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)

At present in vivo NMR spectroscopic studies of brain glutamate and glutamine concentrations relative to encephalopathy have mainly been performed in hepatic encephalopathy (HE). In vivo proton NMR studies were performed in rats with hyperammonemia and acute HE due to acute liver ischemia as well as in rats with hyperammonemia due to either repeated urease i.p. injection or i.p. administration of methionine sulfoximine, a well known inhibitor of glutamine synthetase. In man, in vivo proton NMR is described in patients with chronic liver disease: cirrhosis of different etiology and associated with different degrees of HE. In the experimental models proton NMR spectroscopy of the cerebral cortex revealed an increase in glutamine concentration, a decrease in glutamate concentration and a decrease in phosphocholine compounds. In humans no clear distinction between cerebral cortex glutamate and glutamine concentration could be made by in vivo 1H NMR spectroscopy. However, the combined glutamate/glutamine peak increased in a way compatible with an increased cerebral cortex glutamine concentration during chronic HE. In the cirrhotic patients too a decrease in cerebral cortex phosphocholine compounds was observed, the explanation of which is unclear. Both the experimental work and the clinical observations support the hypothesis that impairment of the glutamate/glutamine cycle between astrocytes and neurons plays a role in the pathogenesis of hepatic encephalopathy.
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PMID:What the clinician can learn from MR glutamine/glutamate assays. 167 85

The metabolism of methanethiol was studied in rats. Administration of a noncomatogenic dose of methanethiol through inspired air or injection into the upper colon resulted in an elevation of the concentrations of methanethiol mixed disulfides in serum (protein--S--S--CH3 and X--S--S--CH3, X yet unknown) and in urine (X--S--S--CH3). The concentrations of methanethiol mixed disulfides proved to be a relative measure of exposure to methanethiol. The levels of volatile sulfur compounds methanethiol, dimethylsulfide and dimethyldisulfide in the air expired by rats exposed to a noncomatogenic dose of methanethiol through the colon were also elevated. Rats with acute hepatic encephalopathy caused by liver ischemia also showed elevation of methanethiol mixed disulfide levels on challenge of methanethiol through the colon or inspired air, but to a significantly smaller extent than did the corresponding sham-operated rats. This suggests that the liver is at least partly responsible for formation of methanethiol mixed disulfides. No additional toxic effects were observed in the rats with ischemic livers on methanethiol exposition when compared with normal rats, suggesting that the liver does not play an essential role in methanethiol detoxification. Metabolism of methanethiol by blood to sulfate, for example, might be more important. In rats with acute hepatic encephalopathy caused by liver ischemia and in dogs suffering from hepatic encephalopathy resulting from chronic liver disease, large and significant increases in ammonia levels were measured. However, the mean levels of methanethiol mixed disulfides in rats and dogs with hepatic encephalopathy were not different from the mean normal levels in these animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Methanethiol metabolism and its role in the pathogenesis of hepatic encephalopathy in rats and dogs. 232 60

We reviewed the clinical histories and autopsy records of 35 pediatric patients (ranging in age from 9 months to 18 years) who underwent orthotopic liver transplantation using ciclosporin and corticosteroids for immunosuppression. At the time of death, 19 children (54%) had encephalopathy, 16 (46%) were lethargic or in coma, 10 (29%) had seizures, and 10 were normal. Neuropathological lesions were found on postmortem examination in all 35 patients. Vascular lesions such as infarction, ischemia, thrombosis, and hemorrhage were the most common neuropathological findings (86%) followed by infectious processes (29%). Candida albicans (2 patients) and Aspergillus fumigatus (3 patients) were the only offending organisms identified, both causing meningoencephalitis. Alzheimer type II astrocytes, a characteristic feature of chronic liver disease, were the single most common autopsy finding (69%). Central pontine myelinolysis was seen in 3 children and basilar artery thrombosis affected 1 child. Neurological complications and their subsequent neuropathology are a significant cause of morbidity and mortality after pediatric liver transplantation. Vascular insults, electrolyte abnormalities, and infections that involve the central nervous system are directly related to liver function and the immunosuppression necessary to maintain graft viability. Only with continued observation after surgery combined with rapid medical and surgical treatment can we hope to improve the prognosis following liver transplantation in the pediatric population.
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PMID:Neuropathology of pediatric liver transplantation. 248 84

