Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

The relationship between oxygen consumption (VO2) and oxygen delivery (DO2) is of interest in critically ill patients. Various studies of these parameters have resulted in different concepts for optimizing DO2 and VO2. During liver transplantation without anhepatic veno-venous bypass, caval cross-clamping initiates a series of haemodynamic and metabolic alterations including the rapid change from hyperdynamic to hypodynamic conditions. In addition, simultaneous changes in DO2 and VO2 occur in these patients. The goal of our present study was to test the clinical relevance of therapeutic interventions based on metabolic monitoring in patients with terminal liver disease undergoing orthotopic liver transplantation. PATIENTS AND METHODS. One hundred sixty-two consecutive patients were evaluated. According to outcome, patients were divided into survivors (n = 115, group A), nonsurvivors (n = 30, group B), and patients with primary nonfunction of the liver graft (n = 17, group C). One hundred twenty patients were cirrhotics due to either alcohol (n = 36), aggressive hepatitis (n = 30), or biliary cirrhosis (n = 54); 42 had a neoplastic disease. Haemodynamic measurements, data for calculations of DO2 and VO2, and blood samples for arterial and mixed-venous blood gases and subsequent laboratory analysis were taken during the surgical procedure at six timepoints: after induction of anaesthesia (I); during preparation of the recipient liver, before cross-clamping (II); 10 min after clamping of the inferior vena cava (III); 10 min before unclamping (IV); with all vessels open, 10 min after declamping during reperfusion (V); and 60 min after declamping (VI). Anaesthesia was induced with thiopentone (3-5 mg/kg i.v.) and fentanyl (15 micrograms/kg min i.v.). Muscle relaxation was achieved with pancuronium (0.1 mg/kg i.v.). Anaesthesia was maintained with i.v. supplements of fentanyl (5-10 micrograms/kg) and pancuronium (4 mg) as required. Volume-cycled ventilation was established with a mixture of O2 in air with a positive end-expiratory pressure of 5 mm H2O to keep the PaO2 above 100 mm Hg and the PaCO2 around 35 mm Hg (Servo 900 C-Ventilator, Siemens). To maintain body temperature, all patients were positioned on a heating blanket set at 38 degrees C. The inspired gases were warmed and humidified using a dual servo-heated humidifier. Mannitol (20-40 g i.v.) or sorbitol (16-24 g i.v.) was given to prevent renal dysfunction during the cross-clamping procedure. Lactated Ringer's solution and fresh frozen plasma administration was guided by cardiovascular performance and requirements for clotting factors, respectively. Cardiac output was measured by the thermodilution method using a pulmonary artery catheter. Blood lactate, haemoglobin concentration, arterial and mixed-venous oxygen content, and oxygen saturation were measured (Hemoxymeter OSM3). VO2 and DO2 were calculated according to standard formulas. STATISTICAL ANALYSIS. The data from groups A, B, and C were compared using a multivariate analysis of variance with Tukey's method for multiple comparisons. A least-square regression was used to correlate metabolic data. RESULTS. The perioperative course of the determinants of oxygen transport is shown in Table 1. After cross-clamping, the cardiac index (CI) decreased in groups A (47%), B (53%), and C (51%) and increased to pre-anhepatic levels after reperfusion of the new liver. This was associated with distinct decreases in DO2 (A: 42%, B: 47%, and C: 45%) and VO2 (A: 8%, B: 19%, C: 25%). After reperfusion of the new allograft (V), VO2 increased in groups A (24%) and B (18%) as compared to controls (I). By contrast, in group C, a distinct further decrease in VO2 (13%) was detected. In these patients, there was a significantly greater increase in mixed-venous saturation accompanied by a further decrease in body temperature. As shown in Figures 1 and 2, no significant relationship was found between O2 transport, VO2, and blood lactate. DISC
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PMID:[Anesthesia-relevant changes in metabolic parameters with different circulatory and liver functions]. 152 56

From 1987 to February 1991, we have repaired or replaced the aortic arch in ten patients using deep hypothermic systemic circulatory arrest with continuous retrograde cerebral perfusion (CRCP). CRCP can be implemented using the bypass connecting the arterial and venous lines of the extracorporeal circuit to reverse the flow into the superior vena cava cannula after induction of circulatory arrest. CRCP flow required to maintain an internal jugular vein pressure of 20 mmHg ranged from 100 to 500 ml/min. After completion of suturing of the aortic arch graft, air is evacuated retrogradely from the open arch vessels prior to reestablishing the usual arterial return. Two patients died, one from sepsis and the other from liver cirrhosis 1 month postoperatively. CRCP times ranged from 11 to 56 min, and minimal nasopharyngeal temperatures ranged from 16 degrees to 18 degrees C. The difference in oxygen content between the perfused blood and the blood draining from the arch vessels during CRCP most likely reflected the steady-state metabolism of the brain during the deep hypothermic state. This technique offers advantages including the need for dissecting and clamping the arch branches, providing sufficient metabolic support to the brain during deep hypothermia, and eliminating embolism of particulate debris from the aortic arch.
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PMID:Deep hypothermic systemic circulatory arrest and continuous retrograde cerebral perfusion for surgery of aortic arch aneurysm. 154

