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

Changes in biochemical and electroencephalographic parameters were followed over time during the development of acute hepatic encephalopathy (HE) in two different experimental models. In the rat, (sub)acute liver failure was obtained either by ligation of the hepatic artery in previously portacaval-shunted animals or by intraperitoneal injection of a high dose of galactosamine (GALN). The EEG changes were characterized in both models by a significant increase in low-frequency activity of the EEG power density spectra: the so-called 'left shift'. This 'left shift' was significant in liver ischemia after 4-5 h and in GALN hepatitis after about 30 h. The changes in plasma biochemical indices also showed a great similarity in both models. The concentration of all measured plasma amino acids (except histidine and arginine in GALN hepatitis and arginine in liver ischemia), NH3 and ALAT were significantly increased during the development of (sub)acute HE. Correlation of the combined data of electroencephalographic and biochemical indices showed a significant (P less than 0.01) correlation between the 'left shift' and NH3, taurine, threonine, proline, alanine, methionine, cystathionine, phenylalanine, tryptophan, ornithine and histidine. It is concluded that EEG spectral analysis is a useful parameter for following the development of (sub)acute hepatic encephalopathy in relation to biochemical parameters.
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PMID:Correlation between electroencephalographic and biochemical indices in acute hepatic encephalopathy in rats. 359 63

The incidences of endotoxemia and bacteremia were evaluated in 30 pigs with ischemic hepatic necrosis treated by hemodialytic procedures. Prior to induction of hepatic ischemia, ten pigs underwent bowel cleansing by means of an oral dose of magnesium sulfate, and 20 received a combination of magnesium sulfate and lactulose. Endotoxemia and bacteremia seldom occurred during the development of hepatic encephalopathy, but the incidence of both increased markedly shortly before death. Pigs pretreated with magnesium sulfate and lactulose however did not develop preterminal endotoxemia. A significant relation between endotoxemia or bacteremia and survival was not found, irrespective of pretreatment with lactulose. Of the positive limulus tests, 67% were accompanied by a positive blood culture, while 42% of all positive blood cultures were associated with a positive limulus test. Dialysis with dialysates contaminated with endotoxins did not increase the risk of endotoxemia. It is concluded that in an animal model of ischemic hepatic necrosis (1) endotoxemia and bacteremia appear mainly in the preterminal stage, but do not influence the duration of survival significantly; (2) lactulose prevents endotoxemia and (3) dialytic procedures do not increase the risk of endotoxemia and bacteremia.
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PMID:Incidence of endotoxemia in pigs with ischemic hepatic necrosis treated by hemodialysis. Prevention of endotoxemia with lactulose. 667 44

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

The aim of this study was to investigate the possible role of N-methyl-D-aspartate (NMDA)-receptor overactivity in two different experimental rat models of encephalopathy: subacute encephalopathy caused by severe hyperammonemia in portacaval-shunted rats (AI-PCS rats) and acute hepatic encephalopathy caused by complete liver ischemia (LIS rats). The effect of the noncompetitive NMDA-receptor antagonist memantine (intraperitoneal [i.p.] 10-20 mg/kg bw or intravenous [i.v.] 5 mg/kg bw) was studied on the severity of encephalopathy by assessment of clinical grading and electroencephalogram (EEG) spectral analysis, on plasma ammonia concentrations, amino acid concentrations in cerebrospinal fluid (CSF), intracranial pressure (ICP), and brain water content. Both rat models developed encephalopathy within 3 to 6 hours, associated with increased CSF glutamate and aspartate concentrations and increased ICP and brain water content. Memantine administration in AI-PCS and LIS rats resulted in a significant improvement in clinical grading and less slowing of EEG activity (P < .05), and smaller increases in CSF glutamate (P < .05) concentrations. Moreover, ICP and brain water content were significantly lower in memantine-treated AI-PCS rats than in untreated AI-PCS rats (P < .05). Memantine had no significant effect on ICP and brain water content in LIS rats, and on ammonia concentrations in both models. These results indicate that NMDA-receptor activation might be involved in the pathogenesis of hyperammonemia-induced encephalopathy and of acute hepatic encephalopathy caused by LIS.
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PMID:Memantine, a noncompetitive NMDA receptor antagonist improves hyperammonemia-induced encephalopathy and acute hepatic encephalopathy in rats. 909 16

The basic principles of proton MR spectroscopy as well as newer and more advanced related techniques are reviewed. Spectroscopy is capable of differentiating normal from pathologic brain and provides tissue specificity greater than that of imaging in many instances. Spectroscopic mapping allows for the visualization of the concentration of different metabolites and their distribution within a lesion. This article emphasizes the utility of proton MR spectroscopy in the diagnosis of brain tumors, postradiation therapy changes, infections, degenerative brain disorders, hepatic encephalopathy, ischemia, and demyelination.
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PMID:Proton MR spectroscopy in neoplastic and non-neoplastic brain disorders. 944 37

