Intracerebral haemorrhage is a strong stimulus for both microglial and astroglial activations. There are some important pathophysiological features during haemorrhage that do not occur in ischaemic or traumatic brain injuries, and may influence the dynamics and intensity of glial activation. Studies on the evolution of glial reaction may have practical importance to the introduction of new therapeutic methods for influencing the inflammatory reaction during haemorrhage. Microglial and astroglial responses to experimental intracerebral haematoma were studied in 50 adult rats for 5 minutes after injection of 100 microl autologous arterial blood into the striatum. The survival period varied from 1 to 21 days. Microglial-macrophage lineage cells were immunocytochemically stained with antibodies OX42, OX6 and ED1. The astrocytic population was studied by means of anti-GFAP staining. Changes in cellular morphology and intensity of staining were time-dependent reactions in both microglial and astroglial cells. Strong activation of microglial-macrophage lineage cells revealed with OX6-and OX42-immunoreactivity started during the first postoperative day. The complete pattern of activation for ED1-immunoreactivity was observed from the third postoperative day. At this stage, numerous phagocytic macrophages started to appear in the perihaematoma region. Morphological changes were most intensive during the second postoperative week. The astroglial (anti-GFAP) reaction was observed after the third postoperative day and proceeded less dynamically. The glial reaction gradually stopped but not completely during the period of observation. The early occurrence of glial activation, pattern of morphological changes and characteristic sequence of antigens expression indicate a very intense type of glial reaction. Evolution of glial response to haemorrhage reveals characteristic features. In our opinion, the initial phase of glial activation, comprising 72 hours after the occurrence of haemorrhage, is potentially the most promising period for influencing the extent of glial reaction with therapeutic agents.