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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hepatic cellular damage induced by liver ischemia was investigated in rats with obstructive jaundice. Hepatic tissue blood flow in obstructive jaundice was decreased in the relation to the duration of jaundice. The value of lipid peroxide and cathepsin D activity of the hepatic tissue increased in the obstructive jaundice. Therefore, it was suggested that cell membrane and lysosomal membrane injury were induced in obstructive jaundice. The value of lipid peroxide of hepatic tissue in obstructive jaundice was more increased after partial liver ischemia. The survival rate following hepatic ischemia in jaundiced rats was remarkably lower than that of normal rats, and also it related to the duration of jaundice. In addition, histological changes of the liver after partial ischemia are severe in obstructive jaundiced liver. These data suggest that more remarkable hepatic cellular damage than in normal liver may be induced by liver ischemia in obstructive jaundice.
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PMID:[Experimental study on cell damage of ischemic liver in obstructive jaundiced rats]. 188 Sep 52

Mechanisms of gastric bleeding under obstructive jaundice were studied in adult male Wistar rats. Following ligation of the common bile duct, mucosal noradrenaline significantly decreased in both the pyloric and fundic gland areas of the gastric mucosa by 20 days after the operation. Serotonin increased only in the pyloric gland area, and histamine increased in the fundic gland area. Urinary excretion of free noradrenaline significantly increased after the ligation. Three weeks after the ligation, restraint and water immersion experiments were conducted. Under water immersion, gastric blood flow significantly reduced in rats with obstructive jaundice compared to controls. Acid output decreased in both groups. Gastric bleeding was noted in the fundic gland area significantly earlier in the ligated rats than in the non-ligated rats. Administration of noradrenaline s.c. 30 minutes before immersion significantly blocked the reduction in gastric blood flow and protected the gastric mucosa against acute bleeding under immersion. These results suggested that prolonged obstructive jaundice may deplete noradrenaline in the gastric mucosa, and that gastric mucosal ischemia caused by this sympathetic dysfunction plays an important role in the formation of acute gastric bleeding under obstructive jaundice.
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PMID:Studies of the mechanisms of gastric bleeding under obstructive jaundice. Role of biogenic amines. 660 80

The effects of OKY-046, a thromboxane A2 synthetase inhibitor, on hepatic dysfunction produced by liver cell ischemia were studied in an experimental model of rats with obstructive jaundice. The experiments were performed 7 days after the rats underwent bile duct ligation. Warm total ischemia of the liver was induced by Pringle's method over a 20-min period and the animals were divided into two groups according to whether or not OKY-046 was administered. The reperfusion time was 30 min in each group. OKY-046 was administered via the femoral vein at a rate of 100 micrograms/kg per min from 15 min before the blockade to the end of the experiment. The level of ATP in the liver tissue of the OKY-046 group was elevated slightly, but not significantly, compared to that of the control group. The ratio TXB2/6-keto PGF1 alpha in the liver tissue was lower in the OKY-046 group than in the control group, and significant differences were found between the two groups in the water content of the liver and the mitochondrial score as examined by transmission electron microscopy. Thus, it was observed that an improvement in the balance of TXA2 and PGI2 associated with OKY-046 administration proctected the cellular structure of the mitochondria in the rat liver.
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PMID:The effects of thromboxane A2 synthetase inhibitor (OKY-046) on complete hepatic ischemia in rats with obstructive jaundice. 868 Jan 15

