[Revealing of the role of NO in the pathogenesis of hypothyroidism].
There have been studied changes in blood and tissue NO levels and its correction in rats exposed to thyrectomy. NO levels were measured by the method of EPR using spin-trap sodium diethyldithiocarbamat. In 22 hours after thyrectomy contents of free nitric oxide in myocardium and liver tissues increased by 33% and 43,3% respectively. At the same time, intensive EPR signals of nitrosyl complexes of non-heme iron (FeSNO, g=2,03) were registered in EPR spectra of liver and myocardium tissues, at that free nitric oxide levels in blood of animals significantly decreased. In conclusion, NO-dependent signal system plays important role in the regulation of redox-homeostasis at hypothyroidism; long-term inadequate activation of NO synthesis may cause intensification of body oxidative stress, which in turn results in oxidative degradation of vasoactive nitric oxide, disturbance of blood vessel reactivity, alteration of tissue blood and oxygen supply, that in turn facilitate farther aggravation of oxidative metabolism disorder and the development of irreversible alterations in tissues. In case of treatment with L-thyroxin or L-thyroxin + oligocrin oxidative metabolism markers and content of NO in blood and tissues normalize, at that oligocrin enhances thyroxin efficacy. Thus, based on the obtained results of the conducted research we suggest that application of pharmaceutical preparations with antioxidant activity along with specific hormonal therapy is appropriate for treatment of hypothyroidism.
D000818:Animals; D004195:Disease Models, Animal; D004578:Electron Spin Resonance Spectroscopy; D007037:Hypothyroidism / Q000209:etiology* / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012307:Risk Factors
D009569:Nitric Oxide