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At least 325 records · Page 18Linked to original sources
PubMed2001

Assessment of hepatic function in cystic fibrosis by lidocaine metabolism.

BACKGROUND: To determine hepatic drug metabolism in patients with cystic fibrosis, as measured by monoethylglycinexylidide formation after lidocaine injection and indocyanine green (ICG) clearance. METHODS: The following study is a case-control study, which included 19 patients with cystic fibrosis and 13 control subjects. Serum monoethylglycinexylidide concentration was measured after intravenous injection of 1 mg/kg (maximum, 50 mg) lidocaine. Indocyanine green (0.5 mg/kg) was injected concomitantly, and absorbance (805 nm) of serum was measured over time to determine its volume of distribution, serum half-life, and hepatic blood flow. RESULTS: Monoethylglycinexylidide formation was decreased in patients with cystic fibrosis compared with controls (39.4+/-16.9 microg/L versus 70.3+/-45.7 microg/L, mean +/- SD, respectively, P < 0.02). Indocyanine green half-life (4.6+/-2.7 min versus 3.0+/-1.0 min), volume of distribution (8.6+/-5.5 L versus 8.3+/-3.4 L), and hepatic blood flow (10.9+/-5.9 ml x kg(-1) x min(-1) versus 7.4+/-2.0 ml x kg(-1) x min(-1)) were similar in both groups. CONCLUSION: Monoethylglycinexylidide formation after lidocaine injection is impaired in patients with cystic fibrosis. This impairment may have clinical implications when using hepatically metabolized medications in patients with cystic fibrosis.

Adolescent↗
PubMed1987

Changes in hepatic function tests to induced toxicity in the bovine liver.

Graded hepatic damage was induced in mature lactating dairy cows to measure the sensitivity of several hepatic diagnostic tests. In a preliminary study, cows were dosed with .05, .10 and .20 ml/kg body weight of carbon tetrachloride. Extreme changes occurred in hepatic tests by 24 h post-dosing, and all died by 35 h with massive diffuse centrilobular necrosis of hepatic cord cells. Dosing was decreased to induce non-fatal hepatic changes. Cows in Groups 1, 2, 3 and 4 were orally dosed with .002, .004, .006 or .01 ml/kg body weight of carbon tetrachloride, respectively. Serum enzymes of hepatic origin, bilirubin, plus bromosulfophthalein dye clearance were assayed before dosing and up to d 14 post-dosing. Liver biopsies were performed 24 h post-dosing for histological evaluation and cytochrome P-450 content. Hepatic concentrations of cytochrome P-450 were decreased in all the dosed cows. Serum activities of sorbitol dehydrogenase and gamma-glutamyl transferase were elevated in cows of Groups 3 and 4 and glutamic-oxaloacetic transaminase in cows of Group 4 by 24 h. Serum alkaline phosphatase, glutamic-pyruvate transaminase, lactate dehydrogenase, bilirubin, urobilinogen and bromosulfophthalein dye clearance were not significantly different. Mild to moderate diffuse centrolobular necrosis was observed in livers of cow of Groups 3 and 4, but no pathological changes were seen in Groups 1 and 2.

Animals↗
PubMed1994

Closed-circuit anesthesia with sevoflurane in humans. Effects on renal and hepatic function and concentrations of breakdown products with soda lime in the circuit.

BACKGROUND: Sevoflurane reacts with CO2 absorbents, resulting in the generation of breakdown products. The concentrations of sevoflurane breakdown products in a low-flow system within 5 h have been reported, but concentrations in low-flow anesthesia exceeding 5 h or in closed-circuit anesthesia have not. In this study, the breakdown products of sevoflurane in closed-circuit anesthesia exceeding 5 h were examined. METHODS: Closed-circuit sevoflurane anesthesia was administered to ten patients. Laboratory tests of hepatic and renal function were performed before and after anesthesia. Gas samples were obtained from the inspiratory limb of the anesthesia circuit, and breakdown products were analyzed by gas chromatography. The temperature of the soda lime was measured during anesthesia. RESULTS: Among the breakdown products of sevoflurane, two products, CF2 = C(CF3)-O-CH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B), were detected. Compound A was detected in all measurements, and its concentration reached 19.5 +/- 5.4 ppm 1 h after anesthesia and decreased after 5 h. The highest concentration observed for compound A was 30.0 ppm. Compound B was detected in seven of the ten patients; its concentration was 0.17 +/- 0.37 ppm after 0.5 h of anesthesia and remained at similar concentrations thereafter. The highest mean temperature of the soda lime was 46.0 +/- 1.7 degrees C. Postanesthetic clinical laboratory tests showed no abnormalities in hepatic or renal function associated with anesthesia. CONCLUSIONS: Two breakdown products were detected in the patients anesthetized with sevoflurane using a closed-circuit technique. No abnormalities were observed during anesthesia, and no evidence of hepatic or renal dysfunction was noted in postoperative laboratory tests.

