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PubMed1985

Protective adaptation of low serum triiodothyronine in patients with chronic renal failure.

Low serum triiodothyronine (T3) concentration is frequently found in patients with chronic renal failure (CRF). To test the hypothesis that this may serve to minimize protein catabolism in these patients, we measured nitrogen balance (Nb) in seven CRF and four control subjects in the basal state and when serum T3 concentration was elevated by L-triiodothyronine (LT3) and suppressed by sodium ipodate administration. In the basal state, both the controls and the CRF patients were in positive Nb, 0.02 +/- 0.51 and 0.58 +/- 0.34 g/day, respectively. During LT3 administration, Nb decreased to -0.80 +/- 0.39 g/day in the CRF patients (P less than 0.01), but remained positive, 0.22 +/- 0.67 g/day, in the controls. There was a significant negative correlation between serum T3 concentration and Nb in the CRF patients (r = -0.63, P less than 0.005), but not in the controls. Furthermore, urea nitrogen generation rate, calculated from urea kinetics, increased from a baseline of 4.6 +/- 0.55 to 6.0 +/- 0.50 mg/min during LT3 administration in the CRF patients (P less than 0.01). Sodium ipodate, which significantly lowered serum T3 concentrations, had little effect on nitrogen metabolism in the controls and the CRF patients. These data support the concept that low serum T3 concentrations may confer a protective effect on CRF patients regarding protein-nitrogen conservation and provide a rationale for not correcting such deficiency.

Adaptation, Physiological↗

PubMed1987

Blunted peripheral tissue responsiveness to thyroid hormone in uremic patients.

To understand the biologic significance of the low triiodothyronine (T3) syndrome in patients with chronic renal failure (CRF), we examined thyroid hormone profile, basal O2 uptake (VO2), and peripheral blood mononuclear leukocyte (PBL) ouabain binding in these patients and in the control subjects before and after L-triiodothyronine (T3) and sodium ipodate treatment. In the controls (N = 8), T3 administration increased serum total T3 from 136 +/- 15 to 232 +/- 11 ng/dl, and reduced total thyroxine (T4) from 8.14 +/- 0.56 to 6.08 +/- 0.43 micrograms/dl, free T4 from 1.59 +/- 0.12 to 1.03 +/- 0.05 ng/dl and thyroid-stimulating hormone (TSH) from 1.74 +/- 0.24 to 0.41 +/- 0.09 microU/ml. VO2 increased from 2.66 +/- 0.11 to 3.15 +/- 0.09 ml/kg/min. Ipodate treatment, on the other hand, resulted in a reduction of serum total T3 to 102 +/- 21 ng/dl, an increase in total T4 to 9.59 +/- 0.50 micrograms/dl, free T4 to 1.91 +/- 0.13 ng/dl and TSH to 3.64 +/- 1.14 microU/ml. VO2 decreased to 2.43 +/- 0.06 ml/kg/min. P values ranged from less than 0.05 to less than 0.001. In the CRF patients (N = 14), T3 treatment also resulted in a rise in serum total T3 from 75 +/- 5 to 185 +/- 8 ng/dl. Total T4 declined from 6.68 +/- 0.34 to 5.18 +/- 0.48 micrograms/dl, free T4 from 0.85 +/- 0.1 to 0.67 +/- 0.08 ng/dl and TSH from 3.67 +/- 0.86 to 0.94 +/- 0.3 microU/ml. VO2, however, did not change (from 2.91 +/- 0.12 to 2.99 +/- 0.17 ml/kg/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Identification of thyroxine-sulfate (T4S) in human serum and amniotic fluid by a novel T4S radioimmunoassay.

Recently, we identified significant amounts of thyroxine sulfate (T4S) in fetal sheep serum, meconium, bile, and amniotic and allantoic fluids. Little is known, however, about sulfate conjugation of thyroxine in humans. In this study, we employed a novel, sensitive T4S RIA to address this question. The rabbit antiserum was quite specific; T4, T3, rT3, and 3,3'-T2 showed less than 0.002% cross-reactivity. Other analogs cross-reacted less than 0.0001%. Only rT3S and T3S cross-reacted significantly (9.9% and 2.0%, respectively). The mean serum T4S concentration (ng/dL) was 8.6 in euthyroid subjects, 14.4 in hyperthyroid subjects, 5.0 in hypothyroid subjects, 5.9 in pregnancy, and 4.5 in patients with nonthyroid illnesses. T4S concentration in amniotic fluid from women at 18-19 weeks of gestation (25.5 ng/dL) was higher than that at 14-15 weeks of gestation (14.3 ng/dL). A significant rise in serum T4S was detected in hyperthyroid patients 1 day after ingestion of 1 g of ipodate. These data suggest that T4S is a normal component of human serum and amniotic fluid, and it is mostly derived from T4 peripherally and accumulates when type I 5'-monodeiodinating activity is low in fetuses or inhibited by drugs, such as ipodate.

