MODULATION OF THE IMMUNOLOGICAL RESPONSE TO ACUTE STRESS IN HUMANS BYBETA-BLOCKADE OR BENZODIAZEPINES

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.