UMLS:C0011570 - FACTA Search

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were made with a total of 272 fattening pigs. Iodine deficiency both in rations of soya bean meal and rape seed meal increased the weight of the thyroid gland and the height of the epithelium cells and significantly reduced the T4 and T3 level in the serum. Iodine supplements to the rape seed meal rations distinctly diminished the goitrogenic effect, did not, however, cancel it out. Stage of goiter and depression of consumption were--different shown by the T3 and T4 level in the serum. Highly significant relations were calculated between live weight gain, weight and the height of the epithelium cells on the one hand and the T4 level in the serum on the other. Iodine supplementations of rations without thyrostatic components should amount to greater than or equal to 0.1 mg/kg. Iodine supplementations of 0.5 mg/kg feed are at present recommended to rations with rape seed meal quotas of less than 8%.
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PMID:[Effect of iodine, copper and zinc supplements to rations with a high quota of rapeseed extract meal on the growth and thyroid function of fattening swine. 3. The effect on weight and the histomorphometric findings in the thyroid and on the serum T3 and T4 concentrations]. 374 Nov 30

The chemistry of low-osmolality contrast agents is reviewed, the effects of these agents on vascular and organ physiology are compared with the effects of conventional ionic contrast media, and guidelines for intravascular use of the low-osmolality agents in selected high-risk patients are presented. Three low-osmolality contrast agents, the nonionic media iohexol (Omnipaque, Winthrop-Breon) and iopamidol (Isovue, Squibb) and the dimeric medium ioxaglate meglumine-sodium (Hexabrix, Mallinckrodt) have recently been introduced into the contrast-media market. Compared with conventional ionic contrast media, these new agents demonstrate approximately one third of the osmolality per given iodine concentration (degree of roentgenographic opacification). Therefore, the risks of hyperosmolarity-induced reactions to contrast media are lower with the new agents. The low-osmolality agents may be associated with a reduced incidence of contrast-media-induced hypersensitivity reactions. Because of their lower osmolality, these agents produce less vessel dilation, vascular endothelial damage, and associated pain and discomfort than equi-iodine concentrations of the conventional ionic media. They also demonstrate a reduction in the incidence and severity of contrast-media-induced renal vasoconstriction and proteinuria, hemodynamic alterations, negative chronotropic effects, depression of myocardial contractility, and neurotoxicity in the presence of an altered blood-brain barrier. These low-osmolality agents produce fewer undesirable physiological effects than conventional contrast agents, but the cost of the new products can be more than 10 times as great. Therefore, the new products should be used selectively in patients known to be at increased risk for reactions to intravascular contrast media. A scoring system was developed to permit rapid recognition of documented single or multiple risk factors and subsequent determination of whether to administer a low-osmolality agent.
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PMID:Evaluation of intravascular low-osmolality contrast agents. 378 Jan 59

To determine the effect of a combined oral progestin on 5 tests of thyroid function, 21 parous women at least 8 weeks postpartum and with histories of regular menses were studied. A complete physical examination showed all to be normal. The 5 tests performed were radioactive iodine uptake (RAI) at 2 and 24 hours, serum protein-bound iodine (PBI), thyroxine iodine by column, triiodothyronine absorption test, and serum cholesterol. 2 baseline determinations of each test except the RAI were performed on each subject on separate days. Only euthyroid subjects were further tested. Of these 16 were given 10 mg of medroxyprogesterone acetate in combination with .05 mg of ethinyl estradiol cyclically for 20 days. Thyroid function tests were repeated at various intervals from the end of the first week of therapy to over 4 months after starting therapy. Cholesterol and RAI determinations were extremely variable precluding any evidence of drug effect. The other 3 tests showed consistent changes in all patients studied. The serum PBI and thyrozine-iodine by column tests both showed slight elevation within the first week of therapy and further elevation 1 months thereafter. These changes approached hyperthyroidism levels. The triiodothyronine absorption test showed little change in the first week but a definite downward shift thereafter with a maximum depression at 3 months of therapy. This change reached hypothyroidism level. If test were done during the 1 week each month patients were not taking the drug, results were the same. These changes are thought to be due to the estrogen component of the contraceptive drugs. Those physicians depending on these thyroid tests for diagnosis should be aware of these changes in patients taking these drugs.
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PMID:The effect of an oral contraceptive on tests of thyroid function. 417 61