Amniotic Fluid↗

PubMedDate not supplied

Hepatic excretion of cholecystopaques introduced into the canine jejunum.

The biliary excretion of five oral cholecystopaques was measured following their introduction into the jejunum of bile fistula dogs. The mean maximal iodine concentration in the bile ranged form a low of 2.2 +/- 0.55 mg per ml following a dose of 33 mg of iodine per kg of iopanoic acid to a high of 12.9 +/- 1.4 mg per ml after the same dose of sodium ipodate. Cumulative excretion at the end of three hours was over five times greater with sodium ipodate in comparison to ipoanoic acid. It is felt that the best explanation of this date is the ability of the more water soluble media to pass through the unstirred water layer of the intestine.

Animals↗

PubMed1985

Modulatory effect of thyroid hormones on uptake of phosphate and other solutes across luminal brush border membrane of kidney cortex.

The mechanism whereby thyroid hormones modulate the transport properties of luminal brush border membrane (BBM) of renal proximal tubules was studied in thyroparathyroidectomized rats. Administration of both T4 and T3 increased BBM capacity for Na+ gradient-dependent uptake of phosphate (Pi) by BBM vesicles (BBMV). This effect of thyroid hormones was present in thyroparathyroidectomized and hypophysectomized rats, and it was not blocked by a saturating dose of propranolol. The stimulatory effect of T3 and T4 on BBM transport of Pi was dose dependent in the range of 5.2-520 nmol/100 g BW. Pretreatment of rats with inhibitors of 5'-monodeiodinase (5'-DI), iopanoic acid or ipodate, prevented the increase in serum T3 in rats injected with T4, but it did not diminish the increase in BBM transport of Pi. Administration of iopanoic acid and ipodate also prevented a 5-fold increase in 5'-DI activity in renal cortical tissue elicited by T4 administration. Treatment with T3 resulted in an increase of Pi transport across BBM from kidneys of rats subjected to dietary Pi deprivation due either to total fasting or to feeding of a low Pi diet. Further, T3 administration enhanced amiloride-sensitive Na+-H+ countertransport across BBM, but the uptake of 22Na+ by BBMV in the absence of pH gradient was not changed. The Na+ gradient-dependent uptake of L-[3H]proline by BBMV was slightly decreased, but the uptake of [14C]citrate was not changed in response to T3. Administration of T3 increased Pi transport in BBMV prepared from juxtamedullary cortex, but not in BBMV from superficial cortex. Conversely, the rate of Na+-H+ countertransport was enhanced, and the enzymatic activity of alkaline phosphatase was decreased in BBMV from superficial cortex; no changes in these parameters were found in BBMV from juxtamedullary cortex. Our results indicate that the stimulatory effect of administered T3 and/or T4 on renal BBM transport of Pi is distinct from the modulatory effect of dietary Pi intake and is not secondary to the beta-effect of catecholamines or to altered secretion of GH. Both T3 and T4 elicit the increase in BBM transport of Pi in a similar manner; T4 is effective even after profound inhibition of in vivo conversion of T4 to T3 by potent 5'-DI inhibitors. Administration of T3 stimulates Na+ gradient-dependent Pi uptake only in BBMV prepared from the juxtamedullary zone, and it stimulates the H+-Na+ countertransport only in BBMV from the outer cortical zone. These findings indicate that thyroid hormones modulate the two distinct transport functions of BBM derived from two different populations of renal proximal tubules.

Animals↗

PubMed1986

Cholecystographic agents and sulfobromophthalein inhibit the binding of L-thyroxine to plasma membranes of rat hepatocytes.

