1 Isolated strips of human or baboon basilar, middle cerebral, vertebral or common carotid arteries were set up in an isolated organ bath or in a superfusion cascade system. 2 These arteries relaxed to prostacyclin but contracted to prostaglandin endoperoxide (PGH2). 3 Human and baboon isolated arteries also generated prostacyclin from exogenous endoperoxide (PGH2). 4 Human arteries generated prostacyclin 36 h post‐mortem but not 40 h post‐mortem. The biologically generated prostacyclin relaxed the basilar artery and overcame the contractile effects of PGH2. 5 Thromboxane A2‐like activity generated during human platelet aggregation by arachidonic acid caused contractions of the human basilar artery. 6 Prostacyclin reversed contractions of human basilar arteries caused by an unidentified vasoconstrictor factor in cerebrospinal fluid obtained from patients with cerebral arterial vasospasm after subarachnoid haemorrhage following rupture of cerebral arterial aneurysms. 7. The above vasospasm may be due at least in part to disordered physiological control of the calibre of cerebral arteries caused by diminished synthesis of prostacyclin.

SYNOPSISThe isolated human basilar artery suspended in Krebs' solution contracts to 5-hydroxytryptamine, noradrenaline, and histamine, which stimulate specific receptors. Normal human serum contains an unidentified contractile substance, and erythrocytes relax the artery. Serum and erythrocytes potentiate 5-HT contractions. This preparation is suitable for studying vasoactive substances released during vasospasm after subarachnoid haemorrhage.

1 The aggregation response of platelets induced by 5‐HT was greatly increased in psychiatric patients receiving chlorpromazine therapy when compared with normal volunteers and psychiatric patients not receiving chlorpromazine. 2 Platelet aggregation responses to ADP were normal during chlorpromazine therapy, but 5‐HT induced aggregation was increased in rate and the typical transient reversible response was converted to an irreversible response in all subjects. This was usually indistinguishable from the ADP response. 3 When chlorpromazine therapy was stopped, plasma concentrations of chlorpromazine, monodesmethylchlorpromazine and chlorpromazine sulphoxide fell rapidly within one week, whereas 5‐HT induced platelet aggregation responses became normal after three weeks. The enhanced responses returned when chlorpromazine therapy was re‐instituted. 4 It is possible that platelet aggregation responses to 5‐HT in vitro could prove to be a useful index of the pharmacological effect of chlorpromazine in vivo.

6. Prostaglandin E1 also reversed ADP aggregation when added to platelet-rich plasma after the nucleotide, with an accompanying decrease in platelet bound [14C]ADP.7. It is concluded that ADP induces platelet aggregation by binding to

1 Platelet aggregation responses to 5-HT and adenosine diphosphate were examined in a population of eighteen patients treated with fluphenazine decanoate for longer than one year.2 5-HT induced aggregation was enhanced in ten subjects. This enhancement was similar to that previously described in patients receiving chlorpromazine. 3 Patients who showed enhanced 5-HT induced aggregation showed less rateable psychopathology and less extrapyramidal side-effects than patients who did not show enhancement. 4 These findings suggest that platelet aggregation responses could be used to identify patients who could be safely withdrawn from long-term neuroleptic therapy.