Regional cerebral blood flow (rCBF), cerebral metabolic rate of oxygen (rCMRO2), and oxygen extraction fraction (rOEF) were measured using positron emission tomography (PET) in four patients with cirrhosis (two males and two females, aged 57 to 69 years) in comparison with those in five age-matched controls with previous transient global amnesia. PET studies were carried out when the patients were fully alert and oriented after the episodes of encephalopathy. In the patients, rCBF tended to be lower, while rCMRO2 was significantly lowered in almost all hemisphere cortices, more markedly in the frontal cortex. Our results suggest that the brain oxygen metabolism is diffusely impaired in patients with advanced cirrhosis, and the frontal cortex seems to be more susceptible to the systemic metabolic derangements induced by chronic liver disease.
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PMID:Marked reduction of cerebral oxygen metabolism in patients with advanced cirrhosis: a positron emission tomography study. 154 88

Although arterial vasodilation is a well-known feature in patients with cirrhosis, the venous system remains unexplored. To measure total effective vascular compliance, a reflection of the properties of the venous system, rapid volume expansion (300 ml of a gelatin solution in 3 min) was performed in 23 patients. Eleven patients had compensated cirrhosis (Child-Pugh grade A or B), and eight had decompensated cirrhosis (Child-Pugh grade C). Four control patients had mild chronic hepatitis, normal hepatic venous pressure and normal liver architecture. Cardiac index, hepatic venous pressures, hepatic and azygos blood flow and renal plasma flow were measured before and immediately after volume expansion. Right atrial pressure was recorded during volume expansion. This allowed the calculation of total effective vascular compliance, which was higher in patients with decompensated cirrhosis than in those with compensated cirrhosis (4.65 +/- 4.21 vs. 1.34 +/- 0.63 ml.mm Hg-1.kg-1; p less than 0.05). In response to volume expansion, renal vascular resistance decreased significantly in patients with compensated cirrhosis, but not in those with decompensated cirrhosis (-30% +/- 33% vs. +2% +/- 23%; p less than 0.05). No change was seen in glomerular filtration rate. Systemic oxygen consumption increased in patients with compensated cirrhosis, but not in those patients with decompensated cirrhosis (25% +/- 33% vs. -4% +/- 9%; p less than 0.05). Although in all patients with cirrhosis volume expansion increased central venous pressures, azygos blood flow and the hepatic venous pressure gradient did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total effective vascular compliance in patients with cirrhosis: a study of the response to acute blood volume expansion. 156 22

The effects of vaso-active agents on hepatic function and splanchnic oxygenation were studied in 17 patients with cirrhosis and portal hypertension. Eight patients received vasopressin (0.3 iu/min) and nine patients received nitroglycerin (50 micrograms/min). Both drugs caused a significant reduction in the portal venous pressure gradient. Vasopressin infusion significantly decreased intrinsic clearance of indocyanine green (-23%, P less than 0.01). This may be due to a decreased hepatic perfusion (-28%, P less than 0.01) and portal venous oxygenation (-15% in portal venous oxygen tension, P less than 0.05). In contrast, no changes in hepatic perfusion and portal venous oxygenation were observed after nitroglycerin infusion. Nitroglycerin did not decrease intrinsic clearance of indocyanine green. These results suggest that vasodilators, rather than vasoconstrictors, might be welcome in the treatment of patients with cirrhosis and portal hypertension.
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PMID:Effects of vaso-active agents on hepatic function and blood gases in patients with cirrhosis: a study of vasopressin and nitroglycerin. 157 96

Excessive consumption of ethanol results in reversible redox changes in the liver that are mainly responsible for the accumulation of triglycerides and the fatty liver of the alcoholic patient. In spite of continuing alcohol abuse, only a fraction of all alcoholics will develop alcoholic hepatitis and eventually cirrhosis. Genetic predisposition and environmental factors (in particular the often poor nutrition of the alcoholic) probably play an important role in the evolution of these complications. The generation of reactive oxygen species increases during the metabolism of ethanol, but their pathogenetic role in alcoholic liver disease in man is not clear. Acetaldehyde, a metabolite of ethanol, can react with proteins and form stable adducts. Such neoantigens may elicit an immunologic response which could in part be responsible for the liver cell damage associated with excessive alcohol consumption. Since no satisfactory animal model for alcoholic liver disease exists, the relative importance of the various factors involved in alcoholic liver disease is difficult to assess.
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PMID:[Pathogenesis of alcoholic liver disease]. 158 33

