The Fate of Pancreatic Proteolytic Enzymes in the Course of Acute Hemorrhagic Pancreatitis

Beck, Ivan T.; Pintér, Erika; McKenna, Richard D.; Ritchie, A. C.; Solymar, J

doi:10.1159/000389214

Cited by 4 publications

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“…23,24 In the present study, hemorrhagic pancreatitis was observed in two cases, one with pulmonary tuberculosis and the other with hydrargyriasis. In this case of tuberculosis the patient had fallen into dyspnea with transient heart failure two days before death.…”

supporting

confidence: 53%

Vascular and Ductal Patterns of Pancreas by Microradiography and Their Relation to Lesions of Pancreatitis

Hayasaka

Sasano

1970

Tohoku J. Exp. Med.

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supporting

confidence: 53%

Vascular and Ductal Patterns of Pancreas by Microradiography and Their Relation to Lesions of Pancreatitis

Hayasaka

Sasano

1970

Tohoku J. Exp. Med.

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“…Grossman (1959) found that dog gall-bladder bile did not activate trypsinogen in dog pancreatic juice, a finding supported by the work of White and Magee (1960). Beck, Pinter, Solymar, McKenna, and Ritchie (1962) showed that dog bile did not activate trypsinogen derived from extracts of the dog pancreas. Haverback, Dyce, Bundy, and Edmondson (1960) were unable to activate trypsinogen in human pancreatic juice by the addition of human hepatic bile.…”

Section: Discussionmentioning

confidence: 87%

The effect of bile on the activation of trypsinogen and the activity of trypsin in pancreatic juice

Elmslie

1965

Journal of British Surgery

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“…Nonquantitative estimations of the sever ity of pancreatic damage have been made in bile [4,7], bile salt [16] and enzyme-induced [5], as well as in duodenal [10] and metabolic (ethionine) [29] forms of acute pancreatitis. In these studies the disease has been graded, e.g., from 0 to 4 or from 'minimal' to 'se vere'.…”

Section: Discussionmentioning

confidence: 99%

Experimental Pancreatitis in the Rat

Aho¹,

Nevalainen²,

Aho

1983

Eur Surg Res

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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.

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The Fate of Pancreatic Proteolytic Enzymes in the Course of Acute Hemorrhagic Pancreatitis

Cited by 4 publications

References 0 publications

Vascular and Ductal Patterns of Pancreas by Microradiography and Their Relation to Lesions of Pancreatitis

Vascular and Ductal Patterns of Pancreas by Microradiography and Their Relation to Lesions of Pancreatitis

The effect of bile on the activation of trypsinogen and the activity of trypsin in pancreatic juice

Experimental Pancreatitis in the Rat

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