Khara M R, Pavlovych S I, Mykhaĭliuk V M
Fiziol Zh (1994). 2013;59(2):18-22.
In experiments on sexually mature rats we studied specific cholinergic regulations of the heart and the degree of its structural damage in hypothyroidism, depending on gender and hormone-productive activity of the gonads. Hypothyroidism in sexually mature males and females was modelled with mercazolil intragastric administration (75 mg/kg) daily during 15 days. We also studied the intensity of bradycardia, which occurred in response to electrical stimulation of vagus nerve and intravenous acetylcholine administration. The degree of structural heart damage was assessed by the percentage of damaged cardiomyocytes in the ventricles of myocardium. It was found that one of the mechanisms of bradycardia in merkazolil-induced hypothyroidism is an increase of the sensitivity of sinus node cholinergic receptors and release of more quanta of acetylcholine from stimulated nerves vagus endings, what was more intense in females. The intensity of bradycardia in hypothyroidism was more significant in gonadectomized animals than in individuals with preserved gonads. The mechanisms of its occurrence in males consist of release of greater amount of acetylcholine from the endings of the nerves vagus, and in females it was the result of significant increase of the sensitivity of sinus node cholinergic receptors. Regardless of the gonads activity, structural damage of the myocardium in merkazolil-induced hypothyroidism was more intensive in female rats.
在对性成熟大鼠的实验中，我们研究了甲状腺功能减退时心脏的特定胆碱能调节及其结构损伤程度，这取决于性别和性腺的激素分泌活性。性成熟的雄性和雌性大鼠通过每天灌胃给予甲巯咪唑（75毫克/千克），持续15天来模拟甲状腺功能减退。我们还研究了迷走神经电刺激和静脉注射乙酰胆碱后出现的心动过缓强度。通过心肌心室中受损心肌细胞的百分比来评估心脏结构损伤程度。结果发现，甲巯咪唑诱导的甲状腺功能减退时心动过缓的机制之一是窦房结胆碱能受体敏感性增加，以及受刺激的迷走神经末梢释放更多乙酰胆碱量子，这在雌性中更为明显。甲状腺功能减退时心动过缓的强度在去势动物中比性腺保留的个体更显著。其在雄性中发生的机制包括迷走神经末梢释放更多乙酰胆碱，而在雌性中则是窦房结胆碱能受体敏感性显著增加的结果。无论性腺活动如何，甲巯咪唑诱导的甲状腺功能减退时雌性大鼠心肌的结构损伤更严重。