Cholecystographic agents and sulfobromophthalein (BSP) cause a major discharge of labeled T4 from the liver in man in vivo. In the present study we sought to determine if this discharge is partially due to inhibition of T4 binding to plasma membrane sites. Plasma membranes were isolated from hepatocytes of female Sprague-Dawley rats, and 5'-nucleotidase levels were measured to demonstrate plasma membrane viability. Specific binding of T4 (Ka, 1.01 X 10(8) M) was confirmed by displacement of labeled T4 by unlabeled hormone (10(-10)-10(-5) M). Displacement of labeled hormone was also produced by addition of tyropanoate, iopanoate, ipodate, or BSP. At 5-mM concentrations of inhibitor, the Ka for T4 declined to 4.00 X 10(7) M with BSP, 5.07 X 10(7) M with ipodate, 5.62 X 10(7) M with tyropanoate, and 7.43 X 10(7) M with iopanoate. Thus, a portion of the discharge of hepatic T4 after administration of these agents may be due to competitive inhibition of binding to plasma membrane sites.

Animals↗

PubMed1989

Thyroxine, triiodothyronine, and reverse triiodothyronine processing in the cerebellum: autoradiographic studies in adult rats.

Well confirmed evidence has demonstrated that the cerebellum is an important target of thyroid hormone action during development. Moreover, the presence of nuclear receptors and strong 5'-deiodinase activity in cerebella of adult rats have suggested that this region may continue to respond to thyroid hormones during maturity. Recent autoradiographic observations have focused attention on the cerebellar granular layer, in that [125I]T3 administered iv to adult rats was found to be selectively and saturably concentrated there. To determine the specificity of iodothyronine localization in the granular layer, we have now compared film autoradiographic observations made after iv [125I]T4 and iv [125I]rT3 with those found after iv [125I]T3. The results demonstrated that, as in the case of the latter hormone, labeling within the cerebellar cortex after iv [125I]T4 was both selective and saturable. Moreover, except for a lag in time to resolution and a longer retention time, the distribution of cerebellar radioactivity after iv labeled T4 was qualitatively similar to that seen after iv [125I]T3. However, the ability of T4 to become differentially concentrated in the granular layer of cerebellum was absolutely dependent on its ability to be converted intracerebrally to T3. Thus, pretreatment with ipodate, which blocks brain 5'-deiodinase activity and, therefore, the intracerebral formation of T3 from T4, completely prevented cerebellar granular layer labeling after iv [125I]T4 even though it did not interfere with differential labeling of this region by iv delivered [125I]T3. In the same experiments, propylthiouracil, a potent peripheral, but not central, 5'-deiodinase inhibitor, had no qualitative effect on the distribution of either T4 or T3 in cerebellum. By contrast with the results obtained after administering labeled T3 or T4, brain labeling after iv delivered [125I]rT3 was found to be no different from that produced by markers of cerebral blood flow, which rapidly enter and leave the brain without becoming incorporated into brain cells. This was so even during treatment with propylthiouracil and ipodate, both of which markedly prolonged the normally brief residence time of this iodothyronine in serum and brain. Overall, the autoradiographic results served to highlight the importance of the morphological approach for investigating thyroid hormone action and metabolism in brain. They demonstrated that only T3, whether entering as such from the circulation or formed in situ from T4 (but neither T4 itself nor iv administered rT3) was strongly, selectively, and saturably concentrated in the cerebellar granular layer of adult rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1987

Circadian and pulsatile thyrotropin secretion in euthyroid man under the influence of thyroid hormone and glucocorticoid administration.

