Zwillich C W, Matthay M, Potts D E, Adler R, Hofeldt F, Weil J V
J Clin Endocrinol Metab. 1978 Mar;46(3):491-500. doi: 10.1210/jcem-46-3-491.
To elucidate the role of the beta-sympathetic system in thyrotoxicosis (THY), we examined cardiac sensitivity to infused beta-agonist and compared the effect of beta-blockade with that of resolution of the hyperthyroid state. Beta-sympathetic (beta-SYM) sensitivity was measured as the heart rate response to isoproterenol in THY patients and in normal subjects. The patients with THY showed both lower threshold (P less than 0.05) and increased slope (P less than 0.05) of the heart rate-isoproterenol response, suggesting beta-SYM hypersensitivity. The beta-SYM like features of THY were measured in 7 patients before and 7 days after beta-SYM blockade with propranolol (mean dose 411 +/- 32 mg/day [SEM]) which was shown to block the heart rate response to isoproterenol. These results were compared with those in a similar group of thyrotoxic patients rendered euthyroid with 131I. During beta-SYM blockade, heart rate decreased from 101 +/- 6.3 to 78 +/- 4.6 (P less than 0.01), but the elevated metabolic rate (V02), resting ventilation (VE), and increased hypoxic and hypercapnic ventilatory responses were not significantly affected. In the group rendered euthyroid with 131I, heart rate decreased from 110 +/- 3.5 to 76 +/- 7.8 (P less than 0.02), but in contrast to the result of beta-SYM blockade, a 28% decrease in VO2 (P less than 0.01), 41% decrease in VE (P less than 0.05), a 38% decrease in hypercapnic ventilatory response (P less than 0.05), and a 66% decrease in hypoxic response (P less than 0.03) occurred. During THY, beta-SYM mechanisms are responsible for part of the tachycardia, but the metabolic and ventilatory abnormalities are not beta-SYM mediated.
为了阐明β-交感神经系统在甲状腺毒症(THY)中的作用,我们检测了心脏对静脉注射β-激动剂的敏感性,并比较了β-受体阻滞剂与甲状腺功能亢进状态缓解后的效果。通过甲状腺毒症患者和正常受试者对异丙肾上腺素的心率反应来测量β-交感(β-SYM)敏感性。甲状腺毒症患者的心率-异丙肾上腺素反应表现出较低的阈值(P<0.05)和增加的斜率(P<0.05),提示β-SYM过敏。在7例患者中,用普萘洛尔(平均剂量411±32mg/天[SEM])进行β-SYM阻断前后测量了甲状腺毒症的β-SYM样特征,结果显示普萘洛尔可阻断心率对异丙肾上腺素的反应。将这些结果与一组用131I治疗使甲状腺功能恢复正常的类似甲状腺毒症患者的结果进行比较。在β-SYM阻断期间,心率从101±6.3降至78±4.6(P<0.01),但代谢率升高(V02)、静息通气(VE)以及低氧和高碳酸通气反应增加均未受到显著影响。在用131I治疗使甲状腺功能恢复正常的组中,心率从110±3.5降至76±7.8(P<0.02),但与β-SYM阻断的结果相反,V02下降了28%(P<0.01),VE下降了41%(P<0.05),高碳酸通气反应下降了38%(P<0.05),低氧反应下降了66%(P<0.03)。在甲状腺毒症期间,β-SYM机制是心动过速的部分原因,但代谢和通气异常并非由β-SYM介导。