Lever E G, Trosser A, Smith C
Department of Medicine, King's College Hospital, London.
Clin Endocrinol (Oxf). 1987 May;26(5):521-30. doi: 10.1111/j.1365-2265.1987.tb00807.x.
The effect of TRH (200 micrograms) on blood pressure, pulse rate, TSH and GH release was investigated in 10 acromegalics, four patients with non-GH secreting pituitary tumours, and seven normal controls. TRH produced a rapid-onset, short-lived pressor response in the acromegalic group (delta mean blood pressure 33 mmHg) compared to the two control groups (P less than 0.001). There was no response to the same volume of saline. The pressor response in the acromegalic group was not different in those who did or did not release GH. The pressor response to TRH was linearly related over the range 50-200 micrograms. Measurement of plasma noradrenaline and plasma renin activity during TRH testing in six acromegalics indicated that the pressor effect was neither mediated by adrenergic mechanisms, nor the renin-angiotensin system. Echocardiographic monitoring in five of these six patients showed that there was a significant increase in directly measured end systolic, end diastolic dimensions and heart rate (all P less than 0.02), and calculated stroke volume (P less than 0.001) and cardiac output (P less than 0.01) without changes in systemic vascular resistance. These data suggest that increase in preload, probably via venoconstriction, is the most likely factor producing the pressor response to TRH in acromegalics.
在10例肢端肥大症患者、4例非生长激素分泌型垂体瘤患者及7名正常对照者中，研究了促甲状腺激素释放激素（TRH，200微克）对血压、脉搏率、促甲状腺激素（TSH）及生长激素（GH）释放的影响。与两个对照组相比，TRH在肢端肥大症组产生了起效迅速、持续时间短的升压反应（平均血压变化33毫米汞柱）（P<0.001）。给予相同容量的生理盐水则无反应。肢端肥大症组中，无论是否释放GH，对TRH的升压反应均无差异。在50 - 200微克范围内，对TRH的升压反应呈线性相关。对6例肢端肥大症患者在TRH试验期间测定血浆去甲肾上腺素和血浆肾素活性，结果表明升压作用既不是由肾上腺素能机制介导，也不是由肾素 - 血管紧张素系统介导。这6例患者中的5例经超声心动图监测显示，直接测量的收缩末期、舒张末期内径及心率均显著增加（均P<0.02），计算得出的每搏输出量（P<0.001）和心输出量（P<0.01）增加，而全身血管阻力无变化。这些数据表明，可能通过静脉收缩导致的前负荷增加是肢端肥大症患者对TRH产生升压反应的最可能因素。
