Stroke-prone spontaneously hypertensive rats lose their ability to auto-regulate cerebral blood flow prior to stroke

Objectives We hypothesized that the loss of cerebral blood flow (CBF) auto- regulation under hypertensive conditions could promote cerebrovascular over -perfusion and haemorrhage formation. The possibility that CBF autoregulati on becomes defective prior to haemorrhagic stroke development was assessed in Wistar-Kyoto stroke-prone spontaneously hypertensive rats (SHRsp) and re lated to the myogenic responsiveness of the cerebrovasculature to pressure. Methods Laser Doppler techniques were used to measure relative CBF in relat ion to mean arterial pressure (MAP 130-260 mmHg) within the perfusion domai ns of the middle (MCA) and posterior (PCA) cerebral arteries. The ability o f isolated MCAs and PCAs to constrict to a 120 mmHg pressure step (pressure -dependent constriction) was measured using a pressure myograph. Results Two weeks prior to stroke, 10-week-old pre-stroke SHRsp exhibited n ear-constant CBF regulation to a 200 mmHg MAP. Thirteen-week-old pre-stroke SHRsp and age-matched post-stroke SHRsp lost their ability to auto-regulat e CBF in the MCA and PCA perfusion domains. CBF increased at a high rate an d in a linear manner with MAP. A distinct upper limit to CBF auto-regulatio n was absent. Pressure-dependent constriction was attenuated prior to strok e, and lost after stroke in isolated MCAs, but not the PCAs, of SHRsp. Conclusions The loss of CBF auto-regulation prior to stroke in SHRsp could enhance cerebral perfusion and facilitate the initiation of haemorrhage. Su ch dysfunction after stroke could produce secondary haemorrhages. Defects i n pressure-dependent constriction cannot fully account for the pattern of C BF auto-regulation loss observed in post-stroke SHRsp. J Hypertens 1999, 17 :1697-1705 (C) Lippincott Williams & Wilkins.