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

In 15 patients with cirrhosis of the liver, the pressures in a systemic artery, in the inferior vena cava and the portal vein, flows in the portal vein and the hepatic artery, and oxygen content and acid-base balance in the arterial, portal and hepatic venous blood were studied during operation before and after the construction of an end-to-side portacaval shunt. Portal pressure decreased from 23 to 13 millimeters of mercury. Portal flow increased from 660 mililiters per minute to the liver to 1,300 milliliters per minute through the shunt. Hepatic arterial flow increased from 230 to 480 milliliters per minute, but this did not fully compensate for the loss of portal blood flow to the liver. Accordingly, total hepatic blood flow was reduced. There was also a decrease in the oxygen transport to the liver, but in spite of this, there was no change in the oxygen content in the hepatic vein nor any production of acid metabolites. Possible implications of these findings on the preoperative investigation of patients with portal hypertension are discussed.
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PMID:Immediate changes in blood flow and oxygen metabolism of the cirrhotic liver following portacaval shunt operations. 84 2

In 17 patients with cirrhosis of theliver and in 11 controls the pulmonary diffusing capacity for CO (DLCO) was determined at three different levels of alveolar oxygen tensions. The diffusing capacity of the alveolar membrane (DMCO) and the intra-pulmonary capillary volume (VC) were calculated following the formula given by Roughton and Forster. The following results were obtained: 1) Both DLCO and DMCO were lower (p less than 0,01) in the patient group than in the controls. 2) VC showed larger variations in thepatient group than in the controls (p less than 0,01). The mean values did not differ, however. 3) There was a significant linear correlation (p less than 0,001) between DM and 1/VC in the patient group (DM and VC in % of the predicted value). The results suggest, that a change in the configuration of the capillary bed may be responsible for the transfer defect found in cirrhosis.
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PMID:[Diffusion disorders in patients with liver cirrhosis]. 96 81

In 5 patients with liver cirrhosis the measured pulmonary diffusing capacity for oxygen (DLo2) was related to the diffusing capacity of the pulmonary membrane (DM) and to the volume of blood in the pulmonary capillary bed (Vc) as estimated from the measured pulmonary blood flow (Qc) and the value of the presumptive transit time. DL and DM were found to be diminished in 4 of the 5 cases, DM being only once 1,7 times greater than DL. The relationship between the resistance of the red blood cells to diffusion and the resistance of the pulmonary membrane to diffusion (see journal for formula) ranged between 5 and 35% indicating that the resistance of the pulmonary membrane to the uptake of O2 was of greater importance than the resistance of the red cells. A correlation was found to exist between D/Q and DM/ThetaVc (diffusing capacity/blood flow and membrane diffusing capacity/diffusing capacity of the red cells in the pulmonary capillary bed). The possible site and nature of the diffusion defect is discussed.
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PMID:Analysis of factors determining the resistance to diffusion in patients with liver cirrhosis. 111 69

In two groups of patients with liver cirrhosis and normal EEG (Group A) and with pathological EEG (Group B) it was possible to demonstrate a correlation between the severity grade of the EEG changes, the livertypical deviations of serum chemistry and alterations in cerebral oxidative metabolism. The metabolism of the brain showed a reduced oxygen consumption and carbon dioxide output in the patients with pathological EEG changes. All patients showed a raised glucose uptake, an increased lactate release, a raised ammonia uptake and glutamine output. These findings in patients with liver cirrhosis indicate a disturbance of the oxidative energy metabolism of the brain with secondary intensification of glycolysis. Pathological changes in the EEG only appear if the oxygen consumption of the brain is limited (as in the patients of Group B). These EEG changes have a poor prognosis in respect to life expectancy. With consideration of the data from animal experiments and the reported results of cerebral blood flow and oxydative metabolism in patients with liver cirrhosis it might be assumed that liver insufficiency with elevated serum ammonia results in a deranged oxydative cerebral metabolism which might explain hepatic encephalopathy.
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PMID:Comparative studies of the electroencephalogram and the cerebral oxidative metabolism in patients with liver cirrhosis. 120 68

