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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary arterio-venous shunts represent a rare cause of hypoxia in cirrhosis. We present two cases, the first was an alcoholic cirrhotic with anthracosilicosis. This patient rapidly developed a picture of significant hypoxaemia with a raised alveolar-arterial oxygen gradient. The presence of this shunt was confirmed by a scintigraphic analysis. A porto-pulmonary localisation was excluded by a changing angiographic picture. Death supervened after refractory hypoxaemia. Post mortem microangiographic studies confirmed the pulmonary nature of the shunt and its pre-capillary localisation. The second patient was alcoholic, with a compensated cirrhosis and developed severe hypoxaemia which progressed to death in less than two months, when he was being treated effectively with corticosteroids for a diffuse interstitial pulmonary fibrosis confirmed histologically. The pulmonary localisation of the shunt was confirmed by an analysis of the angioscintigraphs. The different techniques for the investigation of intra-pulmonary shunt are discussed, as well as the patho-physiological mechanisms involved. The hormone levels measured (sex hormones, serotonin, prostaglandins, intestinal hormones) remained normal. The therapeutic trials tried out (oestrogen, CPD Choline, indomethacin) were ineffective.
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PMID:[Technics for the exploration of pulmonary arteriovenous shunts in liver cirrhosis. Apropos of 2 cases]. 374 86

To differentiate between the "intact" and "sick" cell hypothesis explaining decreased clearance of endo- and xenobiotics, we measured uptake of taurocholate and ouabain in hepatocytes isolated from cirrhotic rat liver. Cirrhosis was induced by chronic exposure of male Sprague-Dawley rats to phenobarbital and carbon tetrachloride. Uptake of [14C]taurocholate and [3H]ouabain was measured by a rapid filtration technique. Hepatocytes from cirrhotic liver were as viable as control hepatocytes--as judged by trypan blue exclusion and lactate dehydrogenase release--but consumed 28% less oxygen. Vmax of both taurocholate (3.16 +/- 0.95 vs. 0.40 +/- 0.35 nmoles X min-1 X 10(6) cells-1; p less than 0.001) and ouabain (2.16 +/- 0.78 vs. 0.83 +/- 0.26 nmoles X min-1 X 10(6) cells-1; p less than 0.005) was significantly reduced. These results are compatible with the "sick" cell hypothesis.
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PMID:Decreased uptake of taurocholate and ouabain by hepatocytes isolated from cirrhotic rat liver. 380 7

The authors have refined a model of cirrhosis in the rat and used it to determine whether the administration of halothane anesthesia adversely affects preexisting liver disease. Male Wistar rats were placed on phenobarbital water and were assigned randomly to two groups. Group 1 rats were exposed by inhalation to carbon tetrachloride (CC14) at weekly intervals for 12 exposures while Group 2 rats received only air. All treatment including phenobarbital then was withdrawn for 4 weeks. Rats then were bled for SGOT and SGPT determinations and 24 h later were exposed to 1.8% halothane in oxygen for 3 h (HAL); the remaining rats from each group were exposed to 100% oxygen for 3 h (O2). Twenty-four hours later, rats were killed and blood was obtained for SGOT and SGPT by cardiac puncture. Light microscopic histologic examination was performed blind on liver sections for cirrhosis and scored for superimposed acute focal necrosis. The weekly sublethal CCl4 exposure resulted in histologically demonstrable cirrhosis in all surviving Group 1 animals. The mean (+/- SD) SGOT (128 +/- 32 IU/1) and SGPT (86 +/- 24 IU/1) values for the Group 1 rats were significantly greater (P less than 0.01) than those for Group 2 rats (98 +/- 18 IU/1 and 57 +/- 12 IU/1, respectively). Cirrhotic animals showed neither deterioration in liver function nor acute liver cell necrosis after Hal compared with O2. However, Group 2 rats showed a modest but significant increase in SGOT (P less than 0.05) after HAL, while this change was not noted after O2. Thus, 1.8% halothane anesthesia in oxygen did not result in superimposition of acute liver cell injury in already cirrhotic rats.
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PMID:Halothane anesthesia does not exacerbate hepatic dysfunction in cirrhotic rats. 396 63