Adult↗
PubMed1975

Quantitative assessment of hepatic function by breath analysis after oral administration of (14C)aminopyrine.

The rate of hepatic metabolism of dimethylaminoantipyrine (aminopyrine), which occurs primarily through N-demethylation, was assessed by measurement of the specific activity of 14CO2 excreted in breath samples obtained 2 hours after oral administration of a trace dose of [14C]aminopyrine. The percentage of administered 14C excreted in 14CO2 in 2 hours was 7.0 +/- 1.3 (SD)% in control patients, and significantly less (P less than 0.01) in patients with portal cirrhosis (2.6 +/- 1.2%), fatty liver (4.7 +/- 1.1%), hepatitis (2.6 +/- 1.4%), and hepatic malignancy (3.5 +/- 1.8%). In 16 of 24 subjects with cholestasis not caused by malignant disease the mean 14CO2 excretion was normal. The 14CO2 excretion in patients with portal cirrhosis correlated highly with aminopyrine metabolic clearance rate (r equals 0.92), serum albumin (r equals 0.75), and retention of bromsulphalein (r equals 0.73). Abnormal 14CO2 excretion returned to normal in patients with hepatitis, when the hepatitis resolved. The data suggest that the aminopyrine breath test is a safe, simple, qualitative and quantitative liver function test.

Administration, Oral↗
PubMedDate not supplied

Age-related changes in hepatic function. Implications for drug therapy.

An age-related decrease in the hepatic clearance of many drugs has been reported. Several mechanisms have been proposed, but only some are supported by hard evidence. Liver volume declines with age, as does hepatic blood flow--changes which may largely account for the reduced clearance of capacity- and flow-limited drugs, respectively. Age-related histological changes in the liver are minor and of uncertain significance; standard liver function tests do not change significantly with aging. There is, as yet, no direct evidence of a generalised fall in hepatic drug-metabolising enzyme activities in aging humans measured in vitro, but some in vivo studies suggest that certain very specific cytochrome P450 isoenzymes may be affected by aging, especially in men. Finally, there may be an age-related decline in the response to environmental influences.

Aging↗
PubMedDate not supplied

Validation of deconvolutional analysis for the measurement of hepatic function in dogs with toxic-induced liver disease.

The extraction of the hepatobiliary radiopharmaceutical 99mTc-mebrofenin (Choletec) by the liver can be used to evaluate the severity of hepatocellular disease. The hepatic parenchymal cells extract mebrofenin from the blood by the same active transport mechanism as bilirubin. The ability of the liver to extract 99mTc-mebrofenin is a measure of hepatic parenchymal cell function. In this study, we induced hepatocellular disease by administration of a hepatotoxic drug and compared a direct method of determining the hepatic extraction of 99mTc-mebrofenin to hepatic extraction fraction derived from deconvolutional analysis. We also compared both methods of calculating the hepatic extraction of 99mTc-mebrofenin to liver histopathology. Hepatic extraction fraction derived from deconvolutional analysis correlated very well to the direct measurement technique (R=0.922, p < 0.001). Both methods of determining hepatic extraction correlated well to quantitative histopathology, having the same correlation coefficient and p values. (R=-0.833, p=0.003). As the hepatic extraction 99mTc-mebrofenin decreased, the severity of the histopathologic lesions of the liver increased in a linear fashion. There was a significant correlation of the hepatic excretion T1/2 to quantitative histopathology (R=0.949, p < 0.001). The hepatic excretion T1/2 increased as the severity of the histopathologic lesions of the liver increased. Hepatic extraction (HEF) and excretion of 99mTc-mebrofenin are good predictors of the severity of hepatocellular damage in toxic induced liver disease. This study helps validate the premise that HEF derived from deconvolutional analysis is a good predictor of the actual first pass hepatic extraction of 99mTc-mebrofenin.

