Objective      To investigate the characteristics of intracerebral hemorrhage and cerebral microvascular architecture changes in spontaneously hypertensive rats (SHR) and normotensive WistarKyoto rats (WKY) after high salt intake.  Methods       Sixty SHR rats and 60 WKY (male’ 6 weeks old) were randomly divided into 2 groups though the random number table. One group was fed with high salt diet

and the other with normal salt diet. Tail arterial systolic pressure was measured weekly

and behavioral changes and neurological deficit score were observed and evaluated everyday. HE staining was used to observe the hematoma characteristics

wet-dry weighing was used to detect cerebral water content

Evan’s blue staining  was used to observe the permeability of blood brain barrier

immunofluorescence staining was performed to observe cerebral microvascular changes

and transmission electron microscopy was employed to observe cerebrovascular ultrastructure and tight connection changes after 8 weeks’ feeding.   Results       Compared with the 2 normal salt diet groups

high salt diet induced to increased blood pressure

neurological deficits

enhanced brain water content

and increased permeability of blood brain barrier. HE staining showed ring exudative hemorrhage around the blood vessels. Immunofluorescence staining displayed the discontinuous changes in cerebral microvessels. Transmission electron microscopy showed the widened gap between cerebral blood vessels and surrounding tissues

disappeared tight junctions

uneven thickness and vacuolar changes in the vascular wall. All of above changes were more significant in SHR rats than the WKY rats (P0.01). All of high salt SHR rats died at the age of 18 weeks

and the high salt WKY group died at the age of 19 weeks

but all of normal salt rats survived.  Conclusion       High salt diet induces blood pressure increase and cerebral microvascular structure changes

and hypertension aggravates cerebral microvascular injury in the rats. The 2 conditions can promote the occurrence of cerebral hemorrhage.