In patients with cirrhosis the renal response to amino acid infusion is controversial. In addition, the renal and systemic metabolic effects of amino acids are unknown. Therefore, the present study examined the effects of amino acids on renal hemodynamics, renal and systemic oxygen (O2) consumption, and hormones in patients with cirrhosis. Twelve patients received an 8% amino acid solution for 30 minutes at a rate providing 250 mg of amino acids/kg body wt. Renal blood flow increased by 45% (P less than 0.05) and the glomerular filtration rate by only 9% (P greater than 0.05). Renal vascular resistance decreased by 23% (P less than 0.05), and renal perfusion pressure did not change significantly. Renal and systemic O2 consumption and pulmonary artery plasma glucagon level significantly increased. There were no significant changes in plasma osmolality, plasma volume, and plasma atrial natriuretic peptide concentrations. In conclusion, the results show that amino acid-induced renal vasodilation caused hyperperfusion but not renal hyperfiltration in patients with cirrhosis. In addition, renal hyperemia was associated with renal and systemic hypermetabolism.
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PMID:Hemodynamic, neurohumoral, and metabolic responses to amino acid infusion in patients with cirrhosis. 850 Jul 52

In patients with cirrhosis, it has been shown that abnormal systemic and splanchnic hemodynamics and systemic oxygen (O2) consumption are related to the severity of liver disease. Little is known on the relationship between the severity of cirrhosis, on one hand, and renal hemodynamics and O2 consumption, on the other. We measured renal hemodynamics and renal O2 consumption in 31 patients Pugh's grade A and B and in 13 patients grade C. Systemic and splanchnic hemodynamics as well as systemic O2 consumption were studied. Renal blood flow, glomerular filtration rate, and renal O2 consumption were not significantly different between grades A and B and grade C patients. The renal fraction of systemic O2 consumption was higher (11.4 +/- 5.9 vs 7.9 +/- 4.1 percent respectively; P less than 0.05) and the systemic O2 consumption (111 +/- 23 vs 128 +/- 26 ml.min-1.m-2 respectively; P less than 0.05) lower in patients with grade C than in grades A and B patients. The degree of systemic hyperkineticism and portal hypertension was related to the severity of cirrhosis. In our patients, renal hemodynamics and renal O2 consumption were not related to the severity of cirrhosis. However, liver failure was associated with an increased renal fraction of systemic O2 consumption due to unchanged renal O2 consumption and decreased systemic O2 consumption.
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PMID:[Effect of the severity of liver disease on renal hemodynamics and renal oxygen consumption in patients with cirrhosis]. 139 48

Hypoxemia in liver cirrhosis has been attributed to increased pulmonary perfusion; lung function abnormalities have rarely been found in adults. In infants, however, smaller airways and the disproportion in size between the enlarged liver and abdominal cavity leading to lung compression by elevated diaphragms may well suggest that ventilation disturbances play an important role in the development of hypoxemia. We examined lung functions, ventilation-perfusion scans, chest radiographs, and blood gases in air and 80% oxygen in 19 infants with biliary atresia (mean age 14 months) and found maximum flows at functional residual capacity (VmaxFRC) markedly decreased [48% +/- 29% (mean +/- SD)] and thoracic gas volume (TGV) elevated (156% +/- 30.2%). PO2 was less than 9.3 kPa in seven of 19 patients, in whom TGV was higher compared with the other patients (182% vs. 141%, p less than 0.005). However, the decrease in PO2, was much more closely correlated to the amount of shunting (r = 0.62, p less than 0.05) than to the reduced airway patency (VmaxFRC/TGV, r = 0.41, p = 0.08). We conclude that airway narrowing probably by lung compression is present more frequently in infants than in adults with liver disease. We found some evidence that hyperinflation contributes to the observed low PO2 values, possibly aggravated by inadequate vasoconstriction to hypoxic stimuli. However, pulmonary shunting independent of ventilatory disturbances more readily explained hypoxemia already present in these infants.
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PMID:Hypoxemia in infants with biliary atresia: the role of airway obstruction. 140 65

