Hyperthyroidism is associated with a significant increase in circulating glucocorticoid levels and hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. The aim of this study was to examine whether the HPA axis hyperactivity observed in hyperthyroidism may be explained by a disturbed feedback inhibition of endogenous glucocorticoids through two specific intracellular receptors in the brain: the high affinity mineralocorticoid receptor (MR) and the lower affinity glucocorticoid receptor (GR). Cytosolic receptor binding and gene expression was assessed in rats with short (7 days) and long standing (60 days) eu- and hyperthyroidism. Glucocorticoid receptor number and binding affinity (Kd) in the hippocampus were measured using [(3)H2]-dexamethasone radioreceptor assay. In situ hybridization was employed to examine the effects of hyperthyroidism on the GR and MR mRNA levels in the hippocampus and the pituitary. Both short- and long-term hyperthyroid rats showed pronounced reduction in the concentration of cytosolic GR in the hippocampus, without changes in binding affinity or changes in GR expression. In contrast, GR mRNA in the pituitary increased after 7 days and decreased after 60 days of thyroxin treatment. MR mRNA was moderately affected. Hyperthyroidism is associated with significant decreases in hippocampal GR levels supporting the hypothesis that hyperactivity of the HPA axis observed in experimentally induced hyperthyroidism may be attributed, at least in part, to decreased negative feedback at the level of the hippocampus. These findings further support the notion that a central locus is principally responsible for the hyperactivity of the HPA axis observed in hyperthyroidism.

These results suggest that cerebral protection during HCA may be achieved with erythromycin pharmacological preconditioning in the porcine model.

The external carotid artery (ECA) anterior branches, including the superior thyroid, the lingual, and the facial artery (STA, LA, and FA) present variability among cadaveric studies. These arteries may usually originate as isolated branches from the ECA anterior surface and atypically migrate proximally or distally and/or fused into trunks with the most common fusion that of the LA with the FA, into the linguofacial trunk (LFT), and the rarer ones those of the thyrolingual and thyrolinguofacial trunks. The current report describes a case of a bilateral fusion of the LA with the FA into an LFT and another case of a unilateral origin of the FA from the LA (aberrant FA). In a 75-year-old donated male cadaver, a bilateral symmetrical LFT coexisted with a right-sided STA origin from the ECA proximal origin, at the level of the common carotid artery (CCA) bifurcation. In an 82-year-old donated female cadaver, at the left side, the atypical origin of the FA from the LA proximal origin coexisted with a common trunk of the left CCA with the brachiocephalic artery, and an atypical origin of the STA from the CCA, 3.65 mm inferior to the CCA bifurcation. This report provides a detailed description of the abnormal origin of the ECA anterior branches, the potential fusion of these branches, their exact location, and the existence of an unusual origin proximal or distal to the CCA bifurcation. Aberrant origin and course remain important in surgical and interventional approaches. A thorough understanding of the typical and variable anatomy of the ECA anterior branches ensures safe and successful intervention. Careful preoperative staging and precise dissection are essential components of this process.

Aim: Normal adrenocortical responsiveness to stress involves glucocorticoid negative feedback to terminate hypothalamic-pituitary-adrenal (HPA) axis activation. Hypothyroidism is associated with a centrally mediated adrenal insufficiency associated. The aim of this study was to examine whether this may be explained by a disturbed glucocorticoid feedback through specific brain receptors: the mineralocorticoid (MR) and glucocorticoid receptor (GR). Methods: Cytosolic receptor binding and gene expression was assessed in male Sprague-Dawley rats (350gm) with short- (7 days) and long-standing (60 days) hypothyroidism (thyroidectomy). Glucocorticoid receptor number and binding affinity in the hippocampus were measured using radioreceptor assay. In situ hybridization was employed to examine GR and MRmRNA levels in the hippocampus and the pituitary. Results: No differences in receptor number or affinity were observed after 7days and 60days treatment. Increased GRmRNA expression in the anterior pituitary was observed in 7day hypothyroid rats under basal conditions compared to euthyroid rats (122.77+4.93 vs 99.65+4.83 DPM/mg; p<0.05), which was associated with significantly decreased GRmRNA levels after osmotic stress (100.82+2.8 vs 110.48+4.1 DPM/mg; p<0.05). No differences were observed at 60days. No effect on MR mRNA expression in the hippocampus was seen in basal condition after both 7- and 60days hypothyroidism. MRmRNA was significantly decreased in 60 days-hypothyroid rats compared to euthyroid after normal saline (3995.67+131.54 vs 5121.00+505.2 DPM/mg; p<0.05). Conclusion: Hypothyroidism resulted in significant changes in GR and MR mRNA levels, in the hippocampus and the pituitary, without changes in receptor number and binding affinity.

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