Ekeberg O, Kjeldsen S E, Eide I K, Greenwood D T, Enger E
Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.
Clin Pharmacol Ther. 1990 May;47(5):599-607. doi: 10.1038/clpt.1990.81.
Cardiovascular and sympathoadrenal effects of short-term oral treatment with beta 1-blockade (atenolol, 50 mg, administered two times) and beta 2-blockade (ICI 118,551, 50 mg, administered three times) were compared with placebo during actual flying in subjects with flight phobia (n = 34). beta 1-Blockade lowered resting blood pressure and heart rate and prevented a heart rate response but not a blood pressure response to this psychologic stress. beta 2-Blockade minimally lowered resting heart rate and prevented a heart rate response, but it failed to lower resting blood pressure or blood pressure response to the stress. Plasma epinephrine increased with all three treatments and more with beta 1-blockade than with placebo. Plasma norepinephrine decreased with administration of beta 2-blockade. Thus neither beta 1- nor beta 2-blockade prevents an increase in blood pressure during acute flight phobia stress. Increased plasma epinephrine seems to be the sympathetic variable that is closest related to this increase in blood pressure. Norepinephrine may be less consistently related to the blood pressure rise during flight phobia stress as shown by the decrease in plasma norepinephrine with administration of beta 2-blockade.
在飞行恐惧症患者(n = 34)实际飞行期间,将β1受体阻滞剂(阿替洛尔,50毫克,给药两次)和β2受体阻滞剂(ICI 118,551,50毫克,给药三次)短期口服治疗的心血管和交感肾上腺效应与安慰剂进行了比较。β1受体阻滞剂降低静息血压和心率,并预防了对这种心理应激的心率反应,但未预防血压反应。β2受体阻滞剂轻微降低静息心率并预防了心率反应,但未能降低静息血压或对该应激的血压反应。三种治疗均使血浆肾上腺素增加,且β1受体阻滞剂组比安慰剂组增加更多。给予β2受体阻滞剂后血浆去甲肾上腺素降低。因此,无论是β1受体阻滞剂还是β2受体阻滞剂都不能预防急性飞行恐惧症应激期间血压的升高。血浆肾上腺素增加似乎是与这种血压升高最密切相关的交感神经变量。如给予β2受体阻滞剂后血浆去甲肾上腺素降低所示,去甲肾上腺素与飞行恐惧症应激期间血压升高的相关性可能不太一致。