Hashimoto thyroiditis and obstructive sleep apnea syndrome: is there any relation between them?

Hashimoto thyroiditis (HT), which is an autoimmune disease of thyroid gland, has been declared to present with concomitant several systemic diseases. In this study, the coexistence of the Hashimoto disease with the sleep apnea syndrome has been examined. Seven female patients (33-66 year of age) with Hashimoto thyroiditis were evaluated for sleep apnea syndrome. The diagnosis of Hashimoto disease was based on the high titers of anti-thyroid antibodies and histological findings. None of the patients had any complaints of sleep disturbances. Seven healthy subjects with similar age and sex characteristics were taken as the control group. All the patients and the control subjects were undertaken a full polysomnography (PSG). Five patients with HT showed the characteristics of obstructive sleep apnea syndrome (one severe, one moderate and three mild OSAS), whereas no sleep breathing disturbance was found in the control group. These findings suggest that sleep related breathing problems may develop in the patients with autoimmune thyroiditis even if they are euthyroid.

A study of serological markers of hepatitis B and C viruses in Istanbul, Turkey.

OBJECTIVE: This study was undertaken to investigate the prevalence of HBsAg, anti-HBs and anti-HCV positivity in Istanbul, Turkey. SUBJECTS AND METHODS: The frequencies of HBsAg, anti-HBs and anti-HCV positivity were determined in 1,157 randomly selected patients attending the outpatient clinic of Istanbul University Hospital, Istanbul, Turkey, during the years 1998 and 2001. All patients underwent complete physical and various routine laboratory examinations. RESULTS: Of the 1,157 patients, the prevalence of HBsAg, anti-HBs and anti-HCV was 6.6, 28.1 and 2.4%, respectively. It appeared that having dental and surgical procedures formed the risk factors for HBV infection. HBsAg positivity in the health care workers was not different from that of the other professions, but anti-HBs was significantly higher in this group. CONCLUSIONS: Our findings indicate that HBV infection occurs more frequently than HCV in Istanbul, and this poses an important health problem in the community.

The effects of vasopressin in isolated rat hearts.

The roles of cGMP, prostaglandins, the entry of extracellular Ca2+ through slow channels, endothelium and V1 receptors in the negative inotropic, chronotropic and coronary vasoconstrictor responses to arginine vasopressin (AVP) have been investigated in isolated perfused rat hearts. The bolus injection of 5 x 10(-5) M AVP produced a significant decrease in contractile force, heart rate and coronary flow. AVP also significantly decreased contractile force, heart rate and coronary flow in hearts pretreated with an inhibitor of soluble guanylate cyclase methylene blue (10(-6) M), an effective drug for removing endothelium saponin (500 micrograms/ml), an inhibitor of cyclooxygenase indomethacin (10(-5) M) or a calcium channel antagonist verapamil (5 x 10(-7) M). The potent V1 receptor antagonist [Deamino-Pen1, Val4, D-Arg8]-vasopressin (9 x 10(-5) M) did not alter effects of AVP but the very potent V1 receptor antagonist [beta-Mercapto-beta, beta-cyclopentamethylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin (8 x 10(-5) M) abolished these effects. Our results suggest that AVP produces negative inotropic, chronotropic and coronary vasoconstrictor effects in isolated perfused rat hearts. cGMP, prostaglandin release and Ca2+ entry does not involve in the effects of AVP. These effects are endothelium independent and mediated by V1 receptors. The use of V1 receptor antagonist [beta-mercapto-beta, beta-cyclopentamethylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin may be beneficial for preventing the negative inotropy, chronotropy and coronary vasoconstriction induced by AVP.

Ischemic-reperfused rat skeletal muscle: the effect of vasoactive intestinal peptide (VIP) on contractile force, oxygenation and antioxidant enzyme systems.

The effect of vasoactive intestinal peptide (VIP) on the nerve-stimulated contraction, tissue oxygenation, lipid peroxidation and antioxidant enzymes activities-superoxide dismutase and catalase was investigated in the rat gastrocnemius muscle exposed to 4 h ischemia-4hr reperfusion. Ischemia caused significant decrease in muscle contractile force, oxygenation and superoxide dismutase enzyme activity. Reperfusion of ischemic muscle increased the muscle contractile force and restored the tissue oxygenation to the baseline level. Superoxide dismutase and catalase activities of reperfused muscle increased significantly. However neither ischemia nor reperfusion affected gastrocnemius muscle malondialdehide (MDA) levels. VIP administration at the onset of reperfusion significantly increased skeletal muscle contractile force and tissue oxygenation even higher than baseline and reperfusion values. VIP also normalized the increased superoxide dismutase and catalase activities of reperfused skeletal muscle. In conclusion, VIP, acting as a powerful antioxidant and preserving contractile machinery seems to be a promising endogenous peptide that can salvage the skeletal muscle from severe ischemia-reperfusion injury.

The role of nitric oxide in the regulation of coronary flow and mechanical function of isolated, perfused rat hearts.

The role of nitric oxide (NO) in the regulation of coronary flow and mechanical function under basal conditions and when exposed to nifedipine was studied in perfused rat hearts. Inhibition of basal release of NO by bolus injections of NG-nitro-L-arginine (L-NNA) (90 mM) and NG-nitro-L-arginine methyl ester (L-NAME) (185, 370 and 740 mM) induced significant decrease in coronary flow, contractile force and heart rate. L-NAME in the doses of 185, 370 and 740 mM also decreased significantly contractile force and heart rate during treatment with 170 microM nifedipine. However, the same doses of L-NAME caused an insignificant reduction in coronary flow in the presence of nifedipine. These findings suggest that NO has an important role in the regulation of coronary flow and mechanical performance under basal conditions and during the hearts exposed to nifedipine. Nifedipine may attenuate the myocardial ischaemia induced by the loss of NO production.