Why the study?
Does short-term oral beta 1- or beta 2-blockade prevent blood pressure and sympathetic responses to acute flight phobia stress in subjects with flight phobia?
Does short-term oral beta 1- or beta 2-blockade prevent blood pressure and sympathetic responses to acute flight phobia stress in subjects with flight phobia?
Short-term beta-blockade does not prevent the blood pressure surge associated with acute flight phobia stress, which appears to be driven primarily by increased plasma epinephrine.
Short-term beta-blockade fails to blunt blood pressure surges in acute flight phobia stress; leaves open epinephrine-driven mechanisms and requires prospective confirmation before clinical consideration.
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.
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Ekeberg et al. (1990) studied this question.
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