The inhibitory action of thyroid hormones (TH) and glucocorticoids on circadian and pulsatile TSH secretion was investigated in groups of five normal men by sampling blood every 10 min for 24 h (start, 1750 h). Serum TSH was measured by a sensitive immunoradiometric assay. Continuous infusion of 50 micrograms T3 or 250 micrograms T4 for 8 h (1900-0300 h) significantly suppressed serum TSH levels (T3, P less than 0.025; T4, P less than 0.05; by paired t test). Administration of 3 g sodium ipodate 7 h before TH infusion did not alter the TSH response to T3, but T4-dependent suppression was abolished. Pulsatile TSH secretion [basally, 5.8 +/- 1.3 (+/- SD) pulses/24 h, as analyzed by the PULSAR program; 6.8 +/- 1.9 by the Cluster program] was not significantly altered by any of the experimental conditions. The additional finding of blunting of the TSH response to TRH after TH alone or ipodate and T3 suggests a predominantly pituitary feedback action of TH exerted via conversion of T4 to T3. In contrast, bolus injections of 4 mg dexamethasone (dex) at 1900 and 2200 h abolished TSH pulses for at least 6 h (PULSAR, 6.6 +/- 1.6 pulses/24 h basally vs. 3.6 +/- 3.0 under dex; Cluster, 7.0 +/- 2.7 pulses/24 h basally vs. 1.6 +/- 1.6 under dex). Dex administration also resulted in a prompt, sustained, and significant suppression of basal TSH (P less than 0.0005). Together with a normal serum TSH response to TRH (in separate experiments 1, 9, and 19 h after dex administration), these data suggest that glucocorticoid feedback occurs at a suprapituitary level.

Adult↗

PubMed1979

Determinants of the rate of intestinal absorption of oral cholecystographic contrast agents in the dog jejunum.

Successful opacification of the gallbladder during oral cholecystography depends on adequate absorption of the contrast agent from the intestine. The present studies were undertaken to define the specific characteristics of the intestinal mucosa and the properties of the various contrast agents which determine their rates of intestinal absorption. The polarity of the compounds was established by determining the ratios of their distribution between bulk solvents (benzene and water). In addition, the maximum aqueous solubility of each compound was determined. Using in vivo cannulated segments of dog jejunum, apparent passive permeability coefficients were measured. From these data, the apparent maximal rate of intestinal absorption was calculated. The six cholecystopaques studied differed markedly in polarity as judged by their varying ratios of distribution between benzene and water. The permeability coefficients varied inversely with the polarity of the compounds. However, the incremental changes in the coefficients were considerably less than the corresponding changes observed in the partition ratios. The rates of absorption of the more polar contrast agents (tyropanoate, iopronic acid, and iocetamic acid) were greater than the less polar compounds (iopanoic acid, sodium ipodate, and calcium ipodate) under the conditions in which the resistance of the unstirred water layer is not rate limiting and where bile acid micelles are not present.

Animals↗

PubMed1988

Furosemide, fenclofenac, diclofenac, mefenamic acid and meclofenamic acid inhibit specific T3 binding in isolated rat hepatic nuclei.

Previous studies with phenytoin (DPH) show that this inhibitor of thyroid hormone binding to plasma proteins also interacts with specific nuclear T3 binding sites. In order to further define the nuclear effects of drugs that inhibit plasma protein binding of thyroid hormones, we assessed furosemide and a number of non-steroidal antiinflammatory drugs using isolated rat liver nuclei. The effects were compared with those of DPH, ipodate and amiodarone. The T3 binding site in isolated nuclei (Ka 1.2 X 10(9)M-1) showed relative affinity triac approximately equal to T3 greater than T4. Drugs were studied over the concentration range 10(-3)-10(-7)M, approximating the known therapeutic total plasma concentrations, in competition with 125I-T3 0.1 nM, expressing inhibition as the percent decrement from maximum specific binding of 125I-T3 in drug vehicle (assay buffer or thanol 1-10%). Specific T3 binding was inhibited by furosemide to 78.8 +/- 3.5% at 2 mM, by fenclofenac to 37.6 +/- 2.8% at 1 mM, by meclofenamic acid to 70.2 +/- 2.4% at 0.1 mM, by mefenamic acid to 60.6 +/- 4.6% at 0.05 mM (each p less than 0.02) and by diclofenac to 87.4 +/- 5.6% at 0.2 mM (p less than 0.05). In comparison, DPH inhibited T3 binding to only 88.1 +/- 0.6% at 0.3 mM, as did calcium ipodate (68 +/- 3.5% at 1 mM, p less than 0.02). Amiodarone (0.3 mM), sodium salicylate (1 mM) and phenylbutazone (0.1 mM) were inactive. In order to achieve a level of nuclear receptor occupancy that approaches in vivo occupancy, the concentration 125I-T3 was increased over the range 0.1-0.5 nM.2+t

Amiodarone↗

PubMed1985

The effects of radiographic contrast agents and other compounds on the nuclear binding of L-[125I]triiodothyronine in dispersed human skin fibroblasts.

