Safa-Tisseront V, Ponchon P, Blanc J, Elghozi J L
Laboratoire de pharmacologie, CNRS URA 1482, faculté de médecine Necker, Paris.
Arch Mal Coeur Vaiss. 1998 Aug;91(8):1003-7.
A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). Thyrotoxicosis was produced by a daily intraperitoneal (i.p.) injection of L-thyroxine (0.5 mg/kg body wt in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvant. Autonomic blockers were administered intravenously: atropine (0.5 mg/kg), atenolol (1 mg/kg), atenolol + atropine or prazosin (1 mg/kg). Eight animals were studied in each group. Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423 +/- 6 vs 353 +/- 4 bpm; p < 0.001, unpaired Student's tests), systolic BP elevation (142 +/- 3 vs 127 +/- 2 mmHg; p < 0.001), pulse pressure increase (51 +/- 2 vs 41 +/- 2 mmHg, p < 0.01), cardiac hypertrophy (1.165 +/- 0.017 vs 1.006 +/- 0.012 g, p < 0.001), weight loss (-21 +/- 2 g; p < 0.001) and hyperthermia (37.8 +/- 0.1 vs 37.0 +/- 0.1 degrees C, p < 0.001). The intrinsic HR observed after double blockade (atenolol + atropine) was markedly increased after treatment with thyroxine (497 +/- 16 vs 373 +/- 10 bpm, p < 0.05). Vagal tone (difference between HR obtained after atenolol and intrinsic HR) was positively linearly related to intrinsic HR (r = 0.84; p < 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyrodism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (analyses on 102.4 sec segments, modulus 1.10 +/- 0.07 vs 1.41 +/- 0.06 mmHg; p < 0.01). Prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in experimental hyperthyroidism. Increased intrinsic HR resulting from the direct effect of thyroid hormone on the sinoatrial node is the main determinant of a tachycardia leading to a subsequent rise in cardiac output. The resulting BP elevation could reflexly induce a vagal activation and a sympathetic (vascular and cardiac) inhibition.
关于自主神经活动与甲状腺激素在控制心率（HR）和血压（BP）方面相互作用的确切性质，仍存在大量不确定性。通过每日腹腔内（i.p.）注射L-甲状腺素（0.5 mg/kg体重，溶于1 ml 5 mM氢氧化钠中，共注射5天）来诱发甲状腺毒症。对照大鼠每日腹腔内注射甲状腺素溶剂。静脉注射自主神经阻滞剂：阿托品（0.5 mg/kg）、阿替洛尔（1 mg/kg）、阿替洛尔 + 阿托品或哌唑嗪（1 mg/kg）。每组研究8只动物。甲状腺素治疗足以诱发显著程度的心动过速（423±6 vs 353±4次/分钟；p<0.001，非配对学生检验）、收缩压升高（142±3 vs 127±2 mmHg；p<0.001）、脉压增加（51±2 vs 41±2 mmHg，p<0.01）、心脏肥大（1.165±0.017 vs 1.006±0.012 g，p<0.001）、体重减轻（-21±2 g；p<0.001）和体温过高（37.8±0.1 vs 37.0±0.1℃，p<0.001）。用甲状腺素治疗后，双重阻断（阿替洛尔 + 阿托品）后观察到的固有心率显著增加（497±16 vs 373±10次/分钟，p<0.05）。迷走神经张力（阿替洛尔后获得的心率与固有心率之差）与固有心率呈正线性相关（r = 0.84；p<0.01）。阿替洛尔对甲状腺功能亢进大鼠的心率和血压变异性均无影响。甲状腺毒症与血压变异性的0.4 Hz成分降低有关（对102.4秒片段进行分析，模量1.10±0.07 vs 1.41±0.06 mmHg；p<0.01）。哌唑嗪对这些动物的该0.4 Hz成分无影响。这些数据表明实验性甲状腺功能亢进时血管和心脏交感神经张力功能降低。甲状腺激素对窦房结的直接作用导致固有心率增加，这是心动过速继而导致心输出量增加的主要决定因素。由此导致的血压升高可反射性诱发迷走神经激活和交感神经（血管和心脏）抑制。
