Effects of ethanol,dl-Ethionine, and protein deficiency on rat pancreas

A histologic, histochemical and electron microscopic study was carried out on the rat exocrine pancreas 6–96 h after a single allyl alcohol intake. Histologically, acidophilia, necrosis and vacuolation of the pancreatic acinar cells were observed. Histochemically, a low but evident alcohol dehydrogenase activity could focally be demonstrated in the pancreatic acinar cell cytoplasm of the experimental and control rats. By electron microscopy, cytoplasmic lipid droplets, mitochondrial degeneration and necrosis were found in the acinar cells. Focal cytoplasmic degradation and vacuolation were seen in acinar, centroacinar and ductular cells of the pancreas. The findings are regarded as the consequence of the toxic action of acrolein that originates after allyl alcohol oxidation by alcohol dehydrogenase. Analogies between the liver and the pancreas in their response to acute allyl alcohol and chronic ethanol intake are discussed.

Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 98%

Allyl Alcohol-Induced Changes in the Rat Exocrine Pancreas

Nizze¹,

Lapis²,

Kovács³

1979

“…The histopathological findings consisted of a decrease in the pancreatic parenchyma, replacement of fat, severe inflammatory cell infiltration, extensive fibrosis and tubular complexes. As this model closely resembles human chronic pan creatitis, we conclude that ischemia is an etiological factor in chronic pancre atitis.Experimental models of chronic pancreatitis (CP) have been introduced by many investigators, but there is no model with closely resembling human CP [1][2][3]. Earlier, we have reported that a combination of persistent paren chymal cell damage and pancreatic duct obstruction is important in producing a CP model (combination theory) [4], Clinically, various etiological factors including alco hol intake are recognized, but the pathophysiology of CP still remains obscure.…”

mentioning

confidence: 99%

Canine Model of Chronic Pancreatitis due to Chronic Ischemia

Tanaka¹,

Ichiba²,

Miura³

et al. 1994

An experimental model of chronic pancreatitis was produced by a chronic ischemia which was induced by ligation and separation of branches flowing into the left pancreatic lobe from the splenic artery. Macroscopic findings at 3 and 6 months after model preparation showed that the pancreas was hard, with severe inflammatory change. In the secretin-cerulein test at 3 and 6 months, the flow rate of pancreatic juice, amylase output and bicarbonate concentration were significantly reduced as compared with the controls. The histopathological findings consisted of a decrease in the pancreatic parenchyma, replacement of fat, severe inflammatory cell infiltration, extensive fibrosis and tubular complexes. As this model closely resembles human chronic pancreatitis, we conclude that ischemia is an etiological factor in chronic pancreatitis.

“…To define this patho physiology, an appropriate experimental model is needed. Experimental chronic pan creatitis may be produced by alcohol admin istration [1,2], pancreatic duct obstruction [3][4][5], circulatory disturbance, or malnutri tion [6]. However, all of these methods fail to produce a pathology comparable to hu man chronic pancreatitis.…”

mentioning

confidence: 99%

New Canine Model of Chronic Pancreatitis due to Chronic Ischemia with Incomplete Pancreatic Duct Obstruction

Tanaka

Ichiba²,

Fujii³

et al. 1988

A new experimental model of chronic pancreatitis was produced by a combination of chronic ischemia and incomplete obstruction of the pancreatic duct. Ischemia was induced by ligation and separation of branches flowing into the left pancreatic lobe from the splenic artery. Incomplete ductal obstruction was achieved by ligation and separation of the minor pancreatic duct and placement of a polyethylene tube in the major pancreatic duct. Macroscopic examination at 6 months after model preparation showed that the pancreas was hard, with severe inflammatory change. In the secretin test, the flow rate of pancreatic juice, amylase output and bicarbonate concentration were significantly reduced as compared with the controls. Pancreatography revealed dilatation and meandering of the major pancreatic duct and poor visualization of its secondary and tertiary bifurcations. The histopathological findings consisted of a decrease in the pancreatic parenchyma, replacement of fat, severe inflammatory cell infiltration, extensive fibrosis and tubular complexes. This model most closely resembles human chronic pancreatitis, and is a very useful instrument.