Using a dispersed intact cell assay system, we screened a number of compounds for their ability to compete for nuclear binding of L-[125I]T3 in cultured human skin fibroblasts incubated for 90 min at 37 degrees C. T3 inhibited nuclear [125I]T3 binding by 50% at a concentration of 3.4 +/- 0.3 (+/- SE) X 10(-10) M. 3,5-Dimethyl-3'-isopropyl-thyronine, a nonhalogenated thyroid hormone agonist, had an affinity for the nuclear thyroid hormone receptor (4.4 X 10(-9) M, as judged by 50% inhibition of nuclear [125I]T3 binding) that correlates well with its thyromimetic potency. Of several radiographic contrast agents and other compounds tested (iodipamide, iopanoic acid, sodium ipodate, sodium diatrizoate, sodium tyropanoate, diphenylhydantoin, carbamazepine, amiodarone hydrochloride, propylthiouracil, propranolol, and potassium iodide), only sodium ipodate (Oragrafin) and iopanoic acid (Telepaque) interfered with nuclear [125I]T3 binding, with 50% inhibition at 5 X 10(-5) and 1.8 X 10(-4) M, respectively. Interestingly, diphenylhydantoin and amiodarone, two compounds previously thought to interact with thyroid hormone receptors, did not impair fibroblast nuclear [125I]T3 binding at concentrations up to 10(-3) M. We conclude that this in vitro assay system with intact human cells is useful in evaluating the nuclear T3 receptor affinity of compounds that affect thyroid hormone action or metabolism. These studies more closely approximate in vivo conditions and, therefore, provide information not obtainable by studies with isolated nuclei or nuclear extracts.

Binding, Competitive↗

PubMed1988

Drug and fatty acid effects on serum thyroid hormone binding.

We directly compared the competitor potency for serum T4 binding of 11 nonsteroidal antiinflammatory drugs; the diuretics furosemide, ethacrynic acid, and bumetanide; diphenylhydantoin; the cholecystographic contrast agents iopanoate and ipodate; and six long-chain nonesterified fatty acids (NEFA) using equilibrium dialysis. To avoid artefacts that occur in competitor studies with diluted serum or isolated binding proteins, we used undiluted normal serum, with drugs added at concentrations that achieved high therapeutic total and free serum levels at equilibrium. Drug addition was based on the measured free fraction of each drug in serum. The free T4 fraction in normal serum (Tris buffer, pH 7.4; 37 C) was between 1.40 X 10(-4) and 1.53 X 10(-4). Drug-induced increases in T4 free fraction were: fenclofenac, 90%; aspirin, 62%; meclofenamic acid, 39%; diflunisal, 37%; mefenamic acid, 31%; and furosemide, 31%. Significant increases of 7-15% occurred with diclofenac, flufenamic acid, phenylbutazone, and diphenylhydantoin. Indomethacin, ketoprofen, tolmetin, ethacrynic acid, bumetanide, iopanoate, and ipodate were inactive at the concentrations studied. Addition of 2.0 mmol/L oleic acid had a negligible effect, but 3.5 mmol/L oleic acid inhibited T3 and T4 binding significantly. Other long chain NEFA (addition of 1.5 mmol/L) gave increases in free T4 fraction as follows: arachidonic acid, 26%; linolenic acid, 23%; and linoleic acid, 11%. Stearic and palmitic acids were inactive. The effect of 5 mmol/L oleic acid in serum could be reproduced by addition of 0.5 mmol/L to serum diluted 1:10, indicating that protein binding of NEFA is the major determinant that limits their competitor potency. These findings provide a basis for anticipating which potential inhibitors may cause important changes in serum thyroid hormone binding. The time course of such effects will be influenced by the pharmacokinetics of the inhibitor itself as well as the equilibrium findings described here.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1992

A radioimmunoassay for measurement of 3,5,3'-triiodothyronine sulfate: studies in thyroidal and nonthyroidal diseases, pregnancy, and neonatal life.

