The functional state of platelets and their possible impairment in res
ponse to various stimuli were assessed in saline-diluted citrated bloo
d samples of normal male central subjects (n = 27), and in schizophren
ic patients with (n = 34) and without(n = 23) haloperidol treatment. I
n response to collagen, but not to arachidonic acid (AA) and adenosine
diphosphate, platelet aggregation (as measured by changes in impedanc
e) was significantly higher in both haloperidol-treated and drug-free
schizophrenic patients than in normal control subjects. Comparison of
the secretion traces, however, indicated that only AA-induced adenosin
e triphosphate (ATP) release was significantly lower in haloperidol-tr
eated schizophrenic patients than in normal control subjects. In respo
nse to thrombin, collagen, and AA, the mean values of ATP release from
drug-free patients were significantly higher than those from the same
individuals when they were receiving haloperidol. Furthermore, there
was a trend toward increased ATP release (in response to thrombin or c
ollagen) in the nonrelapsed group of drug-free schizophrenic patients
as compared with the relapsed group. The collagen-induced platelet agg
regation or dense granule secretion in drug-free patients was correlat
ed significantly and negatively with psychosis ratings. Such changes i
n platelet function of schizophrenic patients were not correlated sign
ificantly with daily haloperidol dose, plasma haloperidol levels, age
of subjects, age of onset, or duration of illness.