PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “IOPANOIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMedDate not supplied

[Effect of roentgenocontrast agents on bilirubin absorption by liver sections of rats].

Spectrophotometry was employed to study the effect of radiographic contrast agents (iopanoic acid, bilimin, bilignost, endobil, biligram, verografin, iodamide) on bilirubin absorption by rat liver sections. It was discovered that lopanoic acid, bilignost, endobil, biligram, iodamide and verografin inhibit bilirubin absorption by rat liver sections by the competitiveless while bilimin by the noncompetitive mechanism.

Absorption↗
PubMed1982

Preoperative diagnosis of gallbladder disease.

The following protocols should be observed in evaluating a patient with suspected cholecystitis: In evaluating chronic cholecystitis in patients on a diet containing fat, plain films of the abdomen and oral cholecystogram are the procedures of choice. If the gallbladder fails to fill after ingestion of 3 g iopanoic acid, the procedure is repeated with an additional 3 g the following day. Failure of the gallbladder to visualize after a two-day study, equivocal findings, or persistent symptoms despite a normal study should be followed by ultrasound and, if necessary, cholescintigraphy. The latter two studies should be done in a fasting state, and CCK used to demonstrate gallbladder contraction during both tests. In suspected acute cholecystitis, plain radiography, ultrasound, and Tc-99m-imino diacetic acid derivative scanning should be performed. Again CCK should be used during cholescintigraphy to verify nonvisualization and to stimulate gallbladder emptying.

Cholecystitis↗
PubMedDate not supplied

Pharmacokinetics: an analysis of the method.

The field of radiology in general, and gastrointestinal radiology in particular, can and has benefited by the application of pharmacokinetic principles in contrast agent research and development. The application of basic pharmacokinetic principles can aid in the design of new synthetic analogues. In many cases, the presence or the absence of certain functional groups in particular locations on the aromatic ring system can predictively influence the binding, clearance and half-life values of these compounds. Detailed pharmacokinetic understanding of gastrointestinal contrast agents, particularly cholecystopaques, hold the key for unlocking the "black box" aspects of hepatic/biliary functions. Specific agents are currently quantitating and characterizing hepatic uptake, enzyme transformations, and biliary excretion functions of the liver. Pharmacokinetic principles can also be applied within the clinical radiology setting. Studies are currently underway to correlate blood iodine levels following iopanoic acid (Telepaque) administration with the causes of gallbladder nonvisualization. In summary, the use of pharmacokinetics has and will continue to assist the gastrointestinal radiologist interested in developmental, basic, and/or clinical research.

Animals↗
PubMedDate not supplied

[Interference in the conversion of T4 to T3 and rT3 by medications in man].

Several drugs are known to interfere in thyroid hormone metabolism: 1) They can affect directly and specifically T4 to T3 conversion. This can be observed in vivo and in vitro. In vivo serum T3 concentrations will decrease and rT3 concentrations increase. Amiodarone, other iodinated compounds (cholecystographic agents: ipodate and iopanoic acid), propylthiouracil and propranolol are known to act in this way. 2) Other drugs which induce the hepatic capacity to catabolize drugs will also affect thyroid hormone metabolism, e.g. diphenylhydantoine. Clinically, inhibitors of conversion will increase serum total and free T4, however this finding per se does not proof hyperthyroidism as in some cases serum TSH will increase after i.v. injection of 400 micrograms TRH. Furthermore the increase in serum T4 can be explained in part by a low metabolic clearance rate, T4 production being barely increased.

Amiodarone↗
PubMed1994

Mechanisms of chemical injury of thyroid gland.

