis

Hyun

Lee

2014

Clin Endosc

View full text Add to dashboard Cite

show abstract

“…Direct injury includes those conditions in which a toxic substance directly injures the lung epithelium such as diffuse pulmonary infection (e.g., bacterial, viral, fungal, pneumocystis), toxic gas/smoke inhalation, pulmonary contusion, and aspiration of gastric contents (29,105). Indirect injury is a more common predisposition and occurs by means of blood-borne systemic inflammatory processes such as sepsis, septic shock (10,15,29,35,80,95,100,105,109), acute pancreatitis (1,4,10,11,17,59,77,85), and other clinical events including major surgery, trauma, multiple transfusions, dyspnea, ischemia-reperfusion injury, and decreased lung compliance (15,84). In ARDS, the injured lung is believed to go through three phases: exudative, proliferative, and fibrotic, but the course of each phase and the overall disease progression are variable.…”

Section: Pathophysiology Of Ardsmentioning

confidence: 99%

Chemokines in acute respiratory distress syndrome

Puneet¹,

Moochhala²,

Bhatia³

2005

American Journal of Physiology-Lung Cellular and Molecular Phys

283

238

View full text Add to dashboard Cite

A characteristic feature of all inflammatory disorders is the excessive recruitment of leukocytes to the site of inflammation. The loss of control in trafficking these cells contributes to inflammatory diseases. Leukocyte recruitment is a well-orchestrated process that includes several protein families including the large cytokine subfamily of chemotactic cytokines, the chemokines. Chemokines and their receptors are involved in the pathogenesis of several diseases. Acute lung injury that clinically manifests as acute respiratory distress syndrome (ARDS) is caused by an uncontrolled systemic inflammatory response resulting from clinical events including major surgery, trauma, multiple transfusions, severe burns, pancreatitis, and sepsis. Systemic inflammatory response syndrome involves activation of alveolar macrophages and sequestered neutrophils in the lung. The clinical hallmarks of ARDS are severe hypoxemia, diffuse bilateral pulmonary infiltrates, and normal intracardiac filling pressures. The magnitude and duration of the inflammatory process may ultimately determine the outcome in patients with ARDS. Recent evidence shows that activated leukocytes and chemokines play a key role in the pathogenesis of ARDS. The expanding number of antagonists of chemokine receptors for inflammatory disorders may hold promise for new medicines to combat ARDS.

show abstract

“…Pancreatic (Popper et al 1948;Theve et al 1973;Aho et al 1980a, b) and extra-pancreatic (Aho et al 1983b) lesions are well documented and are similar to those which appear in man (Simon and Giacobino 1970;Kitamura et al 1973;Nevalainen 1980;Rao et al 1980;Aho et al 1983b). However, pathological features of pancreatic and peripancreatic necrosis have not been quantified using objective determinations.…”

Section: Discussionmentioning

confidence: 84%

Acute experimental pancreatitis in rat induced by sodium taurocholic acid: objective quantification of pancreatic necrosis

Rueda

Ortega

Arguello

et al. 1992

Vichows Archiv A Pathol Anat

View full text Add to dashboard Cite

Retrograde injection of 5% sodium taurocholic acid (TA) in Wistar rat pancreatic duct is followed by acute pancreatitis, resulting in 100% mortality within 36 h. Biochemical determinations show raised levels of amylase in ascites and blood. Necrosis has been measured using seven morphometric characteristics of pathological changes that add precise information on the type and extension of the pancreatic lesion. The percentage of necrotic tissue (by area) seems to be the most objective parameter. Necrosis appears 6 h after TA infusion, being 5.77% in extent after 12 h, 14.9% after 24 h and animals die with an area of 29.5% necrosis. This experimental model seems to one in which physiopathological and therapeutic trials on acute pancreatitis may be tried out.

show abstract

Experimental pancreatitis in the rat. Changes in pulmonary phospholipids during sodium taurocholate-induced acute pancreatitis

Cited by 24 publications

References 15 publications

Experimental Models of Pancreatitis

Experimental Models of Pancreatitis

Chemokines in acute respiratory distress syndrome

Acute experimental pancreatitis in rat induced by sodium taurocholic acid: objective quantification of pancreatic necrosis

Contact Info

Product

Resources

About