The biochemistry of alcohol liver disease as it relates to clinical medicine and experimental alcohol liver disease is presented. Clinical features are emphasized in the diagnosis of alcohol liver disease, particularly as it relates to staging the disease and predictors of prognosis. Currently, it is true that the biochemical diagnosis of alcohol liver disease is at best very limited in terms of the sensitivity tests and specificity of the test. It is particularly difficult to detect alcohol liver disease biochemically in the early stages when steatohepatitis is not severe. Consequently, 50% of the patients have already developed cirrhosis at the time they are diagnosed clinically. In this review indicators of malnutrition are emphasized because they have the strongest implications regarding survival during the acute hospitalization stage of the disease. They are also the best indicators of response to therapy during the recovery phase. With respect to experimental work on the pathogenesis of alcohol liver disease, it appears that necrosis is due to the inability to increase blood flow to compensate for increased oxygen utilization. The hypothesis that mitochondrial damage is the cause of liver cell damage is regarded as less important in the pathogenesis of necrosis. The shift in the redox state during alcohol metabolism accounts for the fatty change noted in the central lobular area of the liver in animals fed alcohol. Apparently, there is strong experimental evidence that highly reactive intermediates are important in the pathogenesis of liver damage due to the induction of the isozyme cytochrome P450 IIE1 by alcohol ingestion. This mechanism is enhanced by a diet high in polyunsaturated fatty acids.
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PMID:Biochemistry of alcoholic liver disease. 141 99

Since adenosine may play a role in the hyperdynamic circulation of cirrhosis, we examined the effects of theophylline (an adenosine receptor antagonist) on systemic and splanchnic hemodynamics, tissue oxygenation and sympathoadrenal activity in patients with cirrhosis and liver failure. Theophylline (aminophylline) was administered intravenously for 30 min. Six patients received a dose of 3 mg/kg and eight others a dose of 6 mg/kg. The low dose caused plasma theophylline concentrations of 7.4 +/- 1.8 mg/ml (mean +/- S.E.), and induced a significant increase in heart rate from 84 +/- 5 to 93 +/- 8 beats/min. This dosage did not significantly change other hemodynamic values, oxygen (O2) consumption, or sympathoadrenal activity. The high dose elicited plasma theophylline concentrations of 15.8 +/- 4.0 mg/ml. This dose significantly increased heart rate from 78 +/- 5 to 87 +/- 7 beats/min and significantly decreased right atrial pressure from 2.5 +/- 1.0 to 1.4 +/- 0.8 mmHg, stroke volume from 52 +/- 3 to 47 +/- 5 ml.beat-1.m-2 and systolic arterial pressure from 140 +/- 5 to 129 +/- 6 mmHg. In contrast, O2 consumption, sympathoadrenal activity, and all other hemodynamic values (including azygos blood flow) were not significantly modified. As a result, we conclude that, in patients with cirrhosis, theophylline may cause decreased stroke volume which lowers systolic arterial pressure. In our patients theophylline also had a positive chronotropic effect but no vasoconstrictor effect on systemic and splanchnic circulation. Finally, theophylline did not improve tissue oxygenation in patients with cirrhosis.
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PMID:Effects of theophylline on hemodynamics and tissue oxygenation in patients with cirrhosis. 144 98

Parenchymal cells isolated from normal and thioacetamide-induced micronodular cirrhotic rat livers were used to evaluate changes in hepatocellular fatty acid (FA) metabolism in cirrhosis. Exogenous free FA (FFA) are rapidly taken up by hepatocytes obtained either from normal or cirrhotic livers. They are predominantly esterified to triglycerides and accumulate intracytoplasmatically as lipid droplets with increasing cellular FFA uptake. In the parenchymal cells of cirrhotic livers, however, the following changes were observed when compared with controls: (i) decreased cellular output of esterified FA derived both from exogenous sources and from de novo FA synthesis; (ii) increased total ketone body production, mainly as beta-hydroxybutyrate; (iii) decreased cholesterol synthesis; and (iv) enhanced incorporation of newly synthesized FA into phospholipids in spite of an unaffected rate of FA synthesis. In summary, the data provide evidence for intrinsic alterations in the lipid metabolism in the parenchymal cells of cirrhotic livers which are preserved in the isolated hepatocytes under optimum incubation conditions for oxygen and substrate supply.
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PMID:Quantitative studies on fatty acid metabolism in isolated parenchymal cells from normal and cirrhotic livers in rats. 150 25


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