A highly sensitive, specific, and reproducible RIA has been developed to measure T3 sulfate (T3S). Only T4 sulfate cross-reacted significantly (approximately 3%) in the RIA; rT3 sulfate, T4, T3, rT3, and diiodothyronine cross-reacted less than 0.01%. T3S was bound by thyronine-binding globulin and albumin in serum. The free fraction of T3S in four normal sera averaged 0.25% compared to a value of 0.35% for T3. Therefore, T3S was measured in ethanol extracts of serum. Recovery of the nonradioactive T3S added to serum averaged 92%. The dose-response curves of inhibition of binding of [125I]T3S to anti-T3S antibody by serial dilutions of serum extracts were essentially parallel to the standard curve. The detection threshold of the RIA was 20 pmol/L (1.5 ng/dL). The coefficient of variation averaged 7.8% within an assay and 11% between assays. The serum concentration of T3S was (mean +/- SE) 76 +/- 7.2 pmol/L in normal subjects, 268 +/- 29 in hyperthyroid patients with Graves' disease, 92 +/- 28 in hypothyroid patients, 201 +/- 32 in patients with systemic nonthyroidal illnesses, 40 +/- 6.2 in pregnant women (15-31 weeks gestation), and 429 +/- 39 in cord sera of newborns; the values in hyperthyroidism, nonthyroidal illnesses, and newborns were significantly different from normal (P less than 0.01). The mean concentration of T3S in amniotic fluid samples at 15-31 weeks gestation (90 +/- 1.3 pmol/L) was significantly higher than the corresponding value in maternal serum (P less than 0.05) and significantly lower than the corresponding value in newborn cord blood serum (P less than 0.001). Oral administration of sodium ipodate (Oragrafin; 3 g) to two hyperthyroid patients was associated with a 76-190% increase in serum T3S at 8 h, followed by a gradual decrease to a nadir that was 25-60% of the baseline value 2-3 days after ipodate ingestion. We conclude that 1) T3S is a normal component of human serum, and its levels change substantially in several physiological and pathological conditions; 2) sulfation pathway plays an important role in the metabolism of iodothyronines in man; and 3) high serum T3S levels in newborns and low normal levels in pregnancy despite elevated thyronine-binding globulin levels may signify markedly different metabolism of T3S in the mother and fetus.

Adolescent↗

PubMed1993

The development of a radioimmunoassay for reverse triiodothyronine sulfate in human serum and amniotic fluid.

Sulfated iodothyronines including T4-sulfate (T4S) and T3-sulfate (T3S) have been identified in human serum and amniotic fluid. Little is known, however, about the existence of sulfate conjugation of reverse T3 (rT3S) in man. In this report, we employed a novel, sensitive, and specific rT3S RIA to address this question. The rabbit antiserum to rT3S was highly specific; T4, T3, rT3, and 3,3'-T2 showed less than 0.002% cross-reaction with the antiserum. Only T4S and T3S cross-reacted significantly (0.3% and 0.01%, respectively); other analogs cross-reacted less than 0.0001%. The detection threshold of the RIA was 14 pmol/L (1.0 ng/dL). The mean serum rT3S concentration (pmol/L) was 40 in euthyroid subjects. Values were similar in hypothyroid patients (38) and pregnant women (52) but significantly (P < 0.01) elevated to 176 in hyperthyroid patient, 74 in patients with nonthyroid illnesses, and 684 in cord sera of newborns. Serum rT3S increased significantly in hyperthyroid patients 1 day after administration of 1 g sodium ipodate orally. Reverse T3S was detected consistently in amniotic fluid at 14 to 22 weeks of gestation and showed a marked rise 1-3 weeks after intraamniotic administration of 500-1000 micrograms T4. The various data suggest that: (1) rT3S is a normal component of human serum and amniotic fluid; (2) it is derived from metabolism of T4 or rT3; (3) circulating rT3S increases in hyperthyroidism and in circumstances where type I 5'-monodeiodinating activity is low, e.g. nonthyroid illnesses, fetal life, and after administration of ipodate.

Amniotic Fluid↗

PubMed1979

Effects of three-day oral cholecystography on serum iodothyronines and TSH concentrations: comparison of the effects among some cholecystographic agents and the effects of iopanoic acid on the pituitary-thyroid axis.