Mitochondrial and cytosolic functions were studied in vivo and in perfused livers from rats with secondary biliary cirrhosis induced by bile duct ligation for 5 wk and in sham-operated controls. The livers were stereologically analyzed, and mitochondrial and cytosolic functions were related to liver structure. Oxygen consumption by perfused livers expressed per stereologically determined mitochondrial volume was decreased by 49% in bile duct-ligated rats compared with control rats. Glucose production (expressed per mitochondrial volume) was reduced by more than 90% in bile duct ligation, whereas urea production was not affected. Lactate production, a cytosolic function, was increased fivefold in bile duct ligation, and both the lactate/pyruvate and the beta-hydroxybutyrate/aceto-acetate ratios were increased in the liver perfusate of bile duct-ligated rats. In comparison with control rats, the stereologically determined mitochondrial volume fraction per hepatocyte was increased by 28% in bile duct-ligated rats. Activities of mitochondrial enzymes expressed per area of mitochondrial membrane or per mitochondrial volume were either unchanged (ATPase, cytochrome c oxidase and glutamate dehydrogenase) or decreased (monoamine oxidase) in bile duct ligation. Thus in comparison with control rats, mitochondrial metabolism is impaired in perfused livers from bile duct-ligated rats; increased mitochondrial volume per hepatocyte may represent a strategy to maintain hepatic energy metabolism in rats with secondary biliary cirrhosis.
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PMID:Stereological and functional analysis of liver mitochondria from rats with secondary biliary cirrhosis: impaired mitochondrial metabolism and increased mitochondrial content per hepatocyte. 159 55

Vasopressin has been found to impair hepatic function in patients with cirrhosis. The aim of this study was to investigate whether oxygen inhalation could improve hepatic function during vasopressin infusion. Vasopressin (0.3 iu/min) was infused into eight patients with cirrhosis for 50 min. During the first 30 min they were ventilated by room air and for the following 20 min by oxygen (approximate 50% of FiO2). The extra oxygen inhalation caused a typical increase in arterial (+7%, P less than 0.01), portal venous (+8%, P less than 0.05), and hepatic venous (+9%, P less than 0.01) oxygen content. No effect was noted in arterio-hepatic venous and portal venous-hepatic venous oxygen content difference in comparison with the values after vasopressin alone. The hepatic perfusion remained unchanged. These results suggest that the extra oxygen did not increase hepatic oxygen uptake. Similarly, intrinsic clearance of indocyanine green did not improve. It is concluded that oxygen supplement in this setting has no hepatic benefit in patients with cirrhosis.
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PMID:Lack of hepatic benefit by oxygen inhalation during vasopressin infusion in patients with cirrhosis. 161 Oct 13

Liver cirrhosis is sometimes associated with very severe hypoxaemia, which is thought to be the result of intrapulmonary vascular dilatations (IPVDs). These vascular abnormalities, although close to the gas exchange units, are so dilated that diffusion of oxygen molecules to their centre is impaired, causing an increase in alveolar-arterial oxygen tension difference (P(A-a)O2). On the other hand, administration of 100% oxygen provides enough driving pressure to overcome this relative diffusion defect and rules out a true intrapulmonary shunt. We report a case in which, in spite of a normal increase in arterial oxygen tension (PaO2) under 100% oxygen, exercising results in a marked impairment of oxygen exchange and a large intrapulmonary shunt. This is probably due to the increased cardiac output and preferential blood flow through these low resistance IPVDs.
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PMID:Hypoxaemia and liver cirrhosis: a new argument in favour of a "diffusion-perfusion defect". 162 34

The hemodynamics during hemodilution occurred after hepatectomy for hepatocellular carcinoma with liver cirrhosis and its influences on the liver functions were studied. The hematocrit value gradually decreased about 10% until the 4th postoperative day owing to hemodilution after hepatectomy. While anemia progressed, cardiac index inversely increased. Under such a condition, oxygen consumption was maintained so that acidosis did not develop. Arterial blood ketone body ratio was also kept within a normal range except for a case whose hematocrit value decreased to 17.1%. Although the escaped hepatic enzymes such as GOT and GPT increased in the serum after hepatectomy, hemodilution was not responsible for their increase. While total bilirubin increased in the severe hemodiluted group, the increase was not due to hemodilution but caused by blood transfusion. The protein synthesis of the liver measured by rapid turnover protein levels in plasma was depressed after surgery, and this depression prolonged to the 14th postoperative day in the group whose hematocrit value decreased below 20%. These results suggest that it is better to keep hemodynamics without blood transfusion unless the hematocrit value decrease below 20%, and also better to maintain the hematocrit above 20% for liver regeneration after hepatectomy.
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PMID:[The hemodynamics during hemodilution and its influence on the liver functions after hepatectomy for hepatocellular carcinoma with liver cirrhosis]. 165 85


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