1. The iodide space in rabbit brain varies greatly depending on the conditions under which it is determined.2. When (131)I(-) only is used the iodide space 4 hr after administration of the marker is of the order of 2%. The iodide content of the cerebrospinal fluid (c.s.f.) is about 1% of that of the serum.3. Depression of the active iodide transport by perchlorate increases the space to 8.2% and the iodide content of the c.s.f. to 26% of that of the serum.4. The active iodide transport can also be depressed by saturation with unlabelled iodide. Up to a serum iodide concentration of 5 mM the space determined after 5 hr remained constant at 2.7%. The iodide space grew when the serum iodide content was enhanced from 5 to 20 mM, to become constant at a value of 10.6% on further increase of the serum iodide (up to 50 mM). The iodide content of the c.s.f. increased in a similar manner as the space with the iodide concentration of the serum to about 1/3 of the serum concentration. The iodide space of the muscle was independent of the plasma iodide content.5. From 4 to 8 hr after administration of (131)I(-) alone or with unlabelled iodide (to a serum concentration of 15 mM) the iodide space remained relatively constant.6. When (131)I(-) was administered in the fluid with which the ventricles were perfused an iodide space of about 7% was attained after about 5 hr.7. In experiments in which (131)I(-) was administered intravenously and the sink action of the c.s.f. was eliminated by perfusion of the ventricles with a perfusate containing as much (131)I(-) as the plasma, the iodide space was 10.2%. When in addition active iodide transport was depressed by perchlorate the space increased to 16.8%.8. Intravenous administration of labelled and unlabelled iodide (to a serum concentration of 20-40 mM) and ventricle perfusion with the same concentration of (131)I(-) and unlabelled iodide as in the plasma yielded an iodide space of 20.8%. In similar experiments the iodide concentration of the perfusate was so adjusted that after 5 hr perfusion its iodide content hardly changed during the passage through the ventricles. Under these conditions the iodide concentration of the extracellular and perfusion fluids can be considered to be near equal. The iodide space computed on the basis of the iodide content of the outflowing fluid was 22.5%.9. The large iodide space could be equated with the extracellular space if the iodide remained extracellular. This seems to be the case in the muscle where the iodide space is similar to the inulin space.10. The large effects on the iodide space of perchlorate and saturation with unlabelled iodide in experiments in which the marker was administered intravenously and in the perfusate (7 and 8) suggests the presence of an active iodide transport from the brain extracellular fluid into the blood over the blood-brain barrier.
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PMID:The iodide space in rabbit brain. 431 Sep 42

1. Dibutyryl cyclic AMP, injected towards the superior cervical ganglion of the cat, produced no consistent responses.2. Imidazole, injected towards the ganglion, regularly produced facilitation, both during intermittent and continuous preganglionic stimulation. This effect was dose-dependent and lasted 2-10 minutes.3. Aminophylline, injected towards the ganglion, regularly produced depression of ganglionic transmission, both during intermittent and continuous preganglionic stimulation. This effect was also dose-dependent and lasted 1-4 minutes. Papaverine produced the same type of response as aminophylline.4. Imidazole potentiated the ganglionic response to 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), while aminophylline depressed it.5. The results of the present experiments are consistent with the view that cyclic AMP may have a mediating role in the process of ganglionic transmission.
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PMID:The effect of N6-2'-O dibutyryl 3',5' cyclic adenosine monophosphate, imidazole and aminophylline on ganglionic transmission in the superior cervical ganglion of the cat. 436 81

