Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic pancreatitis-like lesions are observed in 100% of male Wistar Bonn/Kobori rats. At 3 mo of age, histopathologic examinations of the pancreas revealed a distinct infiltration of inflammatory cells with interstitial edema in the acini. At the same time, periductal and interstitial fibrosis and adenomatous hyperplasia of the ductular epithelium were observed. Extensive fibrotic exudation developed rapidly with age, and irregular destruction of the parenchyma was noted. The only abnormality, prior to the appearance of glycosuria, that could be detected clinically was lower levels, compared to Wistar rats, of BT-PABA excreted in the urine after oral ingestion. These lower levels indicate a decrease in enzyme secretion in WBN/Kob rats. Ultrastructural observations in histologically normal areas at 2 mo of age showed a swelling of mitochondria, indicating that ischemia was associated with the early pancreatic lesions. Serial pancreatographies were performed at 2-8 mo of age. Irregular widenings of the main pancreatic duct and dilations of the smaller ducts were observed already at 2 mo of age, suggesting a stasis of pancreatic juice in the early stages of the disease. It seems that male WBN/Kob rats are a useful model of human chronic pancreatitis, with an unknown mechanism regulated by the sex hormones.
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PMID:WBN/Kob rats. A new spontaneously occurring model of chronic pancreatitis. 169 93

Five patients with severe acute pancreatitis (AP) underwent subtotal pancreatectomy, and six patients with advanced chronic pancreatitis (CP) were subjected to pancreatic resection. Microangiography and histological studies were performed on the resected pancreata. All patients with AP had histologically verified necrotizing pancreatitis. Pancreatic ducts in the necrotic areas had severe inflammation in their walls and a decrease in their vascularity. The ductal walls of CP patients were indistinguishable from the surrounding fibrosis and the vascular supply of the ducts was markedly diminished. The vessels were reduced in number, and their calibers varied considerably. Ductal ischemia in connection with AP and CP is discussed.
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PMID:Vascular changes of pancreatic ducts and vessels in acute necrotizing, and in chronic pancreatitis in humans. 203 15

The cause of pain in chronic pancreatitis appears to be related to ductal and parenchymal hypertension and possibly to pancreatic ischemia. The management of pain needs a multidisciplinary approach. Medical measures such as abstinence from alcohol and therapy with mild analgesics are useful. Surgery should be considered when the pain begins to interfere with the patient's quality of life. Ductal drainage operations may be indicated when the duct is dilatated. The alternative is pancreatic resection, which, although safe and effective, creates diabetes when much of the pancreas is removed. Newer operations that relieve pain while preserving function are being devised.
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PMID:The cause and management of the pain of chronic pancreatitis. 226 24

Follow-up clinical results have been analyzed for 564 patients with occlusions of visceral arteries, which presented clinically as symptoms of chronic pancreatitis in 115 patients. As a rule, chronic pancreatic ischemia leads to exocrine hyposecretion evident from the derangement of cyclonucleotide metabolism. There were also metabolic shifts in pancreatic cells related to hypoxia. Intravital biopsies revealed dystrophy of the acinar tissue as well as inter- and intralobular infiltrates of the connective and fatty tissue.
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PMID:[Clinico-morphologic characteristics of ischemic involvement of the pancreas]. 247 55

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.
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PMID:New canine model of chronic pancreatitis due to chronic ischemia with incomplete pancreatic duct obstruction. 322 67

Arterial intimal thickening and thrombosis of the pancreatic artery has frequently been found in Watanabe heritable hyper-lipidemic (WHHL) rabbits. Three of the 20 rabbits used in this study showed histopathological findings such as intra- or inter-lobular fibrosis with lymphocytic infiltration, acinar degenerative changes, ductular proliferation and small ductal dilatations which were identical to those of human chronic pancreatitis. These findings were observed in discrete areas clearly demarcated from normal pancreatic parenchyma and adjacent to parenchymal necrosis. These discrete areas were developed just peripheral to regions of necrotic or inflammatory obstruction of the pancreatic duct, which might have been caused by parenchymal necrosis due to severe ischemia. The stasis of pancreatic juice in the ductal tree may result in such findings in the WHHL rabbit. Fat replacement of pancreatic parenchyma was observed in 17 of the 20 WHHL rabbits, and was classified into two types, diffuse and massive. Massive fat replacement may occur from fat necrosis and intra-lobular parenchymal necrosis. Vascular alterations and secondary ischemia in the pancreas is one of the most important factors involved in the pancreatic lesions present in the WHHL rabbit.
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PMID:Ischemic changes in the pancreas of Watanabe heritable hyper-lipidemic (WHHL) rabbits. 338 20

