[Changes in endothelial cellular adhesion molecule mRNA expressions in the cerebral blood vessels of rats with prestroke condition caused by simulated cold wave].

OBJECTIVE: To study the changes in the mRNA expression of endothelial cellular adhesion molecules in the cerebral blood vessels in rats with prestroke condition caused by simulated cold wave. METHODS: Two-kidney two-clip renovascular hypertension was induced in 48 male SD rats, which were subsequently randomly assigned into cold wave exposure and non-exposed group (n=24). Each group was further divided into 4 sub-groups according to their systolic blood pressure, namely the sham-operated group with blood pressure (BP)<140 mmHg, mild hypertensive group with BP of 160-199 mmHg, moderate hypertensive group with BP of 200-219 mmHg, and severe hypertensive group with BP no less than 220 mmHg. Cold wave exposure was simulated by housing the rats in an artificial climate chamber with 3 cycles of 12 h light at 22 degrees celsius; and 12 h dark at 4 degrees celsius;. The non-exposed group was kept at 22 degrees celsius; throughout the experiment. After the exposure, the rats were sacrificed and the tissues of the frontal lobe were slice into 2.0-mm-thick coronal sections for real-time RT-PCR detection of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and p-selectin mRNA expressions. The 5.0-microm-thick frozen sections from the bregma section underwent in situ hybridization of VCAM-1, ICAM-1, and p-selectin. The other sections were stained with HE to observe the infarct lesions, and the rats with cerebral infraction were excluded from the statistical analysis. RESULTS: In rats with cold wave exposure-induced prestroke condition and BP <220 mmHg, VCAM-1, ICAM-1, and p-selectin mRNA expressions all increased compared with those in the non-exposed group. In rats with BP>or=220 mmHg and cold exposure, the expressions all decreased to some extent compared with those in the non-exposed treatment. In the non-exposed rats, a positive correlation of BP to VCAM-1, ICAM-1, and p-selectin mRNA expressions were noted, and this correlation was also found in cold-wave-exposed rats with BP <220 mmHg; VCAM-1, ICAM-1, and p-selectin mRNA expressions decreased dramatically in the exposed rats with BP >or=220 mmHg compared with those in rats with BP <220 mmHg. CONCLUSION: Persistent and severe hypertension impairs the modulatory function of the cerebral vascular endothelia, which is a prerequisite for the stroke vulnerability. The modulatory function deteriorates as the BP further increases.

dl-3n-butylphthalide prevents stroke via improvement of cerebral microvessels in RHRSP.

The purpose of the study is to establish a model of cold-induced stroke in hypertensive rats, and to study the preventive effect of dl-3n-butylphthalide ( NBP ) on stroke. Stroke-prone renovascular hypertension(RHRSP) was created in Sprague-Dawley rats. The animals were assigned randomly to NBP, aspirin treated and vehicle control group, with administration of the medications for 7 days, and then subjected to cold treatment in an environmentally controlled chamber for 3 days to induce the occurrence of stroke. The incidence of stroke, the volume of the brain lesion, patency of the microvessels by FITC-dextran perfusion and the number of microvessels by immunohisochemical detection of vwF were investigated. Cold induced different types of stroke in RHRSP. The incidence of ischemic stroke and the volume of the infarct were decreased, and the perfused microvessels were increased with NBP pretreatment. Our data suggest that NBP prevents cold-induced ischemic stroke via improvement of cerebral microvessels.