Hyperthyroidism developed in three patients during the administration of potassium iodide given for the purpose of blocking the thyroid uptake of radioactive iodine liberated in the course of the 125I-fibrinogen test. In a consecutive series of 31 geriatric patients, who received potassium iodide for the same reason, biochemical hyperthyroidism developed in three instances and significant depression of thyroid function was observed in 10. The performance and the interpretation of the 125I-fibrinogen test are unaffected if iodide is not administered to the patient. The possible hazards to some patients of either induced hyperthyroidism or faulty assessment of thyroid function may be greater than the risk of thyroid irradiation. It is suggested that for the performance of the 125I-fibrinogen test potassium iodide need not be given to the elderly and should be given in a dose of 30 mg daily for two weeks to younger patients. Under certain circumstances potassium perchlorate may be a preferable drug for preventing the accumulation of radioactive iodine by the thyroid.
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PMID:Hyperthyroidism induced by potassium iodide given in the course of 125I-fibrinogen test. 445 24

Previous studies of thyroid function during various infections have yielded conflicting results, but most have suggested an acceleration of peripheral thyroxine (T(4)) turnover during the acute infectious illness. In the present studies, thyroid function was examined by a method allowing simultaneous analysis of both endogenous thyroidal release and peripheral T(4) disposal in normal volunteers after induction of acute falciparum malaria. Subjects received iodide-(125)I, followed in 5-7 days by (131)I-T(4) intravenously. 4 days later, infection was induced by the injection of parasitized red blood cells. Bidaily measurements of serum protein-bound (125)I and protein-bound (131)I, and urinary (125)I and (131)I, together with frequent estimates of serum (127)I-T(4) (Murphy-Pattee) and free T(4) (FT(4)), were made during a control period, during acute illness, and during convalescence. Alterations in the peripheral metabolism of (131)I-T(4) during infection included significant decreases in the fractional disappearance rate for T(4) [(k)], and in the clearance and daily disposal of T(4), all of which returned to control values during convalescence. Total serum (127)I-T(4) increased late in the infected period to become greater during convalescence than either before or during infection, while FT(4) did not increase significantly until convalescence. An analysis of serum (131)I-T(4)/(127)I-T(4) and (131)I-T(4)/PB(125)I ratios confirmed these observations. The slope with time of ratios for urinary (125)I/(131)I, a reflection of thyroidal iodine release, was decreased during infection, but rebounded to control values during the convalescent period. The observed increments in serum (127)I-T(4) concentration in the convalescent phase may reflect in part the slowing of (k), but together with the rising ratios of urine (125)I/(131)I suggests enhanced thyroidal T(4) secretion immediately after the acute illness. Thus, with malarial infection, there appears to be an initial depression followed by a rebound in rates of thyroidal iodine release. In contradistinction to other infections, fractional turnover and daily disposal of hormone is decreased in malaria, perhaps due to hepatic dysfunction and the consequent impairment in cellular deiodinative processes.
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PMID:Alterations in thyroid iodine release and the peripheral metabolism of thyroxine during acute falciparum malaria in man. 456 63

The inotropic effects of five non-depolarizing muscle relaxants were examined using an isolated canine heart muscle preparation. Except for fazadinium, all drugs were studied in their commercially available forms. d-Tubocurarine chloride (dTc) and metocurine iodide (MTC) produced dose-dependent decreases in isometric force (F) and the maximum velocity of force development (dF/dt) at concentrations greater than 22.5 x 10(-3) g/L for dTc and greater than 15.0 x 10(-3) g/L for MTC, concentrations which are 3 and 6 times higher than estimated clinical serum concentrations, respectively. Myocardial depression was about 3 times less with MTC than with dTc at equipotent concentrations. The degree of depression in F and dF/dt produced by MTC was almost identical with that produced by phenol, a preservative of MTC, indicating that MTC-induced myocardial depression may be due to the effect of the preservative. Pancuronium bromide (PC) produced a dose-dependent increase in F and dF/dt and decrease in the time to peak force. PC-induced changes in F, dF/dt, and time to peak force were inhibited by administration of propranolol 10(-6) M. The results indicate that PC possesses a positive inotropic effect mediated by beta-adrenergic stimulation. Alcuronium chloride did not change F or dF/dt at concentrations from 5.0 x 10(-3) to 60.0 x 10(-3) g/L. Frazadinium bromide increased F and dF/ dt slightly at a low concentration (1.875 x 10(-2) g/L), but further increases in its concentration returned the values of F and dF/dt to control levels. F and dF/dt were not altered in vitro by concentrations of relaxants that would be anticipated in plasma in vivo in patients given clinically effective doses of 0.3 mg/kg of dTc, 0.1 mg/kg of MTC or PC, 0.2 mg/kg of alcuronium chloride, or 0.75 mg/kg of fazadinium bromide.
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PMID:Inotropic effects of non-depolarizing muscle relaxants in isolated canine heart muscle. 610 62