The purpose of the present study was to elucidate the effect of hepatic reflow following ischemia on the remnant liver after hepatectomy with occluded hepatic blood inflow in dogs with obstructive jaundice. When 40% hepatectomy was performed with 10-min occlusion of hepatic blood inflow in dogs with obstructive jaundice, the lipid peroxide content in the remnant liver increased significantly, together with a reduction in superoxide dismutase (SOD)-like activity. The levels of endotoxin and beta-N-acetyl hexosaminase (NAH) in peripheral blood also increased. The phagocytic index increased transiently after 30 min, followed by a marked decrease after 3h. Histologically, degeneration and necrosis of the hepatic parenchymal cells were demonstrated, and survival rate at 7 days was only 23.1%. With the administration of coenzyme Q10 (CoQ10) or styrene-co-maleic acid SOD (SM-SOD), these phenomena were significantly inhibited, and the survival rate improved. After hepatectomy, Kupffer cells in the remnant liver were activated by increased endotoxin levels in the portal vein, inducing the production of free radicals, which, in turn, damaged the Kupffer cells by reducing endotoxin clearance. Finally, the impaired functional reserve in the remnant liver provoked liver failure. The administration of CoQ10 or SM-SOD prevented the occurrence of these phenomena triggered by the free radicals generated by Kupffer cells, stimulated by endotoxin in the portal vein.
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PMID:Pathophysiological effect of hepatic ischemia and reperfusion after hepatectomy in dogs with obstructive jaundice, focusing on the effect of coenzyme Q10 and styrene-co-maleic acid superoxide dismutase. 872 30

Oxidant injury is considered to be an important mechanism in the pathophysiology of acute renal failure. It has been thought that decrease in extracellular and intracellular fluid and endotoxemia seen in obstructive jaundice may cause an increase in production of oxygen free radicals and impairment in antioxidant defense mechanism. This study is designed to investigate the possible role of oxidant injury in renal failure seen in jaundiced patients. In this study, 28 rats were divided into four groups: Control (C)(N = 7); Renal ischemia (RI)(N = 7); Obstructive jaundice+renal ischemia (OJ+RI)(N = 7); Obstructive jaundice (OJ)(N = 7). All groups were compared with each other according to renal failure findings and enzyme activities, such as Xanthine oxidase (XOD), Superoxide Dismutase (SOD) and Catalase in renal cortex and Glutathione Peroxidase (GSH-Px), in blood at 3rd day after ischemia and reperfusion. Renal failure findings monitored by blood urea and creatinine levels, seemed more evident in OJ+RI than RI group (p < 0.05). When compared with RI, in OJ+RI group, increase in XOD activity at 3rd day was statistically significant [0.259 +/- 0.01 U/g (tissue) and 0.362 +/- 0.03 U/g (tissue) respectively] (p < 0.05). SOD and GSH-Px activities of each ischemic group at 3rd day were decreased compared to non-ischemic groups. This fall was significant (p < 0.05). But there was no statistical difference between jaundiced and non-jaundiced groups. Alterations in catalase activities also had no statistical significance. These findings may suggest that the injury induced by oxygen free radicals at re-oxygenation of tissue after ischemia may also play a role in the pathogenesis of acute renal failure developed in obstructive jaundice.
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PMID:The role of oxygen free radicals in acute renal failure complicating obstructive jaundice: an experimental study. 951 37

Results of clinical study of 87 biliary sepsis patients and experimental study on 54 rats with obstructive jaundice and cholangitis are presented. Own and literary data are compared. Specific immune and portal haemodynamic changes, provoced by obstructive jaundice are main pathogenic factors defining specific course of biliary sepsis. These changes are: 1) gut bacterial and endotoxin translocation, portal endotoxaemia; 2) reduction of RES and Kupfer cell function and endotoxin break into the systemic circulation; 3) liver parenchyma ischemia and milliary abscess formation; 4) portal blood flow shunting into the general circulation additionally increasing systemic endotoxaemia. These factors determine rapid, even fulminate development of milliary abscesses of the liver and multiorganic failure. The authors suggest that etiologic and pathogenic factors, causing peculiarities of the clinical course should be indicated in the diagnosis of septic patient.
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PMID:[Biliary sepsis: some peculiarities of pathogenesis]. 1054 May 49