An increasing number of patients with severe liver dysfunction are admitted to the ICU for stabilization and organ-specific support, including liver transplantation. Global impairment of hepatic performance frequently results in pathologic organ interactions that limit the potential for recovery. One of the most notable of these interactions is the hepatorenal syndrome, an otherwise uniformly fatal complication of end-stage liver disease characterized by the progressive development of oliguria and low urine sodium excretion. The syndrome can occur in the setting of either acute or chronic liver disease, and portal hypertension may be important in the pathogenesis. The patient with the hepatorenal syndrome also has a number of systemic circulatory abnormalities induced by liver disease and/or portal hypertension, but the exact pathologic role of these abnormalities in the development of oliguria is uncertain. It is reasonably well established that diminished systemic BP characteristic of liver failure is not the primary cause of renal insufficiency. Rather, intrarenal preglomerular vasoconstriction mediated by unknown stimuli is the major defect in the hepatorenal syndrome, manifested by relative ischemia. Current data point to abnormal renal sympathetic innervation as one of the more likely major causes of this vasoconstriction. After exclusion of systemic intravascular volume depletion and other causes of oliguria, dialytic therapy is indicated when liver transplantation or recovery of liver function is anticipated; terminal supportive care is appropriate when these outcomes are not options.
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PMID:Organ interactions in the hepatorenal syndrome. 780 2

Endothelial injury occurs as a result of oxygen free radical production after ischemia and reperfusion of transplanted livers, causing hemodynamic disturbance. Patients with chronic liver disease generally have low levels of fat-soluble vitamins, which have important antioxidant roles. We therefore assessed circulating levels of the antioxidants vitamin A, vitamin E, beta-carotene and lycopene, indices of lipid peroxidation and hemodynamic changes during elective orthotopic liver transplantation in 12 patients. We found that initial antioxidant levels were severely depleted compared with healthy subjects, and in some patients carotene and lycopene levels were undetectable. Increased lipid peroxidation was also evident, as shown by thiobarbituric acid-reactive substances. On reperfusion of the liver graft, vitamin A and E levels fell (p < 0.01) and were associated with decreases in systemic vascular resistance (p < 0.02). These data show that patients undergoing liver transplant have lowered antioxidant defenses and evidence of free radical damage, which compound the additional insult of reperfusion injury. Antioxidant therapy in these patients before transplantation may ameliorate the effects of reperfusion.
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PMID:Reperfusion injury, antioxidants and hemodynamics during orthotopic liver transplantation. 829 93

Seventeen patients with chronic liver disease underwent prolonged warm ischemia of hemi-lobe during liver resection. Those included 15 cirrhotic patients and two with chronic hepatitis. The hemi-hepatic ischemia was carried out with a liver clamp. The normothermic liver ischemia time of 40 to 70 minutes (53.8 +/- 10.4 minutes, mean +/- SD) were tolerated well with an acceptable postoperative course and no mortality. The liver with cirrhosis or chronic hepatitis can tolerate a hemi-hepatic ischemia of up to 70 minutes for patients with no high-risk factors.
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PMID:Tolerance of chronically-diseased liver to prolonged hemihepatic ischemia during hepatectomy. 853 Feb 22

The incidence of hepatic artery thrombosis (HAT) following orthotopic liver transplantation in children varies from 4% to 26% and represents a significant cause of graft loss. The purpose of this study was to analyze the risk factors for HAT following liver transplantation in children less than 5 years old. Seventy-three transplants were performed in 62 children under 5 years of age, including 16 for acute hepatic failure, 46 for chronic liver disease, and 11 retransplants. Twenty-four whole liver grafts (WLG) and 49 reduced size grafts (3 right lobes, 16 left lobes, and 30 left lateral segments) were transplanted. The recipient common hepatic artery was used to provide arterial inflow in 22 transplants and an infrarenal iliac conduit in 51 transplants. The overall incidence of HAT was 8 out of 73 transplants (11%). The cold ischemia time (14.3 +/- 3.03 hr) in this group was significantly longer than the cold ischemia time for those without HAT (11.7 +/- 3.94 hr) (P = 0.049). The incidence of HAT for whole and reduced grafts was 25% (6/24) and 4% (2/49), respectively (P = 0.01). HAT occurred in 6 of 22 grafts (27.3%) revascularized from the recipient common hepatic artery, compared with 2 of 51 grafts (3.9%) using an infrarenal arterial conduit (P = 0.008). The combination of recipient hepatic arterial inflow to a WLG resulted in HAT in 50% (6/12), whereas there were no cases of HAT with an iliac conduit to a WLG (P = 0.01). Of the eight patients with HAT, five are alive (median follow-up, 20 months; range, 7-27 months). Five patients were retransplanted, three within the first 2 weeks and two at 4 and 5 months for abnormal liver function in association with clinical and histological features of chronic rejection. Prolonged cold ischemia time and use of a whole graft with recipient hepatic arterial inflow are risk factors for developing HAT. The use of reduced size grafts and infrarenal iliac arterial conduits are associated with a low incidence of HAT.
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PMID:Hepatic artery thrombosis after liver transplantation in children under 5 years of age. 862 96