Methimazole [1-methyl-2-mercaptoimidazole (MMI)] was given to normal male rats in their drinking water in concentrations ranging from 0.0001-0.05% for either 1 week or 1 month. Serum MMI levels in the rats ranged from 0.008-19.6 micrograms/ml, and were similar after 1 week and 1 month of treatment. Serum MMI was linearly related to the MMI concentration in the drinking water (r = 0.98, P less than 0.001). In contrast, intrathyroid MMI content plateaued with increasing MMI concentrations in the water, and was linearly related to the logarithm of the MMI concentration. At the highest MMI concentration (0.05%), thyroid MMI contents were similar in the 1-week and 1-month groups (approximately 1 X 10(-4) M). Surprisingly, at lower MMI concentrations, thyroid MMI content was significantly higher in the 1-week group than the 1-month group. Thyroid function was inhibited by MMI with similar depression of serum T4 or T3 after 1 week or 1 month of MMI treatment. Although the MMI concentration for 50% suppression of thyroid PBI was 0.003% in both groups, thyroid MMI content at this MMI concentration was 97 microM after 1 week but only 15 microM after 1 month. The continued thyroid-inhibiting activity of MMI at 1 month, despite a striking decrease in thyroid MMI content, may relate to intrathyroid iodide depletion, which was more severe after 1 month (thyroid 127I = 40 microM) than after 1 week (thyroid 127I = 140 microM) or in controls (470 microM). Rats were given 0.05% MMI for either 1 week or 1 month, and the drug was then withdrawn. In the 1-week group, serum MMI disappeared biexponentially, with a rapidly declining phase (t1/2 = 3.2 h) and a second, slower disappearance phase (t1/2 = 47.7 h). Similar findings were noted after 1 month of treatment. The disappearance of thyroid MMI was also biexponential after 1 week, but this variable could not be evaluated after 1 month because thyroid MMI fell rapidly to undetectable levels. There was a highly significant correlation in the 1-week group between the disappearance of MMI from the thyroid and the recovery of thyroid function as assessed by thyroid PBI (r = 0.81, P less than 0.01). Despite the very rapid disappearance of MMI from the thyroid after 1 month of treatment, the recovery time of thyroid PBI was significantly longer than after 1 week of treatment (2.1 days vs. 1.4 days for 50% recovery, P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Methimazole pharmacology in the rat: studies using a newly developed radioimmunoassay for methimazole. 619 91

The action of an irreversible inhibitor of acetylcholinesterase (AChE), the organophosphorus compound, ecothiopate iodide, and of a reactivator of phosphorylated AChE, contrathion, were analysed on acetylcholine (ACh) receptors and cholinergic synaptic transmission in the buccal ganglion of Aplysia. At high concentration (above 10(-4)mol X 1(-1), both compounds exerted a curare-like depression on ACh receptors which was reversible with washing. Both compounds reversibly facilitated the current response to ionophoretic application of ACh and increased the evoked postsynaptic current (PSC) as well as the miniature postsynaptic currents (MPSCs). All responses also showed an increase in decay time. These modifications, when induced by ecothiopate iodide were irreversible by washing; however they could be reversed if first washed with contrathion. Neither the organophosphate compound or the oxime did change the number of quanta released per impulse. The current response to ionophoretic application of carbachol also increased after ecothiopate iodide was added. In the limits of the method used, the conductance and opening time of postsynaptic ionic channels opened by ACh were not found to be modified by the two compounds. It was concluded that the facilitatory action of the organophosphorus inhibitors cannot be solely explained by the inhibition of ACh hydrolysis.
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PMID:Direct and indirect effects of an organophosphorus acetylcholinesterase inhibitor and of an oxime on a neuro-neuronal synapse. 630 Jul 51

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