Aniline Compounds↗
PubMed2006

Ablation of PGC-1beta results in defective mitochondrial activity, thermogenesis, hepatic function, and cardiac performance.

The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1beta (PGC-1beta) has been implicated in important metabolic processes. A mouse lacking PGC-1beta (PGC1betaKO) was generated and phenotyped using physiological, molecular, and bioinformatic approaches. PGC1betaKO mice are generally viable and metabolically healthy. Using systems biology, we identified a general defect in the expression of genes involved in mitochondrial function and, specifically, the electron transport chain. This defect correlated with reduced mitochondrial volume fraction in soleus muscle and heart, but not brown adipose tissue (BAT). Under ambient temperature conditions, PGC-1beta ablation was partially compensated by up-regulation of PGC-1alpha in BAT and white adipose tissue (WAT) that lead to increased thermogenesis, reduced body weight, and reduced fat mass. Despite their decreased fat mass, PGC1betaKO mice had hypertrophic adipocytes in WAT. The thermogenic role of PGC-1beta was identified in thermoneutral and cold-adapted conditions by inadequate responses to norepinephrine injection. Furthermore, PGC1betaKO hearts showed a blunted chronotropic response to dobutamine stimulation, and isolated soleus muscle fibres from PGC1betaKO mice have impaired mitochondrial function. Lack of PGC-1beta also impaired hepatic lipid metabolism in response to acute high fat dietary loads, resulting in hepatic steatosis and reduced lipoprotein-associated triglyceride and cholesterol content. Altogether, our data suggest that PGC-1beta plays a general role in controlling basal mitochondrial function and also participates in tissue-specific adaptive responses during metabolic stress.

Adipose Tissue, Brown↗
PubMed2002

Hepatic function during xenon anesthesia in pigs.

BACKGROUND: Inhalation anesthetics decrease liver perfusion and oxygen consumption by changing the distribution pattern of perfusion between the hepatic artery and the portal vein and by direct effects on liver cells. The effects of xenon on liver perfusion and function have been not investigated until now. METHODS: Fourteen pigs were randomly assigned to two groups to receive either 73-78% xenon or 75% nitrogen in oxygen with additional supplementation of pentobarbital and buprenorphine. Microspheres were used to determine the arterial perfusion of the liver and splanchnic organs. Oxygen contents were measured by catheterization of the portal and a liver vein. Lactate and glucose plasma concentrations were measured in hepatic, mixed venous and arterial blood. Alanine aminotransferase (ALT) and lactate dehydrogenase (LOH) plasma concentrations were measured in arterial blood. Urea production rates were calculated to assess hepatic metabolic function. RESULTS: Significant higher oxygen contents were found in the liver venous blood during xenon anesthesia. No differences were found in any other investigated parameters. CONCLUSION: Higher oxygen content in liver venous blood observed during xenon anesthesia was not induced by changes in hepatic perfusion distribution or by an impairment of liver metabolic capacity. However, it can be explained by similar results known from inhalation anesthesia. Additionally, the effect can be caused by the reduction of plasma catecholamine concentrations during xenon anesthesia.

Adjuvants, Anesthesia↗
PubMed2005

[Estimation of efficacy of the correction methods for hepatic functional disorders in cholestasis of mechanical nature].

Efficacy of the prophylaxis and treatment methods for hepatic insufficiency in obstructive jaundice was studied. The role of an energy-dependent processes and the tissue deficit of oxygen in the hepatic insufficiency occurrence and progress, possibility of these disorders medicinal correction was delineated. The expediency of introduction of preparations, improving the erythrocytes function and the oxygen delivery to tissues in conjunction with miniinvasive biliary decompression, in therapeutic complex for hepatic insufficiency of mechanical nature was noted.

Decompression, Surgical↗
PubMed1998

The pharmacokinetics of lamivudine in patients with impaired hepatic function.