A new quantitative method for measuring the prognosis and severity of illness in terms of probability of survival was developed from 224 studies in an index population of 220 critically ill surgical patients. Patients were selected preoperatively to eliminate pre-existing cardiac disease, cirrhosis, nutritional debility, shock or sepsis, in order to evaluate the physiologic relationships of surgical trauma to outcome free of confounding associated medical disorders. The empirically derived numeric severity index was calculated from the probability of survival for each of 28 hemodynamic and oxygen transport variables at each time period after surgery. The score correctly indicated patient outcome in 96% of the index population and 94% of an independent, prospective population. The survivors' score consistently predicted survival within 21.6 +/- 4.4 (SEM) h after the end of surgery. The severity score of those who died consistently predicted nonsurvival within 37 +/- 11 (SEM) h after the end of surgery. We conclude that the score provides a useful, objective, physiologic measure of the severity of illness and prognosis.
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PMID:Probability of survival as a prognostic and severity of illness score in critically ill surgical patients. 396 10

The chemiluminescence level and superoxide dismutase (SOD) activity were determined in the plasma of patients with alcoholic and non-alcoholic liver injuries. Chemiluminescence level was significantly higher in alcoholics than in non-alcoholics. It increased significantly in patients with fatty livers and had a tendency to increase with the progression of alcoholic liver injury from a fatty liver to liver cirrhosis. Mn-SOD activity was elevated in patients with alcoholic liver injuries. Furthermore, there was a positive correlation between the levels of plasma chemiluminescence and plasma Mn-SOD activity. The increases in chemiluminescence and Mn-SOD activity suggests that the generation of a large amount of activated oxygen is associated with the pathogenesis and progression of alcoholic liver injury in humans.
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PMID:Chemiluminescence and superoxide dismutase in the plasma in patients with alcoholic and non-alcoholic liver injuries. 402 67

Halothane, enflurane, isoflurane, and fentanyl were examined for their potential to exacerbate liver dysfunction in rats with preexisting cirrhosis. Male Wistar rats given sodium phenobarbital for 2 weeks are assigned randomly to two groups. One group (cirrhotic) was exposed by inhalation to carbon tetrachloride (CCl4) in air at weekly intervals for 12 weeks to induce cirrhosis. The other group (noncirrhotic) was handled similarly but received air only. Five weeks after the last exposure to CCl4, cirrhotic and noncirrhotic rats were given three hours of 1 MAC halothane, enflurane, or isoflurane in 50% oxygen, or 350 micrograms fentanyl per kg of body weight and 50% oxygen, or 50% oxygen only. Blood gas tensions and blood glucose levels were measured before, during, and at the end of exposure. Forty-eight hours after exposure, serum chemistries were measured in each rat for comparison with preexposure values. Rats were then killed by CO2 overdose, and liver, kidney, and testis were prepared for microscopic examination. Enflurane, isoflurane, and halothane, but not fentanyl, produced mild respiratory acidosis and no change in serum glucose levels. All anesthetics resulted in a mild but similar degree of acute liver dysfunction as indicated by small increases in SGOT or SGPT in both cirrhotic and noncirrhotic rats. Liver histology revealed mild to moderate portal cirrhosis with fibrosis and well-developed micronodules in rats exposed to CCl4, but no superimposed acute hepatocellular damage was noted. It is concluded that all the anesthetics used in this study were associated with the same minimal degree of postanesthetic hepatic dysfunction and that the dysfunction was similar in both cirrhotic and noncirrhotic rats.
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PMID:Effects of volatile anesthetics or fentanyl on hepatic function in cirrhotic rats. 406

The cerebro-hepato-renal syndrome is a rare familial malady with cerebral, renal, and skeletal abnormalities, severe hypotonia, cirrhosis, iron and lipid storage, and death within 6 months. Correlated electron microscopic, histochemical, and biochemical studies demonstrate defects in two oxidative organelles. Peroxisomes cannot be found in hepatocytes and renal proximal tubules. In hepatocytes and cortical astrocytes, mitochondria are distorted in their appearance and glycogen stores are increased. Oxygen consumnption of brain and liver mitochondrial preparations with succinate and with substrates reducing nicotinamide adenine dinucleotide is markedly diminished, but the consumption is normal with ascorbate and tetramethylphenylenediamine, which suggests a defect in electron transport prior to the cytochromes. Histochemical studies of mitochondrial oxidation point to a defect between the succinate dehydrogenase flavoprotein and coenzyme Q, possibly in the region of nonheme iron protein.
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PMID:Peroxisomal and mitochondrial defects in the cerebro-hepato-renal syndrome. 473 55