The release of toxic oxidative free radicals induced by ischemia and reperfusion may jeopardize liver graft function. N-acetylcysteine (NAC) has shown protective effects on hypothermic and warm ischemia reperfusion liver injury in animals. NAC improves hemodynamics and survival rates in patients with fulminant hepatic failure. The aim of this study was to investigate whether intraoperative treatment with NAC would improve hemodynamics and postoperative graft function in liver transplantation. Sixty patients with chronic end-stage liver disease were included in a prospective randomized placebo-controlled study. NAC or the same volume of 5% glucose was started during the anhepatic phase. Hemodynamic data and calculated tissue oxygenation parameters were compared throughout the procedure. Postoperative graft function was assessed by measurements of aminotransferases, prothrombin time, and monoethylglycinexylidide test over the 3 first postoperative days. Patient demographics were similar before the infusion of NAC or glucose. Hemodynamic parameters, oxygen consumption, oxygen delivery, oxygen extraction ratio, and lactates were not different throughout the procedure. One hour after the revascularization of the hepatic artery, the oxygen extraction ratio by the liver was similar (17% +/- 7.6% v 17% +/- 6.2%) in both groups. Postoperative graft function was comparable within the 3 first postoperative days. This study failed to show any beneficial effect of the intraoperative administration of NAC on hemodynamics and graft function in liver transplantation in patients with chronic liver disease.
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PMID:Does N-acetylcysteine improve hemodynamics and graft function in liver transplantation? 951 68

This study was undertaken to evaluate whether topical cooling can alleviate ischemia/reperfusion injury, after continuous inflow occlusion during hepatectomy. Using a canine model of 70% partial liver ischemia (60 min), alteration in the subcellular (cytoplasm, mitochondria, nucleus) elements calcium, sodium, potassium, and chloride, and liver functions following reperfusion were compared between control livers and livers subjected to topical cooling down to 23 degrees +/- 4.9 degrees C by seeding ice slush over the ischemic lobe. The elements were determined by X-ray microanalysis using liver biopsy specimens. A similar clinical study was undertaken examining ten patients with hepatocellular carcinoma and chronic liver disease who underwent right-sided segmentectomy under continuous right inflow occlusion, five of whom were given topical cooling and five of whom were not. In the experimental study, postreperfusion worsening of liver function tests was significantly suppressed in the cooling group, which was associated with the suppression of subcellular Ca, Na, and Cl increases and K decreases after reperfusion. In the clinical study, the occlusion time was significantly longer in the hypothermic patients than in the normothermic patients, but no significant differences in postoperative liver function or postischemic increases in Ca, Na, or Cl and decreases in K were observed. These experimental and clinical findings suggest that topical cooling alleviates ischemic insult and enhances safe prolonged inflow occlusion.
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PMID:Does topical cooling alleviate ischemia/reperfusion injury during inflow occlusion in hepatectomy? Results of an experimental and clinical study. 1103 7

The present paper summarizes the various themes of research which have been developed in the department of medical gastroenterology since it was created in 1977. These include: in pancreatology, the study of chronic pancreatitis pathogenesis, acute pancreatitis pathogenesis and immunomodulation, endoscopic treatment of chronic pancreatitis, the development of new imaging techniques of the bile ducts and the pancreas, as well as the treatment of pancreatic cancer and benign or malignant biliary diseases. in hepatology, the immunomodulation of liver cirrhosis, especially alcoholic liver disease, the modulation of experimental acute and chronic hepatitis, the study of liver ischemia-reperfusion. Clinical hepatology has focused on liver transplantation, prognosis factors of chronic liver disease and treatment of portal hypertension and viral hepatitis. in gut diseases, the treatment of gastro-oesophageal reflux and its complications, the therapeutic endoscopy of the upper and lower GI and the prevention, as well as the treatment, of colon cancer, the pathogenesis and the immunopharmacology of inflammatory bowel diseases and the clinical enteral and parenteral nutrition.
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PMID:[The medical gastroenterology department]. 1258 14


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