Experimental Pancreatitis in the Rat

Abstract

Acute hemorrhagic pancreatitis was induced in rats by injecting sodium taurocholate into the common biliopancreatic duct. The extent of pancreatic necrosis was quantified in histological sections during the course of the disease. The proportion of necrotic acini was low, although the amount of necrosis increased from 3.3% of pancreatic parenchyma at 15 min to 10.5% at 12 h. The degree of ischemia in the inflamed pancreas was estimated by extracting intravenously injected toluidine blue from the gland. The amount of the dye in the gland decreased progressively during 12 h to 58.8% of the amount in normal pancreas. The development of pancreatic edema was studied by recording the water content of the gland. The edema was maximal at 3 h and resolved partly in 12 h after the induction of the disease. Necrosis and ischemia become progressively more pronounced in the edematous pancreas during sodium taurocholate-induced acute hemorrhagic pancreatitis. This kind of pathophysiologic course is also thought to characterize human pancreatitis. The present simple model of acute hemorrhagic pancreatitis in the rat is suitable for quantitative observations on the development of pancreatic damage under various experimental conditions.

Expression of NOD2 in a Rat Model of Acute Pancreatitis

“…It is well established that the survival rate of rats in TAU-induced AP is higher compared with other pancreatitis models. Indeed, it has been hypothesized that TAU can induce a severe form of pancreatitis because it induces hemorrhagic necrotizing effects in the pancreas associated with higher remote inflammation in rats, 36 which is confirmed in the present study. Thus, it also can be concluded from the TAU-induced AP rat experiments that the subsensitivity of inflammatory response to NOD2 may reflect extensive cell damage secondary to massive systemic enzyme generation (AMY and the others).…”

Melatonin Modulates the Severity of Taurocholate-Induced Acute Pancreatitis in the Rat

“…In order to prevent the pancreatic damage caused by released free oxygen radicals and cytokines, substances such as pentoxifylline [23], cyclooxygenase inhibitors [24], melatonin [25,26], allopurinol [27] and octreotide [28] were used in experimental studies. In this study, acute necrotizing pancreatitis was induced by retrograde infusion of taurocholic acid into the biliopancreatic duct, as Aho et al [29,30] described previously. The procedure and dosage for melatonin was selected according to the data presented in the literature [31].…”

Experimental acute pancreatitis: MR relaxation time studies using gadolinium–DTPA

“…These studies indicate that pancreatic lesions are characterized by interstitial edema, necrosis, and hemorrhages observed within minutes after taurocholate injection (18,19). On the basis of light and electron microscopic studies, the course of taurocholate-induced pancreatitis becomes more severe over a period of hours (16,19).…”