Does the radioactive iodine dose affect smell, taste sensation and nose function?

OBJECTIVE: To detect whether the adverse effects of post-operative radioactive iodine therapy following differentiated thyroid cancer on smell, taste and nasal functions were associated with radioactive iodine dose. METHODS: Fifty-one patients who had undergone total thyroidectomy because of differentiated thyroid cancer were divided into two groups depending on the post-operative radioactive iodine therapy dose: low dose group (50 mCi; 21 patients) and high dose group (100-150 mCi; 30 patients). The Sniffin' Sticks smell test, the Taste Strips test and the 22-item Sino-Nasal Outcome Test were performed on all patients one week before therapy, and at two months and one year following therapy. RESULTS: Statistically significant differences were detected in the Sniffin' Sticks test results, total odour scores, total taste scores and Sino-Nasal Outcome Test results between the assessment time points. There was no statistically significant difference between the low and high dose groups in terms of odour, taste or Sino-Nasal Outcome Test scores either before or after therapy. CONCLUSION: Radioactive iodine therapy has some short- and long-term adverse effects on nasal functions and taste and odour sensations, which affect quality of life. These effects are not dose-dependent.

Dietary selenium and vitamin E intakes alter beta-adrenergic response of L-type Ca-current and beta-adrenoceptor-adenylate cyclase coupling in rat heart.

Previously we have shown that both insufficient (combined with vitamin E deficiency) and excess intake of selenium (Se) impairs isoproterenol (ISO)-induced contractions of rat papillary muscle. In the present study, we used patch-clamp and biochemical techniques to investigate mechanisms of this effect in rats fed a Se- and vitamin E-deficient, a Se-excess or a normal diet. Whole-cell configuration of patch-clamp technique was used to investigate L-type Ca(2+) currents (I(Ca,L)) and their regulation by beta-adrenergic receptor stimulation in enzymatically isolated single rat ventricular myocytes. Alteration of Se and vitamin E intake did not affect peak I(Ca,L), but the threshold potential of activation was significantly different among groups. Maximal I(Ca,L) responses to ISO were depressed in both experimental groups, but the EC(50) values were not affected. In the Se-deficient group, basal, ISO- or forskolin-induced adenylate cyclase (AC) activity, measured in cardiac membrane preparations, was reduced when compared to the control, whereas 5' guanylyimidodphosphate (GppNHp) stimulated activity was unaffected. Decreased beta-adrenoceptor density and reduced GppNHp-induced affinity shift in ISO binding were also observed in the deficient group. No such differences were present in the excess group. These results suggest that combined Se and vitamin E deficiency interferes with beta-adrenoceptor-AC coupling, whereas excess intake of Se does not affect it. Thus, in the deficient group, the impairment of I(Ca) responses to ISO may be a result of a defect in beta-adrenoceptor-AC pathway. Impairment of I(Ca) response in the excess group, however, appears to have a different underlying mechanism.

Opioid receptor ligands in human hepatic encephalopathy.

BACKGROUND/AIMS: Opioid peptides may contribute to some of the manifestations of hepatic encephalopathy. To address the role of the opioid system in the pathogenesis of hepatic encephalopathy, three representative opioid ligands were measured in plasma and cerebrospinal fluid of patients with hepatic encephalopathy. METHODS: Plasma and cerebrospinal fluid were obtained in three groups of patients: group 1: patients with hepatic encephalopathy; group 2: patients with lumbar back pain; group 3: healthy controls. Met-enkephalin, leu-enkephalin and beta-endorphin levels were measured in extracted plasma and cerebrospinal fluid samples by radioimmunoassay. RESULTS: Plasma met-enkephalin levels were 656% (p<0.05) and 301% (p<0.05) and cerebrospinal fluid met-enkephalin levels were 1481% (p<0.01) and 645% (p<0.05) higher when compared to healthy control and pain control patients, respectively. Although plasma and cerebrospinal leu-enkephalin levels were elevated in patients with hepatic encephalopathy, the increases were not statistically significant. Plasma and cerebrospinal beta-endorphin levels were similar in the three study groups. CONCLUSIONS: The results of this study support accumulating data on the role of the delta opioid receptor ligand met-enkephalin in the pathogenesis of hepatic encephalopathy, and provide a rationale for the use of opioid receptor antagonists in the treatment of hepatic encephalopathy.

The effects of verapamil and nimodipine on bupivacaine-induced cardiotoxicity in rats: an in vivo and in vitro study.

UNLABELLED: The purpose of this in vivo and in vitro study was to compare the effects of verapamil or nimodipine pretreatment on bupivacaine-induced cardiotoxicity. In the in vivo study, the dose-response curve for the 50% lethal dose (LD50) of bupivacaine was determined for rats. Two separate groups of rats were pretreated with i.v. verapamil 150 microg/kg (n = 35) or i.v. nimodipine 200 microg/kg (n = 35). Each pretreatment group was then subdivided into four groups of at least four rats each. Three minutes after pretreatment, bupivacaine was administered to each of four groups in doses of 2.5, 3.0, 3.25, and 3.5 mg/kg, respectively. Both verapamil and nimodipine pretreatment increased the LD50 and 95% confidence intervals for bupivacaine and increased survival. In the in vitro study, the effects of verapamil or nimodipine perfusion on bupivacaine cardiotoxicity (negative chronotropic, negative inotropic, and arrhythmogenic effects) and coronary perfusion pressure (CPP) were investigated in isolated, perfused rat heart preparations. Depression of heart rate, contractile force, and CPP, and the incidence of arrhythmias caused by bupivacaine alone were similar to those caused by bupivacaine after verapamil pretreatment. In contrast, bupivacaine induced less negative chronotropic effects (P < 0.05, paired t-test) and arrhythmias (P < 0.05, chi2 analysis) after nimodipine pretreatment. The results of this study demonstrate that both verapamil and nimodipine pretreatment decrease bupivacaine-induced cardiotoxicity in vivo, whereas only nimodipine pretreatment decreased bupivacaine-induced cardiotoxicity and arrhythmias in vitro. IMPLICATIONS: In this experimental study consisting of two stages (in vivo and in vitro), we compared the effects of two calcium channel-blocking drugs (verapamil and nimodipine) on bupivacaine toxicity. Bupivacaine is a local anesthetic frequently used in clinical practice, and cardiotoxicity is one of its severe side effects. Verapamil and nimodipine were both effective in decreasing bupivacaine cardiotoxicity in this rat model.