Many goitrogenic xenobiotics that increase the incidence of thyroid tumors in rodents exert a direct effect on the thyroid gland to disrupt one of several steps in the biosynthesis and secretion of thyroid hormones. This includes 1) inhibition of the iodine-trapping mechanism (thiocyanate or perchlorate), 2) blockage of organic binding of iodine and coupling of iodothyronines to form thyroxine (T4) and triiodothyronine (T3) (e.g., sulfonamides, thiourea, methimazole, and aminotriazole, among others), and 3) inhibition of thyroid hormone secretion by an effect on proteolysis of active hormone from the colloid (lithium or an excess of iodide). Another large group of goitrogenic chemicals disrupts thyroid hormone economy by increasing the peripheral metabolism of thyroid hormones through an induction of hepatic microsomal enzymes. This group includes CNS-acting drugs (phenobarbital, benzodiazepines), calcium channel blockers (nicardipine, nifedipine), steroids (spironolactone), retinoids, chlorinated hydrocarbons (chlordane, DDT, TCDD), polyhalogenated biphenyls (PCB, PBB), and enzyme inducers. Thyroid hormone economy also can be disrupted by xenobiotics that inhibit the 5'monodeiodinase, which converts T4 in peripheral sites (e.g., liver and kidney) to biologically active T3. Inhibition of this enzyme by FD&C Red No. 3, amiodarone, and iopanoic acid lowers circulating T3 levels, which results in a compensatory increased secretion of thyroid-stimulating hormone (TSH), follicular cell hypertrophy and hyperplasia, and an increased incidence of follicular cell tumors in 2-year or lifetime studies in rats. Physiologic perturbations alone such as the feeding of an iodine-deficient diet, partial thyroidectomy, natural goitrogens in certain foods, and transplantation of TSH-secreting pituitary tumors in rodents also can disrupt thyroid hormone economy and, if sustained, increase the development of thyroid tumors in rats. A consistent finding with all of these goitrogens, be they either physiologic perturbations or xenobiotic chemicals, is the chronic hypersecretion of TSH, which by receptor-mediated events places the rodent thyroid gland at greater risk of developing tumors through a secondary mechanism of thyroid oncogenesis.

Animals↗
PubMed1997

[Pre-surgical medical therapy of hyperthyroidism].

The Authors analyze the use and the efficacy of antithyroidal drugs administered to the patients affected by hyperthyroidism, that must undergo thyroidectomy. The aim is that the patients arrive to the operation in euthyroidism: this is very important to avoid the complications that can occur during or just after the thyroidectomy. They believe that till today the most effective treatment of hyperthyroidism before thyroidectomy is based on the use of thyonamide and iodine. In case of intolerance to these drugs or if it is necessary an emergency thyroidectomy or in case of a low compliance of the patient, there is the possibility to use different therapeutic approaches with beta-blockers or betametasone plus iopanoic acid and propranolol administered together for a few days. As concerning the possible complications that can occur during or after the thyroidectomy, the Authors analyze in particular the thyrotoxicosis and the "hungry bone" syndrome.

Antithyroid Agents↗
PubMed1980

Rapid thyroxine to 3,5,3'-triiodothyronine conversion and nuclear 3,5,3'-triiodothyronine binding in rat cerebral cortex and cerebellum.

Thyroxine (T(4)) to 3,5,3'-triiodothyronine (T(3)) conversion was evaluated in vivo in cerebral cortex, cerebellum, and anterior pituitary of male euthyroid Sprague-Dawley rats. Tracer quantities of (125)I-T(4) and (131)I-T(3) were injected into controls and iopanoic acid-pretreated rats 3 h before isolation of nuclei from these tissues. Specifically-bound nuclear (131)I-T(3), denoted T(3)(T(3)); (125)I-T(3), denoted T(3)(T(4)); and (125)I-T(4) were extracted and identified by chromatography. Plasma iodothyronines were similarly quantitated. In control rats, nuclear T(3)(T(3)) (percent dose per milligram DNA x 10(-4)) was 174+/-31 in cerebral cortex, 50+/-9 in cerebellum, and 932+/-158 in pituitary (all values, mean+/-SEM). Nuclear T(3)(T(4)) (percent dose per milligram DNA x 10(-4)) was 23.3+/-3.3 in cortex, 3.5+/-0.6 in cerebellum, and 39.4+/-6.9 in pituitary. Two-thirds of nuclear T(3)(T(4)) derived from local T(4) to T(3) conversion. Nuclear T(3)(T(4)) in all tissues was reduced to less than 15% of its control value by iopanoic acid treatment and all of the residual nuclear T(3)(T(4)) could be accounted for by plasma T(3)(T(4)). Nuclear T(3)(T(3)) binding was not inhibited by iopanoic acid. These results indicate there is rapid local T(4) to T(3) conversion in rat brain and nuclear binding of the T(3) produced. We have previously found that local T(3)(T(4)) production is the source of approximately 50% of the T(3) in rat anterior pituitary. The present observations that the ratio of locally derived nuclear T(3)(T(4)) to nuclear T(3)(T(3)) is much higher in cerebral cortex (0.1) and cerebellum (0.04) than in anterior pituitary (0.015) suggest that this locally produced T(3)(T(4)) is the predominant source of intracellular T(3) in these portions of rat brain.

Animals↗