&NA;Intimal accumulation of indium‐111‐labeled platelets in the middle cerebral arteries was examined in two different models of experimental subarachnoid hemorrhage (SAH) in the cat. SAH was produced in 7 subjects by a transorbital rupture of the right middle cerebral artery (RMCA) and in 10 subjects by the transorbital cisternal injection of 2 ml of autologous arterial blood around the RMCA. Animals in both experimental groups were sacrificed at 2, 4, 24, and 48 hours after SAH. The radioactivity (in counts per minute) of the RMCA segment was divided by that of the left middle cerebral artery (LMCA) to produce a radioactivity ratio (RMCA/LMCA). This radioactivity ratio was determined for each animal and was scored as positive if it was 1.25 or greater, and as negative if it was less than 1.25. The scores derived from the radioactivity ratios in both experimental SAH groups were mostly positive (86 and 70%, respectively) and were significantly different (P< 0.05) from those of intact controls (n = 7) or sham‐operated controls (n = 5; n = 4). There was, however, no significant difference (P= 0.35) between the scores of the two experimental groups in the first 48 hours after SAH. The results indicate that subarachnoid blood placed upon the adventitial surface of intact cerebral arteries activates platelet aggregation to a degree comparable to that which occurs after mechanical vessel rupture in the acute stages of SAH. We suggest that the noxious agents responsible for arterial injury and subsequent intimal platelet aggregation after SAH exert their influence primarily from the abluminal surface of the cerebral artery. (Neurosurgery24:487‐490, 1989)