The effects of repeated doses of oral cholecystographic agents on serum thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3) and thyrotrophin (TSH) concentrations were studied in 37 euthyroid male subjects. Iobenzamic acid, tyropanoic acid, iopanoic acid, and ipodate sodium, in a dosage of 3 g for 3 days, respectively, induced a significant decrease in serum T3 and an increase in rT3 within 24 h after the initial dose, followed by an increase in TSH and a slight increase in T4. The extent of the changes in rT3 varied between the agents, ipodate causing the greatest change, but without any relation to the changes in T3 or T4. Responses of serum T4, T3, rT3 and TSH concentrations to exogenous thyrotrophin-releasing hormone (TRH) and bovine TSH were also studied before and after 3-day doses of iopanoic acid. In 11 subjects given iopanoic acid, the response to TSH to TRH (500 micrograms, iv) was increased but the T3 response was unchanged. A dose of TSH (10 U.S.P. units, im) caused a significant increase in serum T3 and a decrease in TSH concentrations in 5 subjects both before and after cholecystography. It is thus suggested that in euthyroid subjects given multiple doses of oral cholecystographic agents, (1) the primary and consistent events are the reciprocal changes of serum T3 and RT3, although the extent of the changes is not coordinately reciprocal; (2) the responsiveness of the pituitary thyrotrophs and thyroid to TRH is preserved; and (3) the high basal and TRH-induced TSH in the serum may be ascribed to the decrease in the serum T3 concentration.

Administration, Oral↗

PubMed1987

Inhibitory effect of various radiographic contrast agents on secretion of thyroxine by the dog thyroid and on peripheral and thyroidal deiodination of thyroxine to tri-iodothyronine.

In previous studies we have found that the cholecystographic contrast agent ipodate induced a rapid, sustained and reversible inhibition of thyroxine (T4) secretion from perfused dog thyroid lobes. This type of inhibition of thyroid secretion has not been observed previously. To evaluate whether this effect is unique for ipodate, ten other iodine-containing radiographic contrast agents were tested. The four agents used for cholecystography (iocetamate, iodipamide, ioglycamate and iotroxate) all induced rapid inhibition of T4 secretion from TSH-stimulated perfused dog thyroid lobes, while none of six agents predominantly excreted through the kidneys (amidotrizoate, metrizamid, metrizoate, iodamide, diodone and ioxithalamate) influenced T4 secretion significantly. All the cholecystographic agents inhibited T4 deiodinases from dog thyroid and liver. Diodone also inhibited the deiodinases while none of the other compounds tested had any effect. The results indicate that the structure necessary to inhibit thyroid secretion is common to a number of cholecystographic agents and that it could be related to the structure responsible for the inhibitory effect of cholecystographic agents on T4 deiodinases.

Animals↗

PubMedDate not supplied

The medical management of Graves' disease.

There are many different approaches to treat Graves' hyperthyroidism. Medical therapy is used short-term to prepare patients for radioiodine or surgery, or it is used long term with the hope of achieving a remission. b-adrenergic blocking agents are useful in all patients without a contraindication, especially selective long-acting agents such as atenalol. Thionamides are the mainstay of medical treatment. Methimazole is more potent, may be used as a single daily dose, and may have less toxicity than PTU. Severe hyperthyroidism or thyroid storm may be treated with methimazole and ipodate. Patients are prepared for surgery with methimazole and SSKI, or b-adrenergic blocking agents and ipodate.

Journal Article↗

PubMed1981

Concentration and excretion of contrast agents during oral cholecystography as measured by computed tomography in dogs.

Nine healthy mongrel dogs were given 2 consecutive doses of 1 of 3 cholecystographic contrast agents (iopanoic acid, sodium ipodate, and sodium tyropanoate), followed by daily computed tomograms (CT) and abdominal radiographs in a randomized crossover study in order to determine: (a) the maximum time for excretion of the contrast material from the gallbladder, (b) the maximum time for elimination of contrast material from the blood, and (c) the correlation between the density of the gallbladder on CT and the actual concentration of iodine in the gallbladder bile. In all 9 animals gallbladder opacification disappeared on CT within 4 days after administration of the contrast material. Plain abdominal radiographs did not show gallbladder opacification after 2 1/2 days. Daily blood iodine measurements showed that all of the contrast material was cleared from the blood within 7 days after administration. In 7 dogs CT imaging of the gallbladder was followed by percutaneous aspiration of bile from the gallbladder using CT guidance. There was a direct linear correlation between the actual concentration of iodine in the bile and the density of the gallbladder on CT (r = 0.925). This suggests that CT measurements can be used to determine the concentration of contrast agents in the gallbladder during oral cholecystography.

Administration, Oral↗