Safa-Tisseront V, Ponchon P, Laude D, Elghozi J L
Laboratoire de Pharmacologie, CNRS URA 1482, Faculté de Médecine Necker, Paris, France.
J Hypertens. 1998 Dec;16(12 Pt 2):1989-92. doi: 10.1097/00004872-199816121-00020.
To study the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP).
Thyrotoxicosis was produced by injections of L-thyroxine (0.5 mg/kg/day for five days). Blockers were atropine (0.5 mg/kg), atenolol (1 mg/kg) or prazosin (1 mg/kg). Eight animals were studied in each group. Spectral analyses was performed using continuous BP time series obtained in conscious rats.
Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423+/-6 vs 353+/-4 bpm, P < 0.001, unpaired Student's t test), systolic BP elevation (142+/-3 vs 127+/-2 mmHg, P < 0.001) and cardiac hypertrophy (1.165+/-0.017 vs 1.006+/-0.012 g, P < 0.001). The intrinsic HR was markedly increased after treatment with thyroxine (497+/-16 vs 373+/-10 bpm, P < 0.05). Vagal tone was positively linearly related to intrinsic HR (r = 0.84, P< 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyroidism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (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 hyperthyroid animals.
These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic HR could be the main determinant of tachycardia. The BP elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.
研究自主神经活动与甲状腺激素在心率（HR）和血压（BP）调控中的相互作用。
通过注射左旋甲状腺素（0.5毫克/千克/天，持续五天）诱发甲状腺毒症。阻滞剂为阿托品（0.5毫克/千克）、阿替洛尔（1毫克/千克）或哌唑嗪（1毫克/千克）。每组研究八只动物。使用清醒大鼠连续血压时间序列进行频谱分析。
甲状腺素治疗足以诱发显著程度的心动过速（423±6对353±4次/分钟，P<0.001，非配对学生t检验）、收缩压升高（142±3对127±2毫米汞柱，P<0.001）和心脏肥大（1.165±0.017对1.006±0.012克，P<0.001）。甲状腺素治疗后固有心率显著增加（497±16对373±10次/分钟，P<0.05）。迷走神经张力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赫兹成分降低有关（模量1.10±0.07对1.41±0.06毫米汞柱，P<0.01）。哌唑嗪对甲状腺功能亢进动物的这一0.4赫兹成分无影响。
这些数据表明，在早期实验性甲状腺功能亢进中，血管和心脏交感神经张力功能减退。固有心率的显著升高可能是心动过速的主要决定因素。血压升高可能通过反射诱发迷走神经激活和交感神经（血管和心脏）抑制。