OBJECTIVE: This study was designed to evaluate the effect of hepatic impairment on the pharmacokinetics of lamivudine. METHODS: Sixteen patients not infected with hepatitis B virus or human immunodeficiency virus who had hepatic impairment due to liver cirrhosis were assigned to moderately or severely impaired groups by clinical signs/symptoms, 14C-aminopyrine metabolic activity and caffeine clearance and compared with eight healthy controls. Following a 300-mg dose of lamivudine, blood and urine samples were taken for drug assay. RESULTS: Lamivudine was well tolerated in patients with hepatic impairment. There were no statistical differences in overall lamivudine exposure (in terms of AUC or Cmax) or other major pharmacokinetic parameters i.e. CLR, tmax and t1/2, between healthy control subjects and patients with moderate or severe hepatic impairment. CONCLUSIONS: Hepatic impairment does not warrant dose modification of lamivudine based on this single-dose pharmacokinetic study.

Adult↗
PubMed1976

Prevention by zinc of cadmium-induced alterations in pancreatic and hepatic functions.

Subacute cadmium treatment (CdCl2, 1 mg/kg twice daily for 7 days) in rats disturbs glucose homeostasis as shown by hyperglycemia and decreased glucose tolerance associated with suppression of insulin release, enhancement of hepatic gluconeogenic enzymes and decrease in hepatic glycogen content. 2 Exposure to cadmium increases hepatic cyclic adenosine 3',5'-monophosphate (cyclic AMP) and this is accompanied by stimulation of basal, adrenaline- as well as glucagon-stimulated form(s) of adenylate cyclase. 3 In contrast to cadmium, subacute administration of zinc (ZnCl2, 2 mg/kg twice daily for 7 days) fails to alter the activities of hepatic gluconeogenic enzymes, cyclic AMP synthesis, as well as glucose clearance and insulin release in response to a glucose load. 4 Zinc, when administered at the same time as cadmium, prevents the cadmium-induced lesions in both hepatic and pancreatic functions. 5 The results are discussed in relation to the possible mechanisms of cadmium toxicity and to the role of sulphydryl groups in the protection exercised by zinc.

Adenylyl Cyclases↗
PubMed1981

Assessment of hepatic function after hepato-porto-enterostomy for biliary atresia using Tc-diethyl-IDA.

A quantifiable biliary function index has been developed from analysis of hepatic time--activity curves. Diethyl-IDA, a technetium-labeled iminodiacetic acid was given intravenously 27 times in 11 patients with proven biliary atresia. An estimated bile bilirubin clearance index derived from the inscribed hepatic absorption and elimination curves appears to be a reliable indicator of bile bilirubin clearance. The actual bile bilirubin clearance, previously shown to be a major determinant of survival, was clinically correlated in five patients studied before and after surgery and confirms the experimental findings. The clearance index should allow objective assessment of the efficacy of surgery for biliary atresia.

Adolescent↗
PubMed1997

Xenobiotic-induced hepatotoxicity: mechanisms of liver injury and methods of monitoring hepatic function.

Xenobiotic-induced liver injury is a clinically important etiology of hepatic disease that, if not recognized, can lead to hepatic failure. In this article we discuss the mechanisms of xenobiotic-induced liver injury, various factors that can alter the risk and severity of injury, the clinical and laboratory manifestations of injury, and the methods used to detect the presence of injury and (or) functioning liver mass.

Animals↗
PubMedDate not supplied

Anti-polymerized albumin antibodies-a test for the evaluation of hepatic function in HBs Ag-positive subjects.

A number of 681 sera collected from hepatic patients and apparently healthy subjects (recruits and blood donors) were tested by immunodiffusion (ID) and hemagglutination (HA) for the presence of anti-polymerized albumin antibodies (AAA). AAA positivity was compared within the categories of patients and healthy subjects, grouped according to the presence of HBsAg. In most of the hepatic patients and healthy subjects both ID and HA were either positive or negative. However, in certain apparently healthy HGsAg carriers, the absence of AAA in ID was associated with high AAA titers in HA. These data point to the possibility of using AAA in order to differentiate an actually healthy HGsAg carrier from a HBsAg carrier with hepatic lesions.

Autoantibodies↗