The Study Of Expression Of NOS And ICAM-1 In Cerebral Ischemia Induced By Homologous Blood Clot Emboli In Rats

Objective: To investigate the temporal profiles of ICAM-1 protein and NOS expression and their relation in multi-focal cerebral infarct induced by homologous blood clot emboli.Methods: 48 male SD rats were subjected to multi-focal cerebral infarct by injection 0.5ml suspension of their homologous clot emboli into the internal carotid artery (ICA) through polyethylene tubing previously retrogradely inserted from external carotid artery (ECA). To gain brain tissues in a variety of durations from 1 h to 14 day after the insult, 6 normal and 6 control animals were employed. Immunohistochemical and NADPH-d histochemical methods were used to identify specific cell types expressing ICAM-1 protein and NOS in brain sections, respectively and synchronously. In addition, 9 male SD rats were subjected to the same model, 9 normal and 9 control rats were employed. They were processed to step-through test by 9th and water maze test by 11th after onset.Results: ICAM-1 protein was detected 1 h after the onset, maximized at 2 h, and persisted out to 3 day, fell toward baseline by 7 day. The number of NOS neurons was increased 1,2,4 and 12h after the insult(P>0.05),mild difference to that of control, decreased by 24h and 3 day ,approached to normal by 7 and 14 day (P>0.05).The time courses of ICAM-1 and NOS expression were equivalent in this study, but NOS expression changes were mild. The latent period and mistakes of model rats were more than that of normal and control rats in step-through test for 2 consecutive days. The rats after the onset showed prolongation of the escape latency in the water maze task starting and enhanced mistakes for 3 consecutive days. The normal and control rats showed less and less the escape latency and mistakes than model rats, indicating learning, memory and spacial function. Conclusions: The endothelium itself upregulates ICAM-1 in response to the stimulus of ischemia/reperfusion. ICAM-1 and NOS commonly participates in cerebral ischemia injury. The rats after embolism show learning ,memory and special dysfunction.