Few studies have been published on the ultrastructural changes which accompany human acute pancreatitis, and these have concentrated primarily on parenchyma. The present study concentrates on extraparenchymal changes, compares acute pancreatitis occurring alone with that on a background of chronic pancreatitis, and tests for similarity with observations made previously in an experimental model. Pancreatic tissue came from 16 patients undergoing surgery for pancreatic disease and five subjects without pancreatic disease. Regressive changes in parenchymal cells were consistent with ischemia, and with previously described studies. Polymorphonuclear leukocytes infiltrated into stroma and parenchyma. Platelets accumulated intra- and extravascularly. Fibrin deposits were common in the connective tissue, and could be observed in intercellular spaces at the base of acini, mingled with degenerating acinar cells and secretion product. Microthrombi occurred in blood vessels. These alterations were consistent with those in experimental acute pancreatitis. Similar changes were observed whether or not acute pancreatitis occurred on a background of chronic pancreatitis. The vascular component is important in acute pancreatitis, and altered epithelial barriers allow interaction between blood-borne material and pancreatic exocrine secretions.
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PMID:Ultrastructure of human acute pancreatitis. 369 80

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.
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PMID:Canine model of chronic pancreatitis due to chronic ischemia. 751 52

A patient with a replaced common hepatic artery originating from the superior mesenteric artery successfully underwent a pylorus-sparing pancreaticoduodenectomy for chronic pancreatitis. This anomalous vessel was discovered by preoperative angiography but at operation the artery coursed ventral to the head of the pancreas, not, as one would predict, through the substance of the pancreas or dorsal to the pancreatic head and lateral to the portal vein. To our knowledge, this is the first case of a replaced common hepatic artery in this position reported in the English literature. Preservation of the entire blood supply to the liver and biliary tree is important to prevent biliary fistula after a Whipple procedure, and, in some cases, hepatic ischemia. In this case the artery was slightly larger and in the same position as the gastroduodenal artery, predisposing the patient to significant potential morbidity with a standard dissection.
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PMID:Sparing a replaced common hepatic artery during pancreaticoduodenectomy. 790 51

Ischemia as a causative factor for acute pancreatitis has been discussed for decades but has only recently gained wider acceptance. Chronic pancreatitis, however, has rarely been attributed to ischemic injury. While experimental evidence is available for the ischemic pathogenesis of acute pancreatitis, no studies have been reported about pancreatic ischemia as a single cause of chronic pancreatitis. Also, the progression from acute to chronic pancreatitis has been a very controversial issue. To address both questions we have injected polystyrene microspheres of 20-microns diameter into the pancreatic branches of the splenic artery of 36 rats. Thirteen more rats were sham operated and injected with saline. The animals were killed at 1, 2, 3, and 9 weeks after operation and macroscopically and histologically examined, and serum alpha-amylase and weight gain were determined. For the pancreas the following parameters were assessed using a score from 0 (no change) to 4 (severe change): atrophy, hemorrhage, edema, fat necrosis, acinar necrosis, polymorphonuclear infiltration, mononuclear infiltration, interstitial fibrosis, and ductal changes. While no difference between control and experiment was observed for serum alpha-amylase, weight gain, edema, and hemorrhage, persistent differences were evident for the parameters characteristic of chronic pancreatitis, most significantly for interstitial fibrosis, ductal changes, mononuclear infiltration, acinar necrosis, and atrophy. No spontaneous deaths occurred. The severity of the lesions remained stationary after the first week. Our work shows for the first time that pancreatic ischemia by microvascular hypoperfusion can cause histopathologic changes characteristic of chronic pancreatitis and that these changes follow acute necrotizing pancreatitis.
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PMID:Does acute pancreatitis progress to chronic pancreatitis? A microvascular pancreatitis model in the rat. 853 54


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