The appropriate treatment for extrahepatic hepatic artery aneurysms remains controversial, with arguments for and against embolization. We describe a case of a giant true aneurysm of the common hepatic artery associated with obstructive jaundice of nonhemobilia origin. The patient, a 49-year-old previously healthy man, presented with upper midepigastric pain, jaundice, and low-grade fever. The diagnosis of the aneurysm was mainly based on computed tomography scan findings. The aneurysm was successfully embolized using wire coils, and the patient was operated on for acute abdomen. Necrotizing acalculus cholecystitis was found, and cholecystectomy followed by aneurysmectomy without hepatic artery reconstruction was performed. The jaundice subsided spontaneously, and the patient was discharged in good condition. Giant common hepatic artery aneurysms can be managed by either surgery or embolization. In the absence of liver ischemia there is no need for common hepatic artery reconstruction unless a bilioenteric bypass has to be performed to resolve the issue of jaundice. If the latter is required, reconstruction of the hepatic artery might be justifiable to maximize the blood supply to the bile duct.
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PMID:True giant common hepatic artery aneurysm associated with obstructive jaundice: a case report. 1240 87

Idiopathic retroperitoneal fibrosis (IRF), usually affects the ureter, although the biliary tree, duodenum and vasculature may also be susceptible. This case report describes a 64-year-old man with IRF, who presented painless watery diarrhea, radiological features of obstructive jaundice and duodenal obstruction, and ultimately an obstruction of the inferior vena cava. We employed tamoxifen for his treatment, but the disease progressed and the patient died of multiple organ failure two years after the onset. While the cause of IRF in this patient was obscure, we suspected his painless watery diarrhea indicated chronic ischemia of the small bowel, and the findings of an abdominal CT scan were extremely valuable in indicating IRF.
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PMID:A rare case of idiopathic retroperitoneal fibrosis involving obstruction of the mesenteric arteries, duodenum, common bile duct, and inferior vena cava. 1451 67

Temporary portal triad clamping (Pringle maneuver) during liver resection reduces intraoperative blood loss. A normal liver can safely tolerate normothermic ischemia for up to 60 min. However, its safety in patients with surgical obstructive jaundice (SOJ) is not known. Therefore, we investigated the effect of hepatic ischemia in an experimental rat model of SOJ created by ligating the bile duct. Four groups of rats were created: Group I (sham operation, 10 days later, liver resection); Group II (sham operation, 10 days later, liver resection with 5 min of hepatic ischemia); Group III (bile duct ligation, 10 days later, liver resection); and Group IV (bile duct ligation, 10 days later, liver resection with 5 min of hepatic ischemia). The ischemic injury was assessed by the survival of rats, liver tissue malondialdehyde and total glutathione (markers of free radical injury), serum alanine aminotransferase, aspartate aminotransferase, and liver histology. The results showed decreased survival (47.6% vs. 90% [p = .046]), increased liver tissue malondialdehyde (161 +/- 35 vs. 129 +/- 33 microg/gm liver tissue [p = .05]), and decreased liver tissue total glutathione (565 +/- 169 vs. 1075 +/- 276 nmol/gm liver tissue [p = .05]) in rats with SOJ subjected to hepatic ischemia when compared to nonjaundiced rats. The changes in serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase showed an increasing trend in the SOJ group but were not statistically significant. Ischemic changes in liver histology were seen more often in the SOJ group but were not statistically significant. These data suggest that temporary portal triad clamping in an experimental model of SOJ is detrimental to the outcome of liver resection.
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PMID:Evaluation of Pringle maneuver during liver resection in a rat model of surgical obstructive jaundice. 1603 81

Portal biliopathy (PB) is a term used to describe biliary ductal and gallbladder wall abnormalities seen in patients with portal hypertension. The pathogenesis of PB is not well known. It has been postulated that external pressure of portal cavernoma and/ or ischemia may play a role. We report a case of a patient with PB presenting with obstructive jaundice that involved endoscopic sphincterotomy and stenting.
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PMID:Portal biliopathy in a 13-year-old Asian girl: a case report and review of literature. 1988 97


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