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SUMMARY
The uptake of technetium-99m (99mTc) by the thyroid was measured 15 min after injection using a directional counting technique. The 'washout' of thyroidal 99mTc after intravenous perchlorate injection was quantitated so that separate measurement of the extrathyroidal activity of 99mTc was unnecessary.
In normal subjects the thyroidal uptake was 1·28 ± 0·61% of the administered dose (mean ± 1 s.d.); in primary myxoedema 0·26 ± 0·28%, in simple goitre 2·18 ± 2·10%, in thyrotoxicosis 11·0 ± 5·4%, in hypothyroid patients with Hashimoto's disease 4·50 ± 3·70% and in three patients with Pendred's syndrome the mean uptake was 9·3%.
The technique has been evaluated and its advantages as a simple alternative to quantitative scintiscanning are discussed.
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The uptake of technetium as pertechnetate by the thyroid is currently accepted as a useful index of thyroid function (Alexander, Harden & Shimmins, 1969). Although Pitt-Rivers & Trotter (1953) have shown thyroidal radioiodide concentration in the colloid using autoradiography, the intrathyroidal site of technetium concentration has not been determined previously.
In this paper, we report the results of autoradiographic studies with [99Tc] pertechnetate in rat thyroid using a method which prevents diffusion of soluble radionuclides until exposure to the autoradiographic emulsion is completed.
Four Sprague—Dawley albino adult male rats were used initially. Two rats received aminotriazole (0·1%) in their drinking water for 3 weeks before the study; the other two rats were on a normal diet. [99Tc]pertechnetate (300 μCi) was administered i.p. to each animal and after 1 h one animal in each group received 10 mg sodium perchlorate by the same route. Ninety minutes
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Endogenous glucocorticoid action is important in the structural and functional maturation of the fetal heart. In fetal mice, although glucocorticoid concentrations are extremely low before E14.5, glucocorticoid receptor (GR) is expressed in the heart from E10.5. To investigate whether activation of cardiac GR prior to E14.5 induces precocious fetal heart maturation, we administered dexamethasone in the drinking water of pregnant dams from E12.5 to E15.5. To test the direct effects of glucocorticoids upon the cardiovascular system we used SMGRKO mice, with Sm22-Cre-mediated disruption of GR in cardiomyocytes and vascular smooth muscle. Contrary to expectations, echocardiography showed no advancement of functional maturation of the fetal heart. Moreover, litter size was decreased 2 days following cessation of antenatal glucocorticoid exposure, irrespective of fetal genotype. The myocardial performance index and E/A wave ratio, markers of fetal heart maturation, were not significantly affected by dexamethasone treatment in either genotype. Dexamethasone treatment transiently decreased the myocardial deceleration index (MDI; a marker of diastolic function), in control fetuses at E15.5, with recovery by E17.5, 2 days after cessation of treatment. MDI was lower in SMGRKO than in control fetuses and was unaffected by dexamethasone. The transient decrease in MDI was associated with repression of cardiac GR in control fetuses following dexamethasone treatment. Measurement of glucocorticoid levels in fetal tissue and hypothalamic corticotropin-releasing hormone (Crh) mRNA levels suggest complex and differential effects of dexamethasone treatment upon the hypothalamic–pituitary–adrenal axis between genotypes. These data suggest potentially detrimental and direct effects of antenatal glucocorticoid treatment upon fetal heart function.