The combination of arterial hypoxemia and low pulmonary vascular resistance in patients with liver cirrhosis is unexplained. Pulmonary microcirculatory dilation, but not gross arterio-venous shunts, has been the usual postmortem finding in patients with liver cirrhosis. When 10 patients with alcoholic liver cirrhosis breathed 10% oxygen in nitrogen, they failed to increase their pulmonary vascular resistance. However, four patients with functional murmurs, three patients with hyperkinetic heart syndrome, six patients with normal pulmonary artery pressures and intracardiac left to right shunts, and five patients with renal failure and anemia all increased their pulmonary vascular resistances when they breathed 10% oxygen in nitrogen. These findings suggested that in liver cirrhosis the normal regulating mechanism (hypoxic vasoconstriction) of the pulmonary circulation may be impaired, resulting in failure of the lung to match perfusion with ventilation.
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PMID:Failure of hypoxic pulmonary vasoconstriction in patients with liver cirrhosis. 505 27

It has been demonstrated that cardiac output and pulmonary, gastroduodenal, pancreatic, and splenic blood flow increases after portacaval shunt operations. This report concerns a study of cerebral haemodynamics and metabolism in eight patients with cirrhosis of the liver, examined both before and after portacaval surgical anastomosis. The patients were fully alert and orientated to mental and neurological examination at all times. In each subject the cerebral blood flow, cerebral vascular resistance, cerebral metabolic rate of oxygen and of glucose, and glucose/oxygen quotient were determined. This investigation showed that a portacaval shunt operation is followed by a significant increase in the cerebral blood flow and a significant decrease in the cerebral vascular resistances. No important variation in the cerebral metabolic rate of oxygen was observed, but both the cerebral metabolic rate of glucose and the glucose: oxygen quotient showed significant increases. The presence of toxic substances which, shunting the liver, enter the general circulation could be the cause of the increased cerebral blood flow, while the increase in the cerebral metabolic rate of glucose could result from a greater cerebral detoxication, for example, the cerebral synthesis of glutamine.
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PMID:Cerebral blood flow and metabolism in hepatic cirrhosis before and after portacaval shunt operation. 535 80

1. The influence of ethanol on the metabolism of perfused livers from normal rats and rats in various stages of development of dietary cirrhosis was studied. A choline-deficient, low-protein and high-fat diet was used. Results were obtained on oxygen consumption and carbon dioxide production, on glucose release and uptake by the liver and on changes in the concentrations of lactate and pyruvate and of beta-hydroxybutyrate and acetoacetate in the perfusion medium. 2. Oxygen consumption and carbon dioxide production were lower in fatty and cirrhotic livers than in normal livers. Ethanol had no effect on the oxygen consumption of any of the various livers. After addition of ethanol to the perfusion medium carbon dioxide production ceased almost completely in normal livers. Only a slight decrease in the carbon dioxide production occurred in fatty and cirrhotic livers. 3. With every type of liver glucose was released from the liver into the perfusion medium during the initial control period. This release continued after the addition of ethanol to the perfusion medium in experiments with normal and fatty livers, whereas with cirrhotic livers a marked uptake of glucose from the medium was found. A simultaneous release of the glycolytic end products lactate and pyruvate into the medium occurred. 4. The production of ketone bodies was equal in normal and early fatty livers (6 weeks on the fat diet). It was smaller in late fatty livers (3-4 months on the fatty diet) and in cirrhotic livers. 5. The lactate/pyruvate concentration ratio in the perfusion medium increased from 11 to 67 with normal livers, from 12 to 16 with early fatty livers, from 13 to 26 with late fatty livers and from 21 to 55 with cirrhotic livers when the livers were perfused with a medium containing ethanol. The beta-hydroxybutyrate/acetoacetate concentration ratio increased from 1.2 to 8.4 in normal livers, from 2.0 to 2.8 in early fatty livers, from 1.2 to 2.4 in late fatty livers and from 2.1 to 4.0 in cirrhotic livers when ethanol was added to the medium. 6. The effects of ethanol on liver metabolism during the development of dietary cirrhosis are discussed and related to human fatty liver and cirrhosis during chronic ethanol consumption.
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PMID:Influence of ethanol on the metabolism of perfused normal, fatty and cirrhotic rat livers. 596 89


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