The purpose of this study was to investigate whether the efficacy of our novel extracorporeal bioartificial liver (BAL) to support rats with complete liver ischemia (LIS) could be improved by extending the culture time of freshly isolated porcine hepatocytes from 14 hours to 38 hours. The results showed that survival as well as porcine hepatocyte integrity improved, the onset of coma delayed, and the ammonia levels decreased in LIS rats of the 38 hour group compared to the 14 hour group, but no statistically significant differences were observed. In the 38 hour group, but not the 14 hour group, the onset of hepatic encephalopathy was significantly delayed and ammonia metabolism significantly improved compared to the LIS rats in control groups that only received a glucose infusion or were connected to a BAL without cells. In conclusion, prolonged hepatocyte recovery favoured all investigated parameters, although not all observed effects were statistically significant. More research is required to find out how long primary hepatocytes should be cultured in a bioreactor for optimal BAL support.
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PMID:Does the extend of the culture time of primary hepatocytes in a bioreactor affect the treatment efficacy of a bioartificial liver? 982 60

A 73-year-old man recurring hepatic encephalopathy due to a congenital splenorenal shunt concomitant with early gastric cancer was successfully treated by surgical intervention. The portal pressures before and after the shunt resection were 13.5 and 18 cm H2O, respectively. The liver was slightly atrophic and the histological specimen showed slight fibrosis and mild infiltration of lymphocytes in the portal area. After the operation, the encephalopathy was improved and the several factors of liver function also recovered. Interestingly, the liver volume estimated by abdominal CT clearly increased 1 month after the shunt resection. The encephalopathy in congenital portosystemic shunt might result from chronic liver ischemia and atrophy. Moreover, the shunt resection may enlarge the functional liver volume by increasing the portal blood flow.
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PMID:Resection of spleno-renal shunt resulting in enhanced liver volume in a patient with congenital portosystemic shunt concomitant with early gastric cancer. Review of Japanese cases. 1124 65

Fulminant hepatic failure (FHF) is an acute and eventually fatal illness, caused by a severe hepatocyte damage with massive necrosis. Its hallmarks are hepatic encephalopathy and a prolonged prothrombin time (< 40%). FHF is currently defined as hyperacute (encephalopathy appearing within 7 days of the onset of jaundice), acute (encephalopathy appearing between 8 and 28 days) or subacute (encephalopathy appearing between 5 and 12 weeks). FHF can be caused by viruses, drugs, toxins, and miscellaneous conditions such as Wilson's disease, Budd-Chiari syndrome, ischemia and others. However, a single most common etiology is still not defined. Factors that are valuable in assessing the likelihood of spontaneous recovery are age, etiology, degree of encephalopathy, prothrombin time and serum bilirubin. The management is based in the early treatment of infections, hemodynamic abnormalities, cerebral edema, and other associated conditions. Liver transplant has emerged as the most important advance in the therapy of FHF, with a survival rate that ranges between 60 and 80%. The use of hepatic support systems, extracorporeal liver support and auxiliary liver transplantation are innovative therapies.
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PMID:[Fulminant hepatic failure]. 1219 94

Hepatic encephalopathy may occur following acute hepatic failure (AHF), which results in the release of toxic compounds from the injured liver. These compounds, which induce cerebral edema, are not well characterized, yet. The aim of this study was to evaluate the potential interest of NMR spectroscopy in the follow-up of different plasma compounds in pigs with ischemia-induced fulminant hepatic failure treated or not with a bioartificial liver (BAL), which has been previously shown to improve the neurological status of the animals. Qualitative analysis of pig plasma was achieved by one-dimensional-(1)H CPMG, two-dimensional homonuclear (1)H-(1)H TOCSY CPMG and heteronuclear (1)H-(13)C HSQC sequences. Semi-quantitative analysis of selected plasma metabolites along the disease evolution was carried out on pigs with ischemia-induced AHF treated with the BAL containing alginate beads with or without hepatocytes. A quantitative longitudinal follow-up was performed on characteristic metabolites via a one-dimensional CPMG sequence, including choline, glutamine, N-acetyl-glucosamine (NAG), pyruvate and trimethylamine-N-oxide (TMAO). The concentrations of choline and TMAO increased from the beginning to the end in animals treated with the BAL containing alginate beads without hepatocytes. Treatment of pigs with BAL containing hepatocytes resulted in an improvement of survival, the plasma concentrations of choline and TMAO being decreased in three out of five animals. Thus, NMR spectroscopy is a useful approach for the identification of toxic compounds which are involved in hepatic encephalopathy associated with AHF. These compounds can be cleared by a BAL resulting in the improvement of survival and neurological parameters of the animals.
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PMID:Follow-up by one- and two-dimensional NMR of plasma from pigs with ischemia-induced acute liver failure treated with a bioartificial liver. 1235 53

Hereditary hemorrhagic telangiectasia (HHT), also known as Osler-Weber-Rendu disease, is an hereditary disorder that results in fibrovascular dysplasia with the development of telangiectasias and arteriovenous malformations. It predominantly involves the skin, mucous membranes, viscera, lungs, and brain. Hereditary hemorrhagic telangiectasia shows great genetic heterogeneity, and its phenotypes have been classified based on the recently identified mutated genes: endoglin (HHT-1) and activin-like kinase receptor-1 (HHT-2). Other families with phenotypic HHT do not bear these mutations; therefore, other genes are probably involved as well. Liver involvement is reported in up to 30% of persons affected by HHT. Large arteriovenous malformations in the liver can lead to significant complications, including high-output congestive heart failure, portal hypertension, hepatic encephalopathy, biliary ischemia, and liver failure. Embolization of large arteriovenous malformations in the liver remains controversial; however, liver transplantation can successfully eradicate these complications.
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PMID:Liver disease in hereditary hemorrhagic telangiectasia. 1254


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