Rj. Benschop et al., MODULATION OF THE IMMUNOLOGICAL RESPONSE TO ACUTE STRESS IN HUMANS BYBETA-BLOCKADE OR BENZODIAZEPINES, The FASEB journal, 10(4), 1996, pp. 517-524
Acute stress evokes immediate responses in the cardiovascular, endocri
ne, and immune systems, In particular, the number and activity of natu
ral killer (NK) lymphocytes increase after stress. Here, we investigat
e the possibility to pharmacologically interfere with these stress-ind
uced immunologic changes. Twenty-five healthy males were subjected to
an acute stressor, a first-time tandem parachute jump. Subjects were r
andomly assigned to a beta-adrenoceptor antagonist (propranolol), a be
nzodiazepine (alprazolam), or placebo group. To analyze the role of th
e spleen in lymphocyte redistribution, splenectomized subjects perform
ed a parachute jump. Propranolol, but not alprazolam, inhibited the he
art rate increase during jumping. Increases in epinephrine and cortiso
l in the propranolol group were comparable to placebo, but were attenu
ated by alprazolam. The number and activity of NK cells significantly
increased in the placebo group but not in the propranolol group immedi
ately after stress. Alprazolam treatment did not alter the increase in
NK cell numbers but did inhibit the increase in Nh activity. In splen
ectomized subjects, NK cell numbers, but not NK activity, increased as
in placebo subjects. We conclude that stress-induced changes in the i
mmune system are controlled by P-adrenergic mechanisms and only partly
depend on the spleen; central interference with alprazolam differenti
ally affects stress-induced changes in the NK cell compartment.