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Hepatobiliary function

ACS Symposium Series American Chemical Society Washington, DC, 1980. [Pg.92]

Tc-macroaggregated albumin, Tc-albumin microspheres, Tc-albumin minimicrospheres, Tc- erric hydroxide aggregates, Tc-sulfur colloid, Tc-antimony colloid, Tc-phytate [Pg.93]

Bone agents, e.g, polyphosphates, pyrophosphates, diphos-phonates, iminodiphosphonates [Pg.93]

Tc-DTPA, Tc-EDTA, Tc-MIDA (methyliminodiacetic acid), Tc-citrate [Pg.93]

Tc-gluconate, Tc-glucoheptonate, Tc-Fe-ascorbate, Tc-inulin, Tc-mannitol, Tc-dimercaptosuccinic acid [Pg.93]


Dietary exposure of rats to 10 ppm (0.5 mg/kg/day) endrin aldehyde or 5 ppm (0.25 mg/kg/day) endrin ketone for 15 days resulted in slight elevations (p<0.05) in SGPT and SGOT (Young and Mehendale 1986). However, no alterations in liver weight or in hepatobiliary function, as measured by phenolphthalein glucuronide or bile flow, were reported. [Pg.53]

Young RA, Mehendale HM. 1986. Effect of endrin and endrin derivatives on hepatobiliary function and carbon tetrachloride-induced hepatotoxicity in male and female rats. Food Chem Toxicol 24 863-868. [Pg.192]

Hewitt LA, Ayotte P, Plaa GL. 1986a. Modifications in rat hepatobiliary function following treatment with acetone, 2-butanone, 2-hexanone, mirex, or chlordecone and subsequently exposed to chloroform. Toxicol Appl Pharmacol 83(3) 465-473. [Pg.260]

Mehendale HM. 1977c. Mirex-induced impairment of hepatobiliary function Suppressed biliary excretion of imipramine and sulfobromophthalein. Drug Metab Dispos 5 56-62. [Pg.272]

Mehendale HM. 1979. Modification of hepatobiliary function by toxic chemicals. Federation Proceedings of the Federation of American Societies for Experimental Biology 38(8) 2240-2245. [Pg.272]

Mehendale HM. 1990a. Assessment of hepatobiliary function with phenolphthalein and phenolphthalein glucuronide. Clin Chem Enzyme Commis 2 195-204. [Pg.272]

Hewitt LA, Ayotte P, Plaa GL. 1986. Modifications in rat hepatobiliary function following treatment... [Pg.79]

The homotaurocholic acid test (SeHCAT) using Se to evaluate the hepatobiliary function (e. g. in the bile-acids losing syndrome) is also worth mentioning here. (40)... [Pg.194]

Vigorous fluid resuscitation and support of respiratory, renal, cardiovascular, and hepatobiliary function may limit systemic complications. " However, there is no proven method to prevent these complications. While hemoconcentration (decreased intravascular volume) is strongly associated with pancreatic necrosis, it is not clear whether aggressive fluid resuscitation alone during the first 24 hours can prevent pancreatic necrosis." Procedures such as ERCP, hypothermia, nasogastric suction, pancreatic irradiation, peritoneal lavage, and thoracic duct drainage remain unproven. ... [Pg.727]

The term cholephil has been proposed (H4) for endogenous and exogenous substances which are removed from the circulation by the liver and concentrated in the bile. Among the cholephils are bromsulfophthalein (BSP) and other dyes which have been used in the study of liver function in patients and experimental animals for over half a century. The uptake of cholephilic dyes, indeed, is widely held to be the most sensitive index of hepatobiliary function. [Pg.310]

Another development has been the study of the conjugates formed when BSP is taken up by the parenchymal cells of the liver (B46, C5, C6, G23). A portion of these regurgitate back into the plasma, and measurement of the absolute or relative amounts of conjugates offers an alternative approach to the clinical study of hepatobiliary function (see Section... [Pg.312]

In persons with impaired hepatobiliary function, the plasma disappearance curve of dye may differ from that observed in normal persons. Sometimes the initial fall of BSP is much slower, so that a plot of the plasma concentration against time is almost linear and the second phase cannot clearly be distinguished. More commonly the curve in the second phase is flattened or shows a temporary rise in BSP concentration which is believed to be due to the passage of BSP or of its metabolites back into the plasma from the liver. [Pg.332]

Following intravenous injection, the Tc-IDA complex is bound to plasma protein (mainly albumin) and carried to the liver (Nicholson et al. 1980). Accumulation in the liver involves the same carrier-mediated, non-sodium-dependent organic anion transport processes as for the uptake of bilirubin. In the space of Disse, the albumin- Tc-IDA conjugate is dissociated to facilitate active transport of the Tc-IDA complex into hepatocytes (Krishnamurthy and Krishnamurthy 1989). In patients with normal hepatobiliary function, maximal liver uptake is measured at 12 min ( Tc-mebrofenin, 10.9 1.9 min Tc-disofenin, 11.5 3.1 min) (Fritzberg 1986). The radioactivity is half this value within approximately 20 min. The gallbladder is well visualized 20 min postinjection. Intestinal activity appears on the average at 15-30 min. The common bile duct may be visualized after 14 min. The upper limit of normal for visualization of these structures is 1 h (Weissmann et al. 1979). [Pg.319]


See other pages where Hepatobiliary function is mentioned: [Pg.53]    [Pg.38]    [Pg.83]    [Pg.84]    [Pg.85]    [Pg.123]    [Pg.128]    [Pg.163]    [Pg.52]    [Pg.1553]    [Pg.92]    [Pg.101]   
See also in sourсe #XX